Download Handbook for Vascular Risk Assessment, Risk Reduction and

A REPORT PREPARED FOR THE UK NATIONAL SCREENING COMMITTEE
BY
MELANIE DAVIES
KAMLESH KHUNTI
UMESH CHAUHAN
BERNIE STRIBLING
ELIZABETH GOYDER
AZHAR FAROOQI
JAYNE HILL
STEVE HILES
NICK TAUB
MARIAN CAREY
MICHAEL BONAR
PROFESSOR OF DIABETES MEDICINE, DEPARTMENT OF
CARDIOVASCULAR SCIENCES, UNIVERSITY OF LEICESTER
PROFESSOR OF PRIMARY CARE DIABETES AND VASCULAR MEDICINE,
UNIVERSITY OF LEICESTER
TRAINING FELLOW, NATIONAL PRIMARY CARE RESEARCH &
DEVELOPMENT CENTRE, UNIVERSITY OF MANCHESTER;
GP ADVISOR TO THE UK NATIONAL SCREENING COMMITTEE
PROJECT MANAGER (CKD): KIDNEY RESEARCH UK
SENIOR CLINICAL LECTURER PUBLIC HEALTH, SCHOOL OF HEALTH &
RELATED RESEARCH, UNIVERSITY OF SHEFFIELD
GENERAL PRACTITIONER, EAST LEICESTER MEDICAL PRACTICE
ADDITION STUDY CO-ORDINATOR DIABETES RESEARCH,
UNIVERSITY HOSPITALS OF LEICESTER
DIABETES RESEARCH ASSOCIATE,
UNIVERSITY HOSPITALS OF LEICESTER
RESEARCH FELLOW IN MEDICAL STATISTICS, UNIVERSITY OF LEICESTER
NATIONAL DIRECTOR : THE DESMOND PROGRAMME
PROGRAMME MANAGER : THE DESMOND PROGRAMME
Copyrights and acknowledgements
Except for as stated below all copyright belongs jointly to the University of Leicester and the UK National Screening Committee:
© University of Leicester and the UK National Screening Committee 2008.
The figures on pages 45, 46 and 130 are reproduced with kind permission from the BMJ Publishing Group. All rights reserved.
All images (including but not limited to images, figures, tables and algorithms, whether labelled as such or not) on pages 11, 34, 35, 59, 60,
61, 62, 63, 64, 67, 82, 83, 107, 108, 109, 110, 114, 115, 124, 131 and 133, are the sole copyright of the University of Leicester.
© University of Leicester 2008
All rights reserved. No part of this publication may be reproduced, or stored in a database or retrieval system, distributed, or transmitted, in
any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without prior written permission of the University
of Leicester and the UK National Screening Committee.
002
FOREWORD
FOREWORD TO UK NATIONAL SCREENING COMMITTEE HANDBOOK ON VASCULAR RISK ASSESSMENT
Cardiovascular disease, diabetes and chronic kidney disease between them cause a huge amount of ill health
and premature death. Our understanding of the most effective approaches to prevention, risk assessment and
management of these diseases has developed considerably in recent years.
These diseases manifest themselves in very different ways, but they share the same set of risk factors: poor diet,
obesity, lack of physical activity, high blood pressure and smoking. And the risk factors interrelate with each
other – somebody with diabetes is at much higher risk of developing heart disease than someone without it.
This handbook brings together in one place information on our current state of knowledge about vascular risk
assessment, risk reduction and risk management. It has been designed to be comprehensive, giving an
overview of the latest state of knowledge. The handbook reviews the clinical context and the available evidence
in relation to risk assessment for these diseases. It goes on to give an overview of interventions and management of specific risk factors. The final section includes standard operating procedures for running risk assessment programmes and has useful examples to help front-line staff.
It draws together existing, guidelines and tools available for CVD, diabetes and chronic kidney disease. It also
builds on the experience and evaluation of the Diabetes and Heart Disease Screening Pilots commissioned by
the UK National Screening Committee, which reported in 2006.
The handbook is the product of great deal of dedicated hard work by Professor Melanie Davies and her team of
colleagues at the University of Leicester. We warmly congratulate her on its publication and we recommend it to
the healthcare and public health community as an invaluable resource.
Dr Anne Mackie
Programme Director
UK National Screening Committee
Sir Muir Gray
Formerly Programme Director
UK National Screening Committee
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CONTENTS
The handbook is intended above all to act as a practical guide and resource to those who provide and commission services for people with, or who have risk factors for, vascular disease.
CONTENTS
PART 1_Section 1
Remit of the Handbook
Background
Overview of this Handbook
Overarching Aims of a Programme
Broad Scope of the Programme
A Strategic Framework for Delivery of Vascular Risk Assessment and Risk Reduction
Record Based Strategy
Population Based Strategies for Vascular Risk Assessment
Sporadic and Opportunistic Risk Assessment Activities
Impact of Health Inequalities
CVD Score and Social Deprivation
Understanding the Purpose and Concept of Vascular Risk Assessment and Reduction
Communication of Risk
Reference List
PART 1_Section 2 Clinical Context & Review of the Evidence
Cardiovascular Disease; Coronary Heart Disease, Stroke, Transient Ischaemic Attacks and
Peripheral Arterial Disease.
The Need for Vascular Risk Assessment in Those at High Risk
The Approach to Multi-factorial CVD Risk Assessment
Cardiovascular Risk Assessment Methods
Choice of CVD Risk Assessment Score
Limitations of Risk Factor Assessment Using CVD Risk Scores
CVD Risk factors not taken into account using conventional CVD Risk Prediction Charts
Evaluation of Scientific Evidence: Bias Towards RCTs of Single Pharmaceutical Therapies
Potential Shortcomings of Using a CVD Risk Assessment Approach in Isolation
Chronic Kidney Disease
Defining CKD
Identifying CKD Earlier
Diabetes Mellitus
Screening, Early Detection and Prevention of Diabetes
Lessons from Diabetes, Heart Disease and Stroke (DHDS) Pilot
Implications for Policy and Practice from the DHDS
Measure-up Campaign from Diabetes UK
The Continuous Relationship Between Blood Glucose Levels and Vascular Outcomes Below
the Threshold for Diagnosing Diabetes
Preventing Progression to Diabetes
Use of Glucose Testing to Detect Undiagnosed Diabetes and Its Utility in Detecting IGR
Recent Data From Screening Studies in Leicester
Activities in Finland Regarding Vascular Risk Assessment and Prevention of Diabetes
The FINDRISC Diabetes Risk Score
Type 2 Diabetes Risk Assessment Form (FINDRISC Test)
Comparison of Different Strategies to Identify those with Impaired Glucose Regulation
Black and Minority Ethnic Issues (BME)
Reference List
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PART 1_Section 4 Implications and Public Health Perspective
Issues for Primary Care Trusts and Directors of Public Health
Review of Current Cardiovascular Risk Reduction Activities
Identification of Resource Implications, Costs and Benefits
Assessing Costs/Resource Implications
Assessing Potential Benefits
Assessing Potential Harm
Reducing Inequalities
Establishing Mechanisms for Evaluation and Audit
Other Issues
Screening Personnel
Data Recording
Reference List
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PART 2_Section 1 Implementation of Vascular Risk Assessment Programme; Broad Overview
Record Based - Existing Disease Registers
What the Practice Needs to Have in Place
Record Based – Procedure 2 ‘At Risk’ Registers
Clinical Assessment of Vascular Risk
List of Additional SOPs for Procedure 2 with Examples of all in SOP Section
Population-based screening
Self Assessment
Sporadic Activities
Reference List
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CONTENTS
PART 1_Section 3 Vascular Risk Management
Overview of the Efficacy of Interventions
Management of Specific Risk Factors
Smoking
Diet
Management of Obesity
Drug Management of Obesity
Lifestyle Advice for Those at High Risk of DM
Other Dietary Factors
Omega 3 Fatty Acids
Dietary Salt Intake
Fruit and Vegetable Intake
Antioxidant Vitamin Supplementation
Stanol Esters and Plant Sterols
Alcohol
Promoting Physical Activity
Hypertension
Interventions for Blood Pressure (BP)
Cholesterol and Lipid Lowering
The Benefits of Lowering Cholesterol for Cardiovascular Risk
Statin Therapy in High Risk Individuals without Cardiovascular Disease
Statin Therapy in Individuals with Established CVD
Cholesterol Targets for Therapy in Patients with Established Cardiovascular Disease
(Secondary Prevention)
Measuring Lipid Levels
Management of Cholesterol in Special Groups
Antiplatelet Therapies
Reference List
PART 2_Appendix
Comparison of Software Available for a Population Based CVD Risk Assessment Strategy
Development of the Vascular Component of the Mid Life Check
- Ongoing work at the University of Leicester
Prototype Life Check Cardiovascular Risk Self Assessment Tool
Screening for Diabetes - Recent Data from Screening Studies in Leicester
Development of the Leicester Diabetes and Pre-Diabetes Risk Score
Comparison of Strategies to Detect DM and (Pre-diabetes or Impaired Glucose Regulation) Using
FPG in all, or ‘Pre-Screening’ with either FINDRISC or the Leicester Diabetes and PDM Risk Score
Example of Prototype Leicester Diabetes and Pre-diabetes Risk Score
Intensity and Energy Expenditure for Common Types of Physical Activity
Comparison of Various Diabetes Risk Scores
Reference List
PART 2_Standard Operating Procedures
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Tables
Table 1 Prevalence of Total Cardiovascular Disease (CVD) (over 10 years)
Risk in Adults aged 40-74 in England, by Age and Sex
Table 2 K/DOQI Stages of CKD
Table 3 Diagnosis of Diabetes Mellitus (DM), Impaired Fasting Glucose (IFG)
and Impaired Glucose Tolerance (IGT)
Table 4 Performance of Screening Strategies for detection of T2DM and
Impaired Glucose Metabolism
Table 5 Dietary Advice for those at Risk of Vascular Disease
Table 6 Optimal and audit standard blood pressure BP targets
Table 7 ‘Record Based’ Procedure 1 Worked Example
Table 8 ‘Record Based’ Procedure 2 Worked Example
Table 9 Population Based Strategy Worked Example
Figures
Figure 1. Implementing Risk Prevention
Figure 2. Clinical Overview for Everyone in the Population to have CVD Risk Managed Appropriately
Figure 3. Implementation Overview of a Programme Framework
Figure 4. Record Based Strategy
Figure 5. Population Based Strategy
Figure 6. Approaches to Identification of IGR in the General Population
Figure 7. An Example of an Algorithm for Identification, Assessment and Intervention for those
at Increased Risk of Developing T2DM
Figure 8. Intervention Thresholds for Blood Pressure
Figure 9. ABCD Treatment Algorithm for Hypertension
Figure 10. ‘Record Based’ Strategy (Existing Disease Register) for Vascular Risk Assessment
Figure 11. ‘Record Based’ Strategy (at Risk Register) for Vascular Risk Assessment
Algorithms
Algorithm 1. ‘Record Based’ Strategy Procedure 1
Algorithm 2. ‘Record Based’ Strategy Procedure 2
Algorithm 3. Population Based Strategy
Algorithm 4. Self Assessment Approach
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PART 1_Section 1
Remit of the Handbook
The handbook, commissioned by the UK National Screening Committee [UK NSC],
u Describes the context, and outlines evidence for a co-ordinated vascular disease control programme to
identify and reduce risks of cardiovascular disease in the population.
u Suggests aims, objectives and a delivery strategy framework appropriate for a Cardiovascular Disease
(CVD) risk management programme.
u Reports key messages from the Diabetes, Heart Disease & Stroke (DHDS) pilot project.
u Provides examples of tools, resources and standard operating procedures that can be used by health
professionals, many of whom are already undertaking some CVD risk assessment in a variety of ways.
Background
u Several groups have highlighted the need for a co-ordinated vascular disease control programme that would
integrate prevention, screening, early detection and disease management for coronary heart disease
(CHD), stroke, transient ischaemic attacks (TIA), peripheral arterial disease (PAD), Type 2 diabetes (T2DM)
and chronic kidney disease (CKD). These conditions overlap considerably and often have similar risk factors.
u Throughout this report, the term CVD is used to include CHD, stroke, TIA, T2DM, PAD and CKD.
u The SIGN guideline on ‘Risk estimation and the prevention of cardiovascular disease’2 takes a similar
approach, as does the Joint British Society Guidelines Group3 in their most recent report on prevention of
cardiovascular disease in clinical practice.
u NICE produced a draft guidance for consultation in June 2007 on ‘Cardiovascular risk assessment: the
modification of blood lipids for the primary and secondary prevention of cardiovascular disease’4.
u The UK NSC advice, following the pilots of screening for T2DM, and a review of current research, is that
screening certain subgroups of the population for Type 2 Diabetes is feasible and should be taken forward,
but this should be part of a programme to detect and manage vascular risk factors.
It is appropriate that such a programme:
●
looks at overall vascular risk in individuals.
●
recognises that everyone in the UK is at some degree of risk of CVD, so that information and support to
reduce risk should be widely available to all, whilst a subset of the population at higher risk may require
more intervention to change lifestyle factors and consideration of pharmacological therapy.
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is proactive in the aim of reducing inequalities in CVD risk identification and management.
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integrates disease prevention with other public health activities aimed at detecting and reducing CVD risk,
as there is considerable overlap.
●
promotes a unified and systematic approach to delivery of preventive strategies for this group of conditions
that meets national standards, is cost effective and can be quality assured.
u In England, the National Service Frameworks for CHD, Diabetes and Renal disease have clear standards for
prevention and early detection of the conditions5-7. This handbook supports local health services in
addressing these standards.
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PART 1_Section 1
u The World Health Organisation defines a disease control programme as the co-ordination of disease
prevention, screening and early detection, as well as disease management1 (Figure 1).
Overview of this Handbook
u Part 1 describes the remit, rationale and clinical evidence for a holistic approach to CVD risk assessment,
which incorporates assessment of diabetes risk. It sets out a possible outline framework for a coherent
programme.
u Part 2 focuses on standard operating procedures (SOP’s) for disease prevention, screening, early detection
and CVD risk management in practice.
u It is important to remember that the evidence base is evolving;
u Figure 1. Implementing Risk Prevention1
Overarching Aims of a Programme
u To reduce premature death from related vascular conditions including CHD, CKD, DM, stroke, TIA and PAD.
u To reduce the incidence of these related vascular conditions.
u To narrow inequalities in premature death from these related vascular conditions.
Broad Scope of a Programme
u Primary reduction of single or multiple risk factors for CVD in the population as a whole
u Identification of those at high risk of CHD, CKD, Stroke, TIA or DM so that interventions can be delivered to
prevent disease*. This includes the opportunity to prevent two-thirds of cases of T2DM diabetes with lifestyle
intervention8-9.
u Identification of those already with CHD, CKD, Stroke, TIA or DM so these can be managed appropriately.
*High risk of DM will be identified at a younger age than high risk for CVD in many people, especially in Black and Minority Ethnic (BME)
populations
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Risk Surveillance
u To reduce future risk of CHD, DM, stroke, TIA, PAD and CKD
u To ensure that all communities have equal access to vascular risk assessment which is appropriate to
their risk factor profile and is appropriately adjusted according to ethnicity and socio-economic status
u To ensure that all potential interventions from single risk factor intervention, to identification of those at high
vascular risk and management of those with existing disease, are described at the level of the individual
across the organisational spectrum, that professional issues are accounted for and that all potential
systems and levers are used
Risk Communication
u To offer all adults undergoing a risk assessment feedback of the results with care planning and an
agreed action plan to help reduce their personal risk10
u To offer adults access, according to need, to an individual risk assessment through a number of different
strategies
u To promote healthy lifestyle with a focus on the determinants of health influence on the risk of DM, CHD,
stroke, TIA, PAD and CKD
u To detect undiagnosed diabetes while undertaking a vascular risk assessment in order to offer microvascular
screening for eye, renal and foot complications and CVD intervention at a lower threshold
Risk Management
u To integrate activities of the programme with primary prevention activities in the general population
u To ensure that all those already identified with CHD, stroke, TIA, PAD, CKD or DM are offered optimal secondary
intervention in line with existing NHS standards updated to reflect the best evidence
u To ensure that those identified as being of higher risk of DM are offered appropriate diagnostic testing
delivered according to agreed SOPs
u To ensure that the programme is properly quality assured and that there is ongoing surveillance of the
programme and its performance
u To ensure that there is clear guidance and SOPs for the implementation of vascular risk assessment
u To ensure that the overall programme of work does not increase, and preferably reduces, inequalities
in health
u To ensure the optimal integration of these policies with existing systems and initiatives, for example
Quality and Outcomes Framework (QOF)11, to avoid duplication and unnecessary testing and assessment.
u To identify those at high risk due to lifestyle factors but who do not reach the traditional CVD risk threshold for
intervention, usually because of their younger age, and offer them intensive lifestyle interventions
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PART 1_Section 1
Risk Assessment
A Strategic Framework for Delivery of Vascular Risk Assessment and Risk Reduction Programme
A clinical plan to ensure wide and equitable opportunity for cardiovascular risk assessment and management is
shown in Figure 2.
u Figure 2. Clinical Overview for Everyone in the Population to have CVD Risk Managed Appropriately
Four broad streams of activity make up a framework for delivering such a programme.
u
u
u
u
1) Record Based
2) Population Based
3) Self Assessment
4) Sporadic Activity or Opportunistic Testing
To ensure wide and equitable coverage all strategies may be implemented in parallel although the priority and
timeframe for implementation may vary (See Figure 3).
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u Figure 3. Implementation Overview of a Programme Framework
u Figure 4. Record Based Strategy
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Record Based Strategy (Figure 4.)
This will comprise two groups.
1. Those with existing vascular disease (CHD/LVD/Stroke/PAD/TIA)
2. Those who can be easily identified from routine practice data or existing registers (e.g. obesity or
hypertension, CKD registers) as being of ‘high’ vascular risk.
An alternative records based approach is using available routine primary care data to estimate CVD risk and
then prioritising risk management to identify those with a CVD risk score over the next ten years of ≥ 20%14.
Optimisation of outcomes for those with established vascular disease and screening for related conditions.
u For those with established vascular disease including those already on the CHD, Stroke/TIA and Left
Ventricular Dysfunction (LVD) registers, the need for detection of undiagnosed diabetes is justified by lower
intervention targets and opportunity for microvascular screening (for example access to National Diabetic
Retinopathy Screening Programme) that is offered once a diagnosis of diabetes is established.
Record based screening of those likely to be at high vascular risk.
u Interrogation of the existing registers of those who may be at higher risk of vascular disease. This would be
focused around the existing Obesity, Hypertension and CKD Registers, with all adults offered a
comprehensive vascular assessment.
Population Based Strategies for Vascular Risk Assessment (Figure 5.)
Refers to risk assessment being offered to those who have not been identified via the self-assessment or record
based approach. This approach was included in the Diabetes, Heart Disease and Stroke prevention (DHDS)
pilot project and has demonstrated that this is feasible in a primary care setting, including the most deprived
inner-city general practices15. Broadly, this approach would proactively target and invite subjects, either not
identified via the Record Based strategy or for whom no record or clinical data is available to allow record based
stratification of risk. This might commence from the age of 40 and be repeated every 5 years (see Figure 5). The
interval between assessments, if 10 year CVD risk is low at first, is likely to be not less than 5 years but subject
to clinical judgement for individuals. The use of formal CVD risk scoring in those over 75 years is not validated;
individual clinical assessment is appropriate.
u Figure 5. Population Based Strategy Example
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A modified version of the FINDRISC diabetes self-assessment tool has been suggested as a potential tool for
identifying people at risk of vascular disease12,13,17. Developed and used in Finland, and validated in other European countries, the tool is easy to complete and calculates an overall risk score ranging from 0 to 24 based on
data supplied by the individual. It does not assess information on BP lipids or blood glucose levels. Notably
FINDRISC does not assess smoking status. However, it has not been validated in a UK setting or in a BME population in the UK.
Sporadic and Opportunistic Risk Assessment Activities
This refers to a number of activities occurring in pharmacy chains, supermarket chains, food companies, occupational health departments or small businesses. These initiatives could make a major contribution, but do
need to;
u Be quality assured
u Ensure that information from such screening activities is integrated into patients’ general practice records.
u Ensure that the SOP for referral, diagnosis, risk management and intervention are clearly defined
and followed.
Impact of Health Inequalities
In England the Public Health White Paper, ‘Choosing Health- making healthier choices easier’ (2004) gave priority to tackling health inequalities so that all groups in society benefit from improvements in public health19.
The gap in life expectancy (at birth) for men between the richest 10% of areas and the poorest 10% is 6 years
(77.4 versus 71.4 yrs). For women, the gap is 3 years (81.2 versus 78.0 yrs)20.
Although people are living longer overall, the long-term trends show that the gap in mortality between the professional (social class I) and unskilled manual men (social class V) has increased by two and a half times in the
last 60 years21. Unemployed men are four times as likely to classify themselves as being in bad health as those
in the top social class22 and the geographical variation in health inequalities can largely be explained by deprivation23. An important target set for the Department of Health in England is to increase life expectancy at birth in
England to 78.6 years for men and to 82.5 years for women by reducing mortality from heart disease and stroke
and related diseases by at least 40% in people under 75, with at least a 40% reduction in the inequalities gap
between the fifth of areas with the worst health and deprivation indicators and the population as a whole24. The
Local Authorities and Primary Care trusts which make up the ‘fifth of areas with the worst health and deprivation
indicators’ the so called Spearhead Group, have been identified and one of the five factors for inclusion was
high CVD mortality rates in under 75 year olds24. An additional target is to narrow the gap in life expectancy between these areas in England by 10% by 2010 compared to the 1995-97 baseline. Work to identify and treat
those at risk of CVD is a key component in achieving these targets24.
CVD Risk Score and Social Deprivation
Any programme must consider its impact on, and aim to minimise, health inequalities. An example of a potential
impact on health inequalities is the choice of the use of the CVD Risk Assessment tool, as there is evidence that
use of conventional CVD risk calculators based on the Framingham data tend to overestimate CVD risk in low
prevalence populations and underestimate it in those at highest risk25-26. This is of particular relevance to the SouthAsian (SA) population and other BME groups living in the UK and all those living in deprived areas. Those at highest baseline risk as defined by ethnicity or socio-economic circumstances are less likely to access or benefit from
screening and early treatment, thus potentially leading to increasing inequalities27. One approach is to develop a
CVD risk score which takes account of social deprivation and uses FH as a proxy for the impact of ethnicity.
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An example of this is Diabetes Screening via pharmacies advocated by the Pharmaceutical Society
(www.rpsgb.org)18.
The ASSIGN score (Assessing cardiovascular risk using SIGN guidelines to ASSIGN preventative treatment) has
been developed to include social deprivation as a risk factor. The inclusion of family history provides an indirect
approach to ethnic susceptibility2,28,29.
ASSIGN uses similar classic risk factors to Framingham, entered as continuous variables rather than categories. It
includes the SIMD (Scottish Index of Multiple Deprivation) score for residential postcode. It also includes family
history of cardiovascular disease, defined as a coronary heart disease or stroke in parents or sibling below the
age 60 years or in several close relatives. Like Framingham it does not include obesity as a risk factor; unlike
Framingham it excludes left ventricular hypertrophy as a risk factor.
ASSIGN tends to classify more people with a positive family history who are socially deprived as being at highest
risk. When used in its own host population it abolished a large social gradient in future CVD victims not identified
for preventive treatment by the Framingham cardiovascular score. It therefore improved social equity, although
overall discrimination of future events was not greatly improved28,29. A demonstration of the ASSIGN tool is available at http://assign-score.com29.
Another approach has been to use QRISK30. This used data from UK practices contributing to the QRESEARCH
Database. A cardiovascular disease risk algorithm (QRISK) was developed in a derivation cohort (1.28 million subjects aged 35-74 years old). This algorithm used age, gender, smoking status, systolic blood pressure, ratio of
total cholesterol to HDL. In addition to conventional CVD risk scores it also used BMI, family history of CVD in first
degree relative, Townsend deprivation score and current prescription of at least one anti-hypertensive agent.
When applied to a validation cohort (0.61 million subjects), the QRISK was better calibrated to a UK population.
Overall the Framingham algorithm over predicted the CVD at 10 years by 35%, ASSIGN by 36% and QRISK by
0.4%30. QRISK has undergone external validation with ongoing pilot work to integrate it into GP systems31.
Understanding the Purpose and Concept of Vascular Risk Assessment and Reduction
All patients should expect to be given targeted and individualised advice about what they can do to reduce their
own individual risk rather than the all or nothing concept of a positive or negative result. The terminology needs
to be clear. Rather than “screening” one should use “risk assessment” and “risk reduction”. There is also a need
to manage patient expectation to avoid increasing dissatisfaction and the recognition that many patients expect
blood tests as part of their assessment process. This is particularly pertinent to blood glucose testing where a
‘negative’ test result for diabetes itself may not be helpful to exclude those at high future risk of DM and vascular
disease.
Communication of Risk
The key factors are;
u Communicating the continuum of risk
u Patient centred decision support
u Standardisation of measurement and recording of risk factors
Risk assessment involves identifying and recording risk factors. Within primary care this may be carried out by a
number of individuals and therefore standardising how these are measured and recorded is a priority. Patients
may have their blood pressure, weight, height, family history, smoking and alcohol status recorded without any
communication as to the reasons why this has been done and yet the act of doing so can be regarded by some
patients as receiving good care.
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Risk communication is defined as ‘the open, two way exchange of information and opinion about risk, leading to
better decisions about clinical management’32. Discussing risk with patients in the clinical consultation has become increasingly important. Patients who are better informed and involved in decisions about their own care
are more knowledgeable and also more likely to adhere to their chosen treatment plan32,33. Patients’ values and
preferences vary widely, as do their attitudes to risk. A two-way exchange of information is therefore important
to explore the patient’s personal beliefs to facilitate treatment decisions. It is possible for the healthcare professional to record risk factors, calculate risk scores and prescribe appropriate treatment without involving the patient in the decision-making process. Our aim should be to create a system where decision support is patient
centred and focused towards increasing patient understanding, and allow patients to use this to their best advantage.
It is increasingly apparent that most risk factors have a continuous relationship to risk of CVD and therefore it is
important to move away from using the “all or nothing” or “positive or negative” concept when talking to our patients, but talk in terms of risk and risk reduction. Although some research has looked at issues of risk communication in the areas of CHD and other areas of health, there is still much to be learned. Changes in attitude or
behaviour mainly occur when the individual or group identify with the threat, and people’s perception of risk may
are socially constructed, and individual behaviours are driven by perception, or beliefs about risks, and not with
the technical risk estimates provided by healthcare professionals.
Communication of risk is not straightforward. Clinicians need to support patients in making choices by turning
raw data into information that can be used to aid discussion of risk. Decision aids are one way of facilitating this
process. Decision aids are systematically developed tools to aid patients to understand and participate in medical decisions. Decision aids often include visual representations of risk information and relate this information to
more familiar risks. They can be in the form of booklets, DVDs, interactive computer programmes, tapes or webbased products. There is, however, very little evidence of the effectiveness of these aids in communicating risk in
patients at high cardiovascular risk34.
It is important to ensure that we develop systems to clearly communicate risks to our patients and to engage
them in prioritising them and implementing the changes that they wish to make in order to reduce their own individual risk. Structured education programmes such as the DESMOND Programme (Diabetes Education SelfManagement Ongoing and Newly Diagnosed) include a health profile in which patients assess their own risk and
then develop action plans to address this35-36. This is important, as a strong predictor of a patient’s readiness for
medical treatment and preventative behaviour is their perceived vulnerability to disease. We will be asking patients to take medicines and change their lifestyle when a combination of risk factors such as smoking, blood
pressure, cholesterol and age results in them breaching a certain threshold for CVD risk.
PART 1_Section 1 Reference List
1. The World Health Report. Reducing Risks, Promoting Healthy Life. 2002. http://www.who.int/entity/whr/2002/en/whr02_en.pdf
2. Scottish Intercollegiate Guidelines Network. Risk estimation and the prevention of cardiovascular disease: A national clinical guideline.
2007 http://www.sign.ac.uk/pdf/sign97.pdf
3. JBS 2: Joint British Societies' guidelines on prevention of cardiovascular disease in clinical practice. Heart 2005;91 Suppl 5:v1-52.
www.bcs.com/download/651/JBS2final.pdf
4. National Collaborating Centre for Primary Care. Cardiovascular risk assessment: the modification of blood lipids for the primary and
secondary prevention of cardiovascular disease - full guideline DRAFT. 2007. http://guidance.nice.org.uk/download.aspx?o=414903
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be inaccurate and influenced by dramatic or sensational causes, e.g. with media coverage. Risk perceptions
5. Department of Health. National Service Framework for Coronary Heart Disease. 2000.
http://www.dh.gov.uk/en/Publicationsandstatistics/Lettersandcirculars/Healthservicecirculars/DH_4004813
6. Department of Health. National Service Framework for Diabetes:Standards. London: DH, 2001.
http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_4002951
7. Department of Health. National Service Framework for Renal Services Part Two: Chronic kidney disease, acute renal failure and end of
life care. 2005. http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_4101902
8. Tuomilehto J, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H, Ilanne-Parikka P et al. Prevention of type 2 diabetes mellitus by
changes in lifestyle among subjects with impaired glucose tolerance. N.Engl.J.Med. 2001;344:1343-50.
9. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA et al. Reduction in the incidence of type 2 diabetes with
lifestyle intervention or metformin. N.Engl.J.Med. 2002;346:393-403.
10. Department of Health & Diabetes UK Care Planning Working Group. Care Planning in Diabetes: Joint report. 2006.
http://www.diabetes.nhs.uk/downloads/care_planning_in_diabetes_report.pdf
11. Department of Health. Quality and Outcomes Framework (updated). 2004.
http://www.dh.gov.uk/en/Policyandguidance/Organisationpolicy/Primarycare/Primarycarecontracting/QOF/DH_4125653
12. Lindstrom J,.Tuomilehto J. The diabetes risk score: a practical tool to predict type 2 diabetes risk. Diabetes Care 2003;26:725-31.
13. Rathmann W, Martin S, Haastert B, Icks A, Holle R, Lowel H et al. Performance of screening questionnaires and risk scores for
undiagnosed diabetes: the KORA Survey 2000. Arch.Intern.Med. 2005;165:436-41.
14. Marshall T. The use of cardiovascular risk factor information in practice databases: making the best of patient data. Br.J.Gen.Pract.
2006;56:600-5.
15. Goyder E, Carlisle J. National Evaluations of DHDS Diabetes Screening Pilot Programme: Interim Report to UK National Screening
Committee, Sheffield: Public Health Section of ScHARR. 2006.
16. Department of Health. Our health, our care, our say: a new direction for community services. 2006.
http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_4127453
17. Silventoinen K, Pankow J, Lindstrom J, Jousilahti P, Hu G, Tuomilehto J. The validity of the Finnish Diabetes Risk Score for the
prediction of the incidence of coronary heart disease and stroke, and total mortality. Eur.J.Cardiovasc.Prev.Rehabil. 2005;12:451-8.
18. The Royal Pharmaceutical Society of Great Britain. RPS e-PIC References on: Diagnostic testing in community pharmacy. 2007.
http://www.rpsgb.org.uk/pdfs/rpsepicdiagtest.pdf
19. Department of Health. Choosing Health: making healthy choices easier. Public Health white paper 2004.
http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_4094550
20. Bajekal M. Healthy life expectancy by area deprivation: magnitude and trends in England, 1994-1999. Health Stat.Q. 2005;18-27.
21. Office of National Statistics. Trends in ONS Longitudinal Study estimates of life expectancy by social class 1972 - 2001. 2006.
http://www.statistics.gov.uk/STATBASE/Product.asp?vlnk=8460&ComboState=&More=Y&Btn.x=14&Btn.y=17
22. Drever F, Doran T, Whitehead M. Exploring the relation between class, gender, and self rated general health using the new
socioeconomic classification. A study using data from the 2001 census. J.Epidemiol. Community Health 2004;58:590-6
23. Woods LM et al. Geographical variation in life expectancy at birth in England and Wales is largely explained by deprivation. J. Epidemiol.
Community Health 2005;115-20.
24. Department of Health. Tackling health inequalities: the Spearhead Group of Local Authorities and Primary Care Trusts. 2004.
http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_4101455
25. Anderson KM, Wilson PW, Odell PM, Kannel WB. An updated coronary risk profile. A statement for health professionals. Circulation
1991;83:356-62.
26. Brindle P, Beswick A, Fahey T, Ebrahim S. Accuracy and impact of risk assessment in the primary prevention of cardiovascular disease:
a systematic review. Heart 2006;92:1752-9.
27. Cappuccio FP, Oakeshott P, Strazzullo P, Kerry SM. Application of Framingham risk estimates to ethnic minorities in United Kingdom
and implications for primary prevention of heart disease in general practice: cross sectional population based study. BMJ
2002;325:1271.
28. Woodward M, Brindle P, Tunstall-Pedoe H. Adding social deprivation and family history to cardiovascular risk assessment: the ASSIGN
score from the Scottish Heart Health Extended Cohort (SHHEC). Heart 2006;93:172-6.
29. Cardiovascular risk assessment score for men and women aged 30-74 years. 2007. http://www.assign-score.com/
30. Hippisley-Cox J Coupland C, Vinogradova Y, Robson J, May M, Brindel P. Derivation and validation of QRISK, a new cardiovascular
disease risk score for the United Kingdom: prospective open cohort study. BMJ, doi:10.1136/bmj.39261.471806.55. 2007.
016
31. Hippisley-Cox J, Coupland C, Vinogradova Y, Robson J, Brindle P The performance of the QRISK cardiovascular risk prediction
algorithm in an external UK sample of patients from general practice: a validation study Heart. Published Online First: 4 October 2007.
doi:10.1136/hrt.2007.134890
32. Edwards A, Elwyn G, Mulley A. Explaining risks: turning numerical data into meaningful pictures. BMJ 2002;324:827-30.
33. Gigerenzer G,.Edwards A. Simple tools for understanding risks: from innumeracy to insight. BMJ 2003;327:741-4.
34. O'Connor AM, Stacey D, Rovner D, Holmes-Rovner M, Tetroe J, Llewellyn-Thomas H et al. Decision aids for people facing health
treatment or screening decisions. Cochrane.Database.Syst.Rev. 2003;CD001431.
35. Skinner TC, Carey ME, Cradock S, Daly H, Davies MJ, Doherty Y et al. Diabetes education and self-management for ongoing and newly
diagnosed (DESMOND): Process modelling of pilot study. Patient.Educ.Couns. 2006;64 (1-3):369-377.
PART 1_Section 1
36. Davies MJ, Heller S, Khunti K, Skinner TC. The DESMOND (Diabetes Education Self-Management Ongoing and Newly Diagnosed)
programme: from pilot to randomised controlled trial in a study of structured group education for people newly diagnosed with type 2
diabetes mellitus. Diabetic Medicine, 2005 22(Suppl.2) :108.P333
017
018
PART 1_Section 2
Clinical Context & Review of the Evidence
Cardiovascular Disease
Cardiovascular disease particularly, coronary heart disease (CHD), stroke/TIA, peripheral arterial disease (PAD)
and diabetes mellitus (DM) are the main cause of death in the UK. Even considering only coronary heart disease
(CHD) and stroke in England and Wales, in 2005 more than one in three people died with 124,000 deaths;
39,000 of those who died were aged under 75 years1. The death rate varies with age, gender, socio-economic
status, ethnicity and UK geographical locality. Death rates from CVD have been falling since 1970, and it has
been estimated that 58% of the CVD mortality decline in the UK in the 1980s and 1990s is attributable to reductions in major risk factors, principally smoking. The risk of CVD is directly related to blood cholesterol level and it
is estimated that over 50% of CVD in developed countries is due to a blood cholesterol in excess of 3.8 mmol/L.
A number of surveys have shown that the majority do not achieve recommended lifestyle, blood pressure (BP)
and lipid targets despite the increase in prescribing of anti-hypertensive and lipid lowering therapies3. Of major
concern is that in apparently healthy individuals there appears to be an increasing prevalence of a combination
of risk factors that puts them at high risk of developing vascular diseases including CHD, cerebrovascular disease, CKD, T2DM and PAD. In the Health Service for England 2003, the prevalence of smoking in those with
established CVD was 28% in men and 25% in women, 64% of men and 55% of women were overweight (BMI
≥25kg/m2), 29% of men and 27% of women had hypertension as defined by a blood pressure of >140/90
mmHg and 68% of men and 67% of women had an elevated cholesterol (>5mmol/L). The overall prevalence of
DM was 4.3% in men and 3.4% in women2.
T2DM is a growing public health concern worldwide. The prevalence is increasing and diabetes contributes
significantly to overall health inequalities within countries. DM leads to significant morbidity and mortality
which can be reduced by effective treatment and preventative measures. BME groups, particularly the SA
and Afro Caribbean populations, generally have a higher prevalence of T2DM and are also at greater risk of
DM associated mortality and complications compared to the White European population. 75% of deaths in
people with diabetes are caused by CVD.
The Need for Vascular Risk Assessment in Those at High Risk
The rationale for estimating “total” CVD risk based on major risk factors is because:
u Risk factors tend to cluster
u Co-existent risk factors tend to have a multiplicative effect on risk
The advantages of this approach are that interventions are considered in the context of overall CVD risk. A
threshold for drug interventions is based on robust scientific evidence. Treatment is targeted on the threshold of
total CVD risk so by definition it tends to be targeted at those at highest risk and therefore the absolute benefits
of such treatment will be greatest.
019
PART 1_Section 2
In the Health Survey for England 2003, the prevalence of CHD (angina and heart attack) was 7.4% in men and
4.5% in women. With stroke added, CVD prevalence was 9.1% and 6.3% in men and women respectively.
From age 65 onwards, between one quarter and one-third of men reported having CHD or stroke, and the
prevalence rises with age: 26% between 65 and 74 years, 34% in those aged >75 years in men, with 14% and
25% respectively in women. The prevalence of cerebrovascular disease is also increasing, between 1994 and
2003 it rose from 7.1% to 9.1% in men, and 5.2% to 6.3% in women2.
The Approach to Multi-factorial CVD Risk Assessment
The NSF for CHD sets out clear standards for prevention and treatment4. This is focused on people with established CHD and other related conditions of high vascular risk but also on offering treatment to apparently healthy
individuals at high multi-factorial risk of developing CHD. At that time, risk calculators used CHD risk and it was
suggested that those whose total CHD risk was >15% (equivalent to the current CVD risk of 20%) over 10 years
should be eligible for both lifestyle and appropriate therapeutic interventions. However, given the scale of the
task in identifying and managing such high risk individuals, it was advocated that a staged approach be used
and that the starting point was those with a CHD risk of >30%. However, it is now clear that this policy of targeting very high risk, particularly with lipid lowering therapy, falls short of the scientific evidence base that now
exists. There are RCTs showing clinical benefit down to levels of CHD risk of 6% (CVD risk of 8%)5.
There has been a focus on lipid lowering therapy and the evidence base for this is now even stronger, such that
recent NICE guidance recommended statin therapy for adults with clinical evidence of CVD and for primary prevention of total CVD risk in those who have a 20% or greater 10 year risk6.
Subsequently the SIGN guidelines advocate that asymptomatic individuals over the age of 40 years with ≥ 20%
risk of CVD over the next 10 years should be considered at high risk and warrant intensive lifestyle change and
drug intervention including statins.7 This is consistent with the advice in the recent public consultation document
on Lipid Modification from NICE8.
Cardiovascular Risk Assessment Methods
The Joint British Society (JBS) CVD Risk Prediction Chart based on the Framingham data can be used to estimate total risk of developing CVD, i.e. CHD and stroke, over a period of 10 years based on 5 key risk factors:
u Age
u Sex
u Smoking habit
u Systolic blood pressure (BP)
u Ratio of total cholesterol to HDL cholesterol.
The estimate is a probability (i.e. percentage chance) of developing CVD over the next 10 years and is therefore
referred to as the total CVD risk. Current definitions state that the total CVD risk of over 20% is defined as “high
risk”, and all those at high risk will require lifestyle intervention and advice and drug therapy focused around antithrombotic, lipid lowering and BP lowering drugs6-8.
SIGN specifically commissioned work to incorporate risk coefficients accounting for both family history and
social deprivation and advocate the use of a new CVD risk score ASSIGN7,9. However the cut off used (≥ 20%)
and the age group targeted (Adults over age of 40 years) is likely to be consistent with the emerging guidance
from NICE8. The consultation document on Lipid Modification currently suggests that all adults aged over 40
years should have a risk score calculated with ≥ 20% defined as high risk8.
020
Choice of CVD Risk Assessment Score
In this handbook we acknowledge that this field is moving rapidly. The latest JBS guidance uses a modified Framingham
method, but SIGN advocate using the ASSIGN Tool, and recent draft NICE guidance also suggested using a Framingham based risk score.8-10 There are a number of other risk assessment methods available. These include the New
Zealand risk calculator, the Heart Score, the Sheffield Risk Table, the ETHRISK and others.11-14 The Heart Score
is based on the SCORE project and has been adopted by the Joint European Society guidelines.15 It has the
advantage of being based on European epidemiological studies, and also predicts CVD risk and not CHD risk
alone. However, it can only predict fatal CVD and therefore underestimates the true burden of total CVD risk.
The latest JBS guidance continues to recommend the Framingham based algorithm10. The principal reasons
stated are:
u That it has been widely adopted
u Physicians in both hospitals and primary care are familiar with the CVD risk threshold of ≥20%,
In order to try to reduce the bias in terms of age group, the charts are provided for 3 age groups: <50 years, 5060 years, and >60 years. However, the actual risk given for these 3 age bands are based on the actual ages of
49, 59 and 69 respectively. Therefore the charts will deliberately tend to overestimate risk within the younger
age bands, and potentially underestimate risk for people aged 70 or over.
The approach used may change with the publication of the new QRISK tool16. This algorithm has used parameters included in the Framingham method but also measures of social deprivation and other factors such as BMI16.
Whichever tool is used, the vascular risk threshold defined for intensive lifestyle and appropriate drug therapies
is ≥ 20% over 10 years7,8,10,16. This threshold for drug treatment cannot be based directly on the evidence from
clinical trials because most clinical trials are uni-factorial in their design. Therefore, extrapolating from clinical trial
results in hypertension or dyslipidaemia to an intervention threshold based on multifactorial risk is not possible.
Nevertheless, absolute CVD event rates of ≥20% were common in most of the uni-factorial intervention trials.
However, it is important that a risk threshold for drug treatment is a matter for clinical judgment. The size of the
populations potentially eligible for intervention based on ≥20% CVD risk alone has been estimated to be around
23% of men and 8% of women aged 40-74 years, based on data from the Health Survey of England 2003
(Table 1)2. However there is some suggestion that these figures will be reduced if the QRISK score is used16.
CVD Risk (%)
40-49 (%)
50-59 (%)
≥30
25<30
20<25
15<20
10<15
1.0
1.6
7.2
20.8
6.0
7.4
14.1
22.5
31.4
≥30
25<30
20<25
15<20
10<15
Source HSE 2003
0.3
0.2
1.4
5.3
0.7
0.9
3.3
8.1
18.8
Age
60-69 (%)
Men
32.9
15.3
22.3
19.7
8.8
Women
4.1
4.0
12.9
19.1
33.3
70-74 (%)
Total (%)
65.5
11.2
14.6
6.8
1.8
10.0
4.9
7.9
10.6
15.1
16.4
10.6
19.4
29.2
15.9
1.9
1.7
4.3
7.5
12.4
u Table 1. Prevalence of Total Cardiovascular Disease (CVD) (over 10 years) Risk in Adults
aged 40-74 in England, by Age and Sex2
021
PART 1_Section 2
u That the new algorithms do not offer sufficient advantage.
Limitations of Risk Factor Assessment Using CVD Risk Scores
u It is vital that clinical intervention and assessment for a vascular risk reduction programme is not based on
CVD risk score alone.
u Conventional risk scores tend to overestimate risk in low risk populations and underestimate in high risk
groups17
u It is important to consider other factors and to ensure that the assessment of vascular risk using a risk
assessment tool does not increase inequalities
u There is no strong evidence supporting the assumption that CVD risk assessment performed by clinicians
improves health outcomes17
Risk assessment tools for vascular disease do present somewhat of a dilemma. This is because:
● A review including 27 studies with data from over 71,000 participants, showed that the predicted to
observed ratios ranged from an underestimate of 0.43 in a high risk population to an over-prediction of 2.87
in a lower risk population so risk scores tend to overestimate risk in low risk populations and underestimate
in high risk groups17. One approach may to be multiply the derived Framingham risk score by 1.4 in the SA
population. Another approach would be use an ethnically-adjusted prediction model, which adjusts the
background risk of different geographical regions and ethnic groups9,16.
In Scotland when they applied the Framingham risk score to an adult population (13,000 aged 25-74 years from
25 districts in Scotland) they found that overall the Framingham risk score overestimated actual observed CHD
risk in the whole cohort but seriously underestimated the large gradient in risk by socio-economic status7. They
concluded that application of the Framingham risk score for essentially what is preventative treatment would
result in relative under treatment of the most socially deprived, potentially exacerbating social disparities in disease rates. They addressed this by using a risk score system (ASSIGN) adjusted for social deprivation9.
A similar approach which may be appropriate is the QRISK tool which also includes Townsend Score and other
risk factors such as BMI16.
● RCTs examining the effect on clinical outcomes of healthcare professionals performing a vascular risk score
in people predominantly without known vascular disease; show a very poor uptake by doctors and health
care professionals in terms of the clinical decision support systems. There is no strong evidence supporting
the assumption that CVD risk assessment performed by clinicians improves health outcomes. It is therefore
important to engage practice staff on the ground in the overall strategy and implementation of the policy in
practice17.
CVD Risk factors not taken into account using conventional CVD Risk Prediction Charts
The current dilemma is that a number of other risk factors not included in the traditional risk assessment tool
should also be taken account of in assessing and managing a person’s overall vascular risk. These include;
u Ethnicity
u Family history of premature CHD
u Family history of DM (first degree relative)
u Weight (as defined by Body Mass Index)
u Abdominal obesity as assessed by waist circumference
u Impaired glucose regulation (both IFT/IGT and HbA1c ≥6%)
u CKD
u Raised triglycerides
u Socio Economic Status
022
Recent guidelines recognise the importance of these additional risk factors and the shortcomings of the conventional CVD risk prediction tool7,8,10; for example:
u In people originating from the Indian subcontinent it is reasonable to assume that CVD risk is approximately
1.4 times higher than predicted from the charts10
u Abdominal obesity as assessed by waist circumference of >94 cms in men and >88 cms in women (in South
Asians 90cms in men and 80 cms in women) increases the risk of both diabetes and CVD18-19
u Impaired glucose regulation as defined by a fasting plasma glucose of ≥6mmol/L (IFG) and IGT (2 hour
glucose during an OGTT of between 7.8 and 11.1 mmol/L) indicates an increased risk of developing DM and
CVD. (Evidence suggests an increase CVD outcome by 50%, so by a factor of 1.5)20
u Raised fasting triglycerides of >1.7 increases the risk of CVD by a factor of 1.310
u A family history of premature CVD and especially coronary heart disease in men <55 years and women <65
years in a first-degree relative increases the risk of CVD by 1.38,21,22
u A first-degree relative history of DM also increases risk of subsequent development of T2DM
u Individuals with Chronic Kidney Disease (CKD) are at significantly increased risk of CVD events23
Evaluation of Scientific Evidence: Bias Towards RCTs of Single Pharmaceutical Therapies
u If we were only to consider clinical trial evidence, drug treatment would always take precedence over
other interventions, principally those related to lifestyle change
u It is important that we value evidence from epidemiological studies that give information as to the benefit
of lifestyle intervention in those at high vascular risk
Evidence-based medicine involves the integration of individual clinical expertise with the best available clinical
evidence from systematic research. It is a holistic procedure, from the definition of important clinical questions,
to searching for the best evidence, critically appraising the evidence, and applying the evidence to individual patient care and evaluating the process. This hierarchy by definition places meta-analysis of clinical trials at the
top. Therefore in this context there tends to be greater emphasis on RCTs of individual drug therapy rather than
epidemiological studies of the adverse effects of lifestyle factors such as smoking, poor diet and physical inactivity, or beneficial effects of healthy diet and increased physical activity.
Another important factor is that whilst clinical trials may be well suited to evaluating a single drug therapy against
a single risk factor, there are inherent limitations in the methodology of clinical trials when evaluating complex
lifestyle interventions in the free-living population. If we were only to consider clinical trial evidence, drug treatment would always take precedence over other interventions, principally those related to lifestyle change. It is
important that we value evidence from epidemiological studies that give information as to the benefit of lifestyle
intervention in those at high vascular risk.
023
PART 1_Section 2
u Presence of Albuminuria and an eGFR < 60 mls/min/1.73m2 are independent predictors of CVD events
Potential Shortcomings of Using a CVD Risk Assessment Approach in Isolation
There are disadvantages of using a CVD risk assessment tool in isolation;
u A number of risk factors are not included in the Framingham based Risk Score as outlined above
u Treatments will tend to be concentrated in older people and especially in those >70 years unless the
potential effect of lifetime risk factor exposure is taken into account
u Evidence-based medicine that favours single intervention RCTs as opposed to complex lifestyle
interventions that may be effectively offered to patients at a much younger age even though they may not
reach ‘high vascular risk’ thresholds
u It may increase inequalities unless adjustments are made, for example, in socio-economically deprived and
BME populations
Chronic Kidney Disease
CKD is a worldwide public health problem. Early CKD (mild to moderate) is very common, with an estimated
11% of the US adult population having CKD24. Early CKD if not treated, can progress to more severe forms of
the disease. In the UK, a recent study has found that 8.5% of the general population have moderate to severe
CKD25. Established renal failure is relatively rare, but treatment with dialysis or transplantation is very costly. In the
UK, it is reported that the number of patients needing dialysis or transplantation is rising rapidly and is unlikely to
reach a steady state for another 25 years26. Therefore, it is important to treat CKD early to prevent the progression of the disease to renal failure.
CKD patients have an increased risk of CVD that accounts for 40-50% of all deaths in CKD27. Risk markers of
CKD have been shown to be highly predictive of cardiovascular events28. This is very important because individuals with CKD are more likely to die of CVD than to develop kidney failure and this has led to the recommendation that these patients should be considered in the “highest risk group” for preventative treatment of CVD28.
Multiple risk factor intervention taking a chronic disease management approach can halt decline of kidney function and there is evidence that the combination of declining kidney function and proteinuria identifies the highest
vascular risk and progressive kidney disease risk group29-32. However there is a lack of evidence of the benefit of
Statin therapy in those with CKD alone.
Defining CKD
CKD is an umbrella term for all types of kidney disease that slowly destroy the kidneys over months or years. In
the UK, CKD is now classified according to the NKF-K/DOQI guidelines (see Table 2)24. This classification system is based on estimated GFR (glomerular filtration rate) as an indicator of kidney function, irrespective of the
cause of the kidney disease. It identifies the progression of CKD in five stages from mild to severe. Proteinuria
refers to the presence of increased protein in the urine. Proteinuria is an important marker of kidney damage and
a potent predictor of increased cardiovascular risk33, and of risk of progression.
From 2006, eGFR has been included with creatinine testing in many laboratories. Studies of general practice
computerised medical records show that it is feasible to identify people with CKD and that computer records are
a valid source of data The compilation of a register of people with CKD will enable appropriate investigation,
advice, treatment and support for the patient to preserve kidney function and to reduce the risk of CVD. Only a
minority of people with stage one or two CKD go on to develop end stage kidney disease and symptoms do not
usually appear until stage four.
024
u For the purpose of this handbook we refer to CKD stages 3-5. However despite the increased
awareness of CKD it is still often considered in isolation24
u Early identification of CKD is important as it allows appropriate measures to be taken to slow or prevent
the progression to more serious CKD
u CKD is an independent risk factor for CVD and a multiplier of other risk factors
u Identification of CKD also allows us to combat the major risk of illness or death due to CVD
Stage
GFR*
1
90+
2
60-89
3
30-59
Moderately reduced kidney function
Observation, control of blood pressure
and risk factors.
4
15-29
Severely reduced kidney function
Planning for endstage renal failure.
5
<15
Very severe, or endstage kidney
failure (sometimes called established
renal failure)
Treatment choices.
Normal kidney function but urine
findings or structural abnormalities or
genetic trait point to kidney disease
Mildly reduced kidney function, and
other findings (as for stage 1) point to
kidney disease
Treatment stage
Observation, control of blood
pressure.
Observation, control of blood pressure
and risk factors.
* All GFR values are normalised to an average surface area (size) of 1.73m2
u Table 2. K/DOQI Stages of CKD24
Identifying CKD
A recent paper describes a screening strategy for patients with CKD34. This is based on data from an 8 year follow-up of 65,000 subjects in Norway. 4.7% of the adult population aged >20 years had CKD as defined by an
estimated GFR filtration rate of <60mls per minute/1.73 m2. The most effective strategy was to restrict screening to those with HT, DM, or aged over 55 years34.
A high risk screening model targeting only those with DM or HT identifies less than half of those with CKD.
However, a model that targets those aged >55 years identifies 93%, with only a few more people needed to
screen than the high risk strategy (9 versus 6 per case). It was noted that the incidence of end-stage renal disease was lower among people with GFR of 30-60mls per minute/1.73 m2 while CVD mortality was much higher
(4.2 per 100 person years). Those with eGFR of <30 mls per minute/1.73 m2 had a high risk of both renal failure
and CVD mortality (2.6 and 10.1 per 100 person years)34.
It is possible that the simple strategy targeting people with DM, HT or aged > 55 yrs has the highest detection
rate for CKD, combined with the low number needed to screen. Most patients detected had a low risk of progression to end-stage renal disease. The cost effectiveness of screening needs further research and at present
we suggest routine eGFR in those with HT or DM until there is further research in this area.
Diabetes Mellitus
T2DM is a growing public health concern worldwide. The prevalence is increasing and diabetes contributes significantly to overall health inequalities within countries. DM leads to significant morbidity and mortality which can
be reduced by effective treatment and preventative measures. BME groups, particularly the SA population, generally have a higher prevalence of T2DM and are also at greater risk of DM associated mortality and complications compared to the White European population. 75% of deaths in people with diabetes are caused by CVD.
025
PART 1_Section 2
Description
u There is now clear evidence that the majority (2/3) of T2DM can be prevented by lifestyle and diet
interventions34-35
u Patients with established T2DM are all at high CVD risk and the use of CVD risk charts is no longer
advocated
u A diagnosis of T2DM means patients are offered vascular interventions at a lower threshold (for example
lower BP targets are used)
u A diagnosis of T2DM means patients are placed on a disease register and in addition are offered
screening for microvascular complications (In particular Retinopathy and Nephropathy)
Screening, Early Detection and Prevention of Diabetes
The increasing evidence base for effective primary and secondary prevention of CVD and T2DM has led to increasing interest in screening, early detection and risk reduction intervention. Despite the lack of randomised
trial evidence and long-term outcomes for the effectiveness of screening for T2DM, screening in high risk populations has been recommended by Diabetes UK, the American Diabetes Association and the Australian Diabetes
Association37,38,39.
Up to 750,000 people with Type 2 DM remained undiagnosed in the UK with evidence that people have the
condition for between 9 and 12 years before diagnosis40,41. The UKPDS showed that up to 50% of people already have complications such as CVD and microvascular complications including neuropathy, nephropathy and
retinopathy at diagnosis42. There is evidence that those diagnosed by screening are as likely to have complications as those diagnosed on the basis of symptoms4. Risk of CVD is increased among patients with previously
undiagnosed diabetes compared to people with normal glucose tolerance.
Patients with established DM are all considered at high vascular risk and therefore the continued use of vascular
risk assessment charts is no longer advocated7,8,10. The importance of a diagnosis of T2DM means that patients
are offered vascular interventions at a lower threshold7,10. Furthermore, patients are placed on a disease register
(the Diabetes Register) and are offered microvascular screening, including for nephropathy and retinopathy44,45.
There is a range of evidence that screening for diabetes in general practice may be feasible, and identifies previously undiagnosed cases46. A number of different approaches have been advocated including the use of risk
questionnaires and risk assessment tools which aim to identify those who would benefit from attending for a
blood test.
Lessons from Diabetes, Heart Disease and Stroke (DHDS) Pilot46
The Diabetes, Heart Disease and Stroke Project (DHDS) looked at the implications of vascular risk assessment
in a general practice setting and provided useful information on its impact and feasibility. Important lessons
learnt from this were:
Testing
u 50% of practices already had some systematic screening for vascular risk and DM in place, but there was
marked variation particularly with regard to diagnostic testing for DM.
u If practices used OGTTs these were often carried in the hospital setting.
Population Screened
u Around 25% of the practice population were eligible on age criteria (between 40 and 74 years) once those
with a known BMI of ≤ 25 and those who had had previous blood glucose testing within the past two years
were excluded.
u Retired people, women and the “worried well” were most likely to attend for screening; patients at low risk
still attended, expecting reassurance.
026
Results
u Around 60% of those invited for screening attended, and around one-third had a positive screen test of
whom 1.4% had newly diagnosed diabetes. This equates to 2 per 1,000 registered population of the practice.
u There was marked variation in the practice yield of new cases of DM. Practices that had the highest yield were in
fact in a predominantly white population in a deprived area who used all three inclusion criteria including age, BMI
and recent blood glucose to select patients and used OGTTs for diagnosis.
Follow Up
u Follow-up of those who undergo initial testing was crucial as one-third of patients with an initial random
capillary blood glucose of ≥ 6mmol (positive, as defined in this project) did not have any results of diagnostic
testing recorded on their screening records, even after updating records from practice information systems.
It is important to have systems that accurately record the results of screening investigation and prepare
patients for the need for further diagnostic testing.
u Patients tended to believe that a negative result gave them the all-clear, and therefore communicating
continuous risk with regard to results of glucose tests, BMI, etc. needs to be clearly and carefully delivered,
i.e. “everyone is at risk”.
An updatable, searchable, clinical database is crucial for identifying eligible patients.
Data collection was crucial and half the practices used their own locally designed templates.
It is important to implement strategies so that the practice can plan and cope with the increased workload.
Opportunistic invitation was popular because of the perceived high success rate with patients already
attending the practice for an unrelated reason.
u Adapting the method of invitation to the type of patient population and ensuring it was appropriate to the
practice, generated better attendance.
u
u
u
u
Staff
u 55% of screening was undertaken by the healthcare assistant, who had a crucial role in implementation of
the programme (see Job Description in SOP Section on page 147).
u A number of practice staff need to be involved in identifying, inviting and providing vascular risk assessment
and discussion of the results.
u Staff felt overall job satisfaction from providing preventative care, and healthcare assistants enjoyed their
increased responsibility.
Barriers
u The procedure was relatively time consuming, taking around 2 hours per person invited, with around
one-third of time spent on identification and two-thrids spent on screening time.
u Staff viewed the criteria for screening as sometimes being too restrictive and unfair to patients, particularly
those in BME communities and those with a positive family history.
u Staff were also concerned about the equity of access for all patients.
u Sending out letters was costly in terms of staff time, but letters sent in English appeared to have a better
uptake than in those other languages.
u Barriers to attendance for screening and diagnostic testing were a lack of availability during the evenings and
weekends.
u Communication with BME populations may be enabled through local organisations, rather than direct
translations of written information.
027
PART 1_Section 2
Logistics
Implications for Policy and Practice from the DHDS
Any programme will need to have:
u A clear and consistent method of data collection
u A system for data audit and continuous quality improvement
u Screening invitation letters should be as simple as possible, and the value of translated materials needs to
be explored in each location
u Integration of assessment in the other ongoing practice activities may increase uptake and represent a
more cost effective strategy
Measure-up Campaign from Diabetes UK
Diabetes UK has long been calling for the early identification of people with T2DM, to reduce the impact on individuals and NHS resources.
Diabetes UK suggest screening those with the following risk factors:
u White Europeans aged over 40 years;
u People from BME groups aged over 25 with one or more of the risk factors below;
u A first-degree family history of diabetes;
u Those with obesity, morbidly obese or those who are overweight with a sedentary lifestyle;
u Waist circumference measurements include >94cms for white/black men and 90cms for SA men,
and >80cms for all women.
u People with a history of IHD, cerebrovascular disease, PAD or treated HT;
u Those with a history of gestational diabetes;
u Women with polycystic ovary syndrome;
u Those with previous IGT or IFG;
u Those with severe mental health problems;
u Those who have hypertriglyceridaemia.
However, the evidence would suggest that whilst family history and WC measurements are ideal to be used for
patients in terms of their self-assessment of risk, they are not often recorded on routine clinical data sets. Furthermore, isolated risk factors such as gestational diabetes and PCO are often not recorded on information systems and may have limited utility as most patients have other more easily ascertained risk factors such as BMI
and a history of HT. Whilst screening those with severe mental health problems may well have a good rationale,
this strategy has not been evaluated and the utility of this approach and its added value above screening for
other more easily identifiable risk factors is not known.
028
The Continuous Relationship Between Blood Glucose Levels and Vascular Outcomes Below the
Threshold for Diagnosing Diabetes
u Glycaemia, whether evaluated by fasting glucose, a 2 hour glucose level during an oral glucose tolerance
test (OGTT) or by HbA1c, has a continuous relationship to the risk of CVD47,48
u This continuous relationship is similar in those both with and without DM
u As is the case for BP and cholesterol, the absolute risk of CVD associated with any level of glycaemia is
also determined by the presence of other risk factors
Although the relationship between glycaemia and CVD is a continuous one, the traditional assessment and categorisation of glycaemic status has been using either a fasting sample or OGTT that categorises individuals as either normal glucose tolerance, impaired fasting glycaemia (IFG), impaired glucose tolerance (IGT) and DM (Table
3)49.
Random Plasma
Glucose test
Oral Glucose
Tolerance test (OGTT)
Random Plasma Glucose ≥ 2-hour plasma
11.1 mmol/l plus symptoms‡ glucose ≥11.1 mmol/l §
Diabetes
FPG ≥7.0 mmol/l
plus symptoms†
Impaired Glucose
Regulation
(IGT, IFG or both)
IFG ≥6.1 and <7.0
mmol/l
IGT + 2 h PG ≥7.8
and <11.1 mmol/l
Normal
FPG ≤6.0mmol/l
2 h PG <7.8mmol/l
* The FPG is the preferred initial test for diagnosis, but any one of the three listed is acceptable. In the absence of unequivocal
hyperglycaemia with acute metabolic decompensation, one of these three tests should be repeated on a different occasion to confirm
diagnosis. Venous plasma samples are used. (symptoms are the classic ones of polyuria, polydipsia, and unexplained weight loss).
† Fasting is defined as no caloric intake for at least 8 hours. Water is allowed.
‡ Random = anytime of day without regard for time since last meal
§ OGTT should be performed using a glucose load containing the equivalent of 75g anhydrous glucose dissolved in water
u Table 3. Diagnosis of Diabetes Mellitus (DM), Impaired Fasting Glucose (IFG) and Impaired Glucose Tolerance (IGT)49
u Focusing CVD prevention solely on diagnosed cases of DM will have a limited impact, and the focus needs to
be broadened to include those with Impaired glucose regulation (IGR), this includes both IFG and IGT.
It is important to recognise that diagnosed diabetes only accounts for about 20% of all subsequent fatal CVD,
with the majority of the events coming from apparently healthy individuals with a HbA1c of >6% but in the absence of DM48. Of patients admitted to the Coronary Care Unit with a myocardial infarction, approximately 40%
have abnormal glucose tolerance and 25% have undiagnosed T2DM50. The total risk of CVD for any value of
HbA1c is further determined by the presence of other risk factors such as smoking, elevated BP and dyslipidaemia. Therefore, focusing CVD prevention solely on diagnosed cases of DM will have a limited impact, and
the focus needs to be broadened to include those with impaired glucose regulation (IGR), this includes both IFG
and IGT.
029
PART 1_Section 2
Fasting Plasma Glucose
(FPG) test (preferred)*
Preventing Progression to Diabetes
u The best evidence for prevention of T2DM is in those with IGR (particularly IGT)35,36
u Diet and Lifestyle has been shown to be the most effective intervention35,36,51
u Fasting or Random Glucose used alone are very poor discriminators of IGT and IFG and will miss the
majority of cases
The best evidence for prevention of progression to T2DM is in IGT and IFG using diet and lifestyle intervention35,36,51,52. IGT and IFG are under-diagnosed in clinical practice. It is well established from a number of epidemiological studies in North America, Europe and Asia that approximately 1 in 7 of the population have either
IFG or IGT20,53,54. There have now been a number of studies published that showed that intensive and effective
lifestyle interventions lead to a 60% reduction in subsequent progression to T2DM in these subjects35,36.
There is a need for effective, feasible and affordable interventions that can be offered to people, in particular
those with IGR (IGT and IFG), as in these groups there is good evidence that lifestyle change can delay progression to diabetes35,36. The dilemma is that the glucose cut-off for diagnosing undiagnosed T2DM should have
reasonable sensitivity and specificity. However, fasting or random glucose are both very poor discriminators of
patients with IGR55. Their use may lead to false reassurance as patients may regard the fact that they have a
‘negative test’ means they are ‘normal’.
There is ongoing work looking at effective behavioural interventions for people identified as being at high risk of
future diabetes and vascular disease. Such subjects are unlikely to be identified using conventional vascular risk
scores, as these tend to be biased in terms of detecting older patients. Diabetes risk scores tend to identify
people decades earlier on the basis of poor lifestyle choices, and offer the opportunity for targeted lifestyle intervention56-63 (See page 78-83 in the Appendix).
It is important that any blood glucose testing done as part of a vascular control programme is focused on those
with other risk factors (based on obesity, family history, hypertension etc.), with clear procedures for those who
may need confirmation with an OGTT. The Diabetes Heart Disease and Stroke (DHDS) Programme showed that
practices that offered widespread testing based on random glucose based on age criteria alone had the lowest
yield of new cases, whereas practices which targeted screening on those with risk factors and followed with
OGTT, had the highest yield of new cases of T2DM46.
When undertaking any vascular risk assessment including screening for diabetes, it is important that the individual is aware of the issues regarding employment, insurance and driving should a diagnosis of either CHD/CKD
or DM be established. Practitioners should have a low threshold in offering diagnostic testing for diabetes in
anybody who presents with symptoms, i.e. polyuria, polydipsia and unexplained weight loss or visual blurring.
Such individuals should be offered an immediate random plasma glucose which, if ≥11.1 mmol/l in the presence
of symptoms indicates a new diagnosis of diabetes.
030
Use of Glucose Testing to Detect Undiagnosed Diabetes and Its Utility in Detecting IGR
The Australian experience regarding screening sensitivity and cut-offs for fasting glucose has been assessed in a
population-based sample of 10,508 Australians55. This study suggested that screening for diabetes is undertaken in those with any one of the following risk factors:
Fasting plasma glucose (FPG) is measured and further testing (OGTT) is offered according to the level of fasting
glucose. This study shows the poor sensitivity of using FPG to detect IGT/IFG, as using a strategy based on a
fasting glucose of ≥ 5.5 mmol/l had a sensitivity of 80%, specificity of 80% to detect diabetes, 20% of the population required an OGTT but the sensitivity to detect IGT and IFG was only 51.9%. In this population, using FPG
of ≥ 6.1 mmol/l, sensitivity for diabetes drops to 63% with a specificity of 93.9%, sensitivity for IGT or IFG falls to
34.6%, but only 6.6% of the population required an OGTT.
u So in general terms using a FPG of 5.5 mmol/l picks up 50% of IFG/IGT using a FPG of 6.0 mmol/l only
picks up 33%
The authors discussed the favourable outcomes of the Finnish and US Prevention Studies that have stimulated
greater interest in the detection of people with IGT and IFG35,36. Any risk assessment programme that includes
testing for blood sugar may offer detection of people with lesser degrees of glucose intolerance (IGT and IFG).
However, even using a lower glucose threshold of 5.5 mmol/l only has a sensitivity of just over 50% for these
conditions. Furthermore, the current assessment of the performance of screening showed that age combined
with obesity and hypertension and parental history of diabetes accounted for 87% of patients with previously
undiagnosed DM and the inclusion of gestational diabetes had little additional effect. The Australian programme, when based on a fasting glucose of 5.5 mmol/l, required 32 to be screened to identify one new case
of DM, with 4 out of 10 people requiring fasting plasma glucose and a further 1 in 5 requiring an OGTT (Table 4).
Newly diagnosed
diabetes
RF & FPG ≥ 5.5 *
RF & FPG ≥ 6.1
RF & FPG ≥ 5.5 then HbA1c ≥ 5.3%
RF & FPG ≥ 5.5 or HbA1c ≥ 5.3%
RF & HbA1c ≥ 5.3%
% Population
requiring test
IGT or IFG
Sensitivity
(%)
Specificity
(%)
PPV
(%)
Sensitivity
(%)
Specificity
(%)
PPV
(%)
Sensitivity
(%)
Specificity
(%)
PPV
(%)
79.9
63.6
73.7
84.9
78.7
79.9
93.9
89.2
73.5
82.8
13.7
29.4
21.4
11.4
15.5
51.9
34.6
33.5
60.3
42.0
86.7
100.0
94.1
80.8
88.2
45.5
100.0
54.8
40.2
43.2
43.4
43.4
43.4
43.4
-
20.7
43.4
43.4
20.7
6.6
11.6
27.1
19.5
All data were weighted to the Australian adult population RF=Risk Factor
*Current guideline according to the National Health and Medical Council in Australia55
u Table 4. Performance of Screening Strategies for detection of T2DM and Impaired Glucose Regulation
u The majority (90%) of people with IGT/IFG will have either a positive family history or be hypertensive
u Use of FPG (or RPG) alone is a poor discriminator of IGT/IFG with 50% missed if a cut off of 5.5 mmol/l is
used and 66% missed if 6.0mmol/l is used
031
PART 1_Section 2
u Those aged over 55yrs
u People aged over 45 with one of more of the following factors: obesity as defined by a BMI of ≥ 30kg/m2,
first degree relative with T2DM, hypertension or a history of taking anti-hypertensive medications, a blood
pressure ≥ 140/90.
u In minority ethnic groups (Aborigines and Torres Strait Islanders) aged over 35 years
u People with IFG or IGT
u All people with clinical CVD including myocardial infarction and TIA or stroke
u Women with gestational DM
u Women with polycystic ovary syndrome who are obese
Recent Data From Screening Studies in Leicester
In Leicestershire in the past 5 years there have been two large population-based screening studies that will help
inform a strategy for detection of undiagnosed T2DM and IGT. They are detailed in the Appendix pages 75-77
but essentially the findings were that in terms of screening for T2DM in people with HT and with a BMI of
≥25kg/m2 using a FPG of 5.5 mmol/l had a sensitivity of 87% in the South Asian population and in the White European population a sensitivity of 86% dropping to 79.5% if a FPG of 6mmol/l was used.
Thus a 2 stage screening procedure using BMI (if 25kg/m2) and presence of HT in both the South Asian and
White European population is reasonably sensitive (in 80%-86%) and only 7-9% required an OGTT if a cut off
6mmol/l is used (See Appendix pages 75-77).
u A two stage procedure using BMI ( ≥ 25kg/m2) and presence of HT in both South Asian and White
European populations has a sensitivity of between 80-86% with only 7-9% requiring an OGTT
u FPG cut off should be ≥ 6 mmol/l to detect undiagnosed diabetes
u This approach will not detect the majority of cases of impaired glucose regulation (IGR) (See page 31)
Moving to IGR (IGT & IFG) even if HT and BMI are included, the use of FPG if 5.5mmol/l in detecting IGT/IFG is
poor with a sensitivity in both South Asian and White European population of about 25-30%. Thus for detection
of IGR a different approach will need to be adopted (See page 34).
Activities in Finland Regarding Vascular Risk Assessment and Prevention of Diabetes
There has been a lot of innovative work in Finland in the area of CVD prevention. At a Public Health level the
Finnish have been successful in implementing behaviour change in the general population to try and reduce the
risk of CVD64.
The unequivocal evidence of DM prevention by lifestyle intervention shown in the Finnish study as well as the
North American Diabetes Prevention Programme is a strong argument for detecting subjects who have an increased risk for future T2DM, such as those with IGR35,36.
There are two approaches to detecting IGR. One is to measure blood glucose levels but, as has been said earlier,
FPG is largely unhelpful and in order to measure the 2 hour glucose and determine the presence of IGT requires
large numbers of OGTTs which are expensive, time consuming and unlikely to be implemented on a large scale in
primary care. The Finns, therefore, have done work looking at risk assessment models for T2DM and have developed the FINDRISC57,58,59.
The FINDRISC is unique in that it focuses on predicting future DM with several factors that are simple and easy
to measure, non-invasive, and are known to be associated with the risk of T2DM. These are easily comprehensible and direct the person’s attention to the modifiable risk factors of DM.
The FINDRISC Diabetes Risk Score
The original FINDRISC included only 7 questions and did not include family history of DM. Using the 7 questions around age, BMI, waist circumference, BP, history of high blood glucose, physical activity and consumption of vegetables, fruits or berries showed that the score was reliable in predicting future DM over a 10 year
period, in two cohorts, with an area under the curve >0.8556. Using this original score with a value of 9 or above
was associated with an increased risk of future DM with a sensitivity of 78% and a specificity of 77% in the 1987
cohort (sensitivity of 81%, specificity 76% in the 1992 cohort). Using this original score of a cutpoint of 9 identified the highest risk 25% of the population, which produced 78% of the incidence cases of DM56. The final
FINDRISC has been amended in two ways; the age categories have been changed, with the addition of an age
category of >64 years with a score value of 4, and the addition of a question regarding family history. The final
FINDRISC is available at www.diabetes.fi/english/risktest and is shown on page 33.
032
PART 1_Section 2
FINRISC Test designed by Professor Jaakko Tuomilehto, Dept Public Health, University of Helsinki, and Jaana Lindstrom,
MFS, National Public Health Institute, Finland
033
Even though the FINDRISC was designed to predict future DM risk, it has proved to be a reasonably reliable
method in identifying previously unrecognised DM. Using the risk cut-off of 11(for the original version) it has a
sensitivity of 66% in men and 70% in women. Furthermore it has also been shown to be strongly associated
with the presence of CVD risk factors, the metabolic syndrome, and also as a future predictor of CHD, stroke
and total mortality58.
The FINDRISC has been tested in other populations. In a German study which compared the Dutch, Cambridge and American risk scores in comparison to the FINDRISC, the FINDRISC had the highest sensitivity
(88%)59. It is important that any risk score is validated in the population it will be used in. Whilst there are other
risk scores available (See page 090 of the Appendix) the FINDRISC compares well and can be used as a self assessment tool56-63.
Comparison of different strategies to identify those with impaired glucose regulation (IGR)
Previous studies have shown that approaches that identify those with Diabetes Mellitus are not particularly helpful
at picking up those with lesser but important degrees of glucose intolerance, such as impaired glucose tolerance
(IGT) and Impaired Fasting Glucose (IFG) (see page 31).
We have compared three approaches to identify those with IGR in a UK, multi-ethnic population (see page 72-82
for full details). The results are summarised in Figure 6. Essentially use of FPG in all has the highest sensitivity. For
FPG of >5mmol/L the sensitivity is approximately 90% but this requires 100% of patients to have an initial FPG and
over 60% to have an OGTT. Clearly this is not feasible. Increasing the FPG cut off to 5.5 mmol/L has a good sensitivity of 70% and reduces the number of required OGTTs to 30% but all patients would be required to have an initial FPG.
An alternative option is to use the FINDRISC (see example on page 33). Using a cut off of ≥12 points will identify
the top 40% of the population, and if a cut off of FPG of 5.0mmol/L is used the sensitivity is 56% and about 30%
require an OGTT. We are in the process of developing and piloting a Leicester Diabetes Risk Score and early results suggest we can improve the performance of the FINDRISC (see page 78-82)
u Figure 6. Approaches to Identification of IGR in the General Population
034
PART 1_Section 2
An example of an algorithm for identification, assessment and management for those at increased risk of developing
T2DM is shown in Figure 7.
u Figure 7. An Example of an Algorithm for Identification, Assessment and Management for those at Increased
Risk of Developing T2DM
Black and Minority Ethnic Issues (BME)
South-Asian (SA) people form an important minority ethnic population in many countries worldwide with SA people originating from India, Pakistan, Sri Lanka and Bangladesh forming the largest minority ethnic group in the
UK, amounting to some 2.3 million65. A consistent finding in these migrant populations is a higher incidence and
prevalence of premature CHD than in the indigenous population. In the UK, mortality from CHD is currently 46%
higher for men and 51% higher for women of SA origin than in the non-Asian population66. South-Asians are not
a uniform group, but include ethnic subgroups with different cultures and practices and the prevalence of recognised risk factors for CVD may vary between these subgroups67. However, even taking these differences into
account, classical risk factors do not fully explain the increased risk of CHD in the SA population.
Systematic reviews have shown that levels of physical activity are lower in all SA groups68. SA people who are
physically active have a more favourable metabolic syndrome risk factor profile. Scientific evidence suggests that
SA populations have different associations between BMI, percentage of body fat and health risk than do European populations. It has been shown that SA people have a high risk of T2DM and CVD at a substantially lower
BMI than the existing WHO cut-off for overweight as currently defined, ≥25 kg/m2 and obesity, currently defined
as 30 kg/m2. Public health action points for SA populations for overweight and obesity have been defined at 23
and 27.5 kg/m2 respectively69,70.
035
Evaluation of the candidate definitions for Metabolic Syndrome in adult SAs suggests modification of the NCEP
ATP III definition with ethnically sensitive waist circumference (WC) cut-offs and BMI cut-offs. For example, for a
definition of the Metabolic Syndrome, a cut-off of 90cms of WC in men and 80cms in women, and a BMI cut-off
of ≥23 kg/ m2 71.
Vascular risk assessment and screening for DM is therefore particularly important in the BME population, particularly the SA population, in the UK. However, there remain a number of difficulties:
u Screening is based on BMI requiring ethnically appropriate adjustments and BMI as trigger points for
intervention, i.e. BMI of 23 and 27.5 kg/m2 are used rather than 25 kg/m2 and 30 kg/m2 to define
overweight and obesity respectively
u If traditional risk factor assessment tools based on the Framingham equation are used, an adjustment is made
based on ethnicity (suggest multiply by a factor of 1.4, i.e. if 15% then multiply by 1.4 = 21%)
u Systems for recording ethnicity are improved in general practice to allow structured and systematic risk
assessment via record based strategies
u The current tool in GP systems does not well categorise ethnicity (An example is shown on page 113)
u That implementation of a programme does not increase inequalities by using tools that underestimate
true vascular risk in BME populations
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037
PART 1_Section 2
22. Sesso HD, Lee IM, Gaziano JM, Rexrode KM, Glynn RJ, Buring JE. Maternal and paternal history of myocardial infarction and risk of
cardiovascular disease in men and women. Circulation 2001;104:393-8.
37. Diabetes UK. Early identification of people with Type 2 diabetes (position statement). 2006.
www.diabetes.org.uk/Documents/Professionals/Earlyid_TYPE2_PS.doc
38. American Diabetes Association. Screening for Type 2 Diabetes (position statement). Diabetes Care 2003;26.
39. Timothy Welborn. ADS: Screening for non-insulin dependent diabetes (position statement). 1996.
http://www.racp.edu.au/ads/screening.pdf
40. Derived from Forouhi etal. Diabetes prevalence in England, 2001 - estimates from an epidemiological model. Diabetic Medicine 2005,
23, 189-197 [Reference states 667,000 for England alone, if this figure is extrapolated pro rata for the rest of the UK, then the
undiagnosed will be closer to 750,000].
41. Harris MI, Klein R, Welborn TA, Knuiman MW. Onset of NIDDM occurs at least 4-7 yrs before clinical diagnosis. Diabetes Care
1992;15:815-9.
42. Manley SM, Meyer LC, Neil HAW, Ross IS, Turner RC, Holman RR. UK Prospective Diabetes Study 6. Complications in newly diagnosed
type 2 diabetic patients and their association with different clinical and biochemical risk factors. Diabetes Res. 1990;13:1-11.
43. Colagiuri S, Cull CA, Holman RR, UKPDS Group. Are lower fasting plasma glucose levels at diagnosis of type 2 diabetes associated
with improved outcomes?: UKPDS 61. Diabetes Care 2002;25:1410-7.
44. Department of Health. Quality and Outcomes Framework (updated). 2004.
http://www.dh.gov.uk/en/Policyandguidance/Organisationpolicy/Primarycare/Primarycarecontracting/QOF/DH_4125653
45. National Institute for Clinical Excellence. Management of type 2 diabetes - retinopathy: Early management and screening. 2002.
http://www.nice.org.uk/download.aspx?o=27922
46. Goyder E and Carlisle J. National Evaluations of DHDS Diabetes Screening Pilot Programme: Interim Report to UK National Screening
Committee, Sheffield: Public Health Section of ScHARR. 2006.
47. Coutinho M, Gerstein HC, Wang Y, Yusuf S. The relationship between glucose and incident cardiovascular events. A meta-regression
analysis of published data from 20 studies of 95,783 individuals followed for 12.4 years. Diabetes Care 1999;233-40.
48. Khaw KT, Wareham N, Luben R, Bingham S, Oakes S, Welch A et al. Glycated haemoglobin, diabetes, and mortality in men in Norfolk
cohort of european prospective investigation of cancer and nutrition (EPIC-Norfolk). BMJ 2001;322:15-8.
49. Alberti KG,.Zimmet PZ. Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and
classification of diabetes mellitus provisional report of a WHO consultation. Diabet.Med. 1998;15:539-53.
50. Norhammar A, Tenerz A, Nilsson G, Hamsten A, Efendic S, Ryden L et al. Glucose metabolism in patients with acute myocardial
infarction and no previous diagnosis of diabetes mellitus: a prospective study. Lancet 2002. 359;2140-4.
51. Gillies CL, Abrams KR, Lambert PC, Cooper NJ, Sutton AJ, Hsu RT et al. Pharmacological and lifestyle interventions to prevent or delay
type 2 diabetes in people with impaired glucose tolerance: systematic review and meta-analysis. BMJ 2007;334:299.
52. Davies MJ, Tringham JR, Troughton J, Khunti KK. Prevention of Type 2 diabetes mellitus. A review of the evidence and its application in
a UK setting. Diabet.Med. 2004;21:403-14.
53. Cardiovascular risk profile assessment in glucose-intolerant Asian individuals--an evaluation of the World Health Organization two-step
strategy: the DECODA Study (Diabetes Epidemiology: Collaborative Analysis of Diagnostic Criteria in Asia). Diabet.Med. 2002;19:549- 57.
54. Nelson KM,.Boyko EJ. Predicting impaired glucose tolerance using common clinical information: data from the Third National Health and
Nutrition Examination Survey. Diabetes Care 2003;26:2058-62.
55. Colagiuri S, Hussain Z, Zimmet P, Cameron A, Shaw J. Screening for type 2 diabetes and impaired glucose metabolism: the Australian
experience. Diabetes Care 2004;27:367-71.
56. Lindstrom J,.Tuomilehto J. The diabetes risk score: a practical tool to predict type 2 diabetes risk. Diabetes Care 2003;26:725-31.
57. Rathmann W, Martin S, Haastert B, Icks A, Holle R, Lowel H et al. Performance of screening questionnaires and risk scores for
undiagnosed diabetes: the KORA Survey 2000. Arch.Intern.Med. 2005;165:436-41.
58. Silventoinen K, Pankow J, Lindstrom J, Jousilahti P, Hu G, Tuomilehto J. The validity of the Finnish Diabetes Risk Score for the
prediction of the incidence of coronary heart disease and stroke, and total mortality. Eur.J.Cardiovasc.Prev.Rehabil. 2005;12:451-8.
59. Franciosi M, De Berardis G, Rossi MC, Sacco M, Belfiglio M, Pellegrini F et al. Use of the diabetes risk score for opportunistic screening
of undiagnosed diabetes and impaired glucose tolerance: the IGLOO (Impaired Glucose Tolerance and Long-Term Outcomes
Observational) study. Diabetes Care 2005;28:1187-94.
60. Glumer C, Carstensen B, Sandbaek A, Lauritzen T, Jorgensen T, Borch-Johnsen K. A Danish diabetes risk score for targeted screening:
the Inter99 study. Diabetes Care 2004;27:727-33.
038
61. Park PJ, Griffin SJ, Sargeant L, Wareham NJ. The performance of a risk score in predicting undiagnosed hyperglycemia. Diabetes Care
2002;25:984-8.
62. Thomas C, Hypponen E, Power C. Type 2 Diabetes Mellitus in Midlife Estimated From the Cambridge Risk Score and Body Mass Index.
Arch.Intern.Med. 2006;166:682-6.
63. Mohan V, Sandeep S, Deepa M, Gokulakrishnan K, Datta M, Deepa R. A diabetes risk score helps identify metabolic syndrome and
cardiovascular risk in Indians - the Chennai Urban Rural Epidemiology Study (CURES-38). Diabetes Obes.Metab 2007;9:337-43.
64. Puska P, Salonen J, Nissinen A, Tuomilehto J. The North Karelia project. Prev.Med. 1983;12:191-5.
65. Office of National Statistics. Census of England and Wales. 2001.
66. Balarajan R. Ethnicity and variations in mortality from coronary heart disease. Health Trends 1996;2.
67. Bhopal R, Unwin N, White M, Yallop J, Walker L, Alberti KG et al. Heterogeneity of coronary heart disease risk factors in Indian,
Pakistani, Bangladeshi, and European origin populations: cross sectional study. BMJ 1999;319:215-20.
68. Fischbacher CM, Hunt S, Alexander L. How physically active are South Asians in the United Kingdom? A literature review. Journal of
Public Health 2004;250-8.
69. WHO expert consultation. Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies.
Lancet 2004;363:157-63.
71. Alberti KG, Zimmet P, Shaw J. Metabolic syndrome--a new world-wide definition. A Consensus Statement from the International
Diabetes Federation. Diabet.Med. 2006;23:469-80.
039
PART 1_Section 2
70. Razak F, Anand SS, Shannon H, Vuksan V, Davis B, Jacobs R et al. Defining obesity cut points in a multiethnic population. Circulation
2007;115:2111-8.
040
PART 1_Section 3
Vascular Risk Management
Overview of the Efficacy of Interventions
The Joint British Society Guidelines on the Prevention of Cardiovascular Disease in Clinical Practice was a joint
collaboration between the British Cardiac Society, British Hypertension Society, Diabetes UK, Heart UK, the Primary Care Cardiovascular Society and the Stroke Association1. The aim was to promote a consistent multidisciplinary approach to the management of people with both established atherosclerotic CVD (those with CHD and
stroke) and also those at high risk of developing symptomatic atherosclerotic disease. An emphasis of this
guideline was that CVD prevention in clinical practice should focus equally on people with established atherosclerotic CVD and people with DM, but also on apparently healthy individuals who were at high risk of developing symptomatic atherosclerotic disease, this being defined as being ≥20% risk over 10 years as defined by a
risk score.1 This has been followed by the SIGN guidance for Risk Estimation and the Prevention of CVD and
most recently the consultation document for Lipid Modification from NICE2-3.
There is a clear recognition that lifestyle and risk factor intervention including appropriate drug therapies mainly
to lower BP, modify lipids and reduce glycaemia are required. These documents all include clear targets for
lifestyle BP, lipid and lifestyle management and also clear specific clinical indications for particular CVD protective
drug therapies1-3.
Smoking
Smoking increases the risk of vascular disease and the adverse effect is related to the amount of tobacco
smoked and the duration of smoking. The impact is greater for patients with HT and DM. Stopping smoking is
followed by a rapid decline in risk of vascular disease. All current smokers should receive advice from a healthcare professional to stop smoking completely, and this advice should be consistent, reiterated and reinforced by
all healthcare professionals. The advice should include a description of the vascular risk of smoking, provide
appropriate information on the approaches to stopping, assessing readiness to stop, and agreeing a specific
action plan with a follow-up arrangement. NICE have published advice on smoking cessation in primary care4.
There is also separate guidance on use of pharmacotherapy5. This advocates that Nicotine Replacement Therapy (NRT) or bupropion should normally be prescribed when the person has made a commitment to stop smoking and agreed a ‘target stop date’5.
Diet
There are complex relationships between diet and vascular disease. Epidemiological data shows that total fat
and saturated fat are positively associated with long-term CHD mortality6. Consumption of saturated fat increases LDL cholesterol. A decrease in fat intake results in a decrease in both HDL and LDL cholesterol. A
meta-analysis of RCTs of reducing saturated fat using monounsaturated or polyunsaturated fats as a replacement has shown a risk reduction in CVD events7.
People at high risk of CVD should be advised to eat a diet in which total fat intake is 30% or less of total energy intake, saturated fats are 10% or less of the total energy intake, intakes of dietary cholesterol is less than 300mg/day
and saturated fats are replaced by increasing the intake of monounsaturated fats. This advice is summarised at
www.eatwell.gov.uk/healthydiet/8. Dietary targets for those at risk of Vascular Disease are highlighted below.
1
Keep total dietary intake of fat to 30% of total energy intake
2
Keep the intake of saturated fats to 10% of total fat intake
3
Keep the intake of dietary cholesterol to < 300 mg/day
4
Replace saturated fats by an increased intake of monounsaturated fats
5
Increase the intake of fresh fruit and vegetables to at least five portions per day
u Table 5. Dietary Advice for those at Risk of Vascular Disease1,2,3,8
041
PART 1_Section 3
Management of Specific Risk Factors
Management of Obesity
As body weight (defined conventionally by Body Mass Index) rises so does the risk of vascular disease.9 However, there appears to be an additional risk from central adiposity which is easily measured by waist circumference (cm)10.
Overweight and abdominal obesity are also associated with other risk factors, including small and dense atherogenic LDL cholesterol, low HDL cholesterol, raised triglycerides, elevated BP, insulin resistance and impaired
glucose regulation (IGR). Clustering of these risk factors has now been defined by the Metabolic Syndrome, of
which there are a number of definitions11-13.
Studies have shown weight loss in the range of 5-10% results in improvements in BP, Lipid Profile and glucose
tolerance and if it can be maintained it is possible to extrapolate the reduction of the cardiac events that would
be predicted by risk analysis14-18.
Weight reduction strategies may be appropriate for those who are;
u Overweight (BMI >25 kg/m2 lower thresholds for those of SA origin, > 23 kg/m2)
u Obese (BMI > 30 kg/m2) (27.5 kg/m2 for those of SA origin)
u Increased abdominal fat as defined by a circumference of >94cms in men and 80cms in women (90 cms
for SA men, 80cms in SA women)
Broad guidelines are that:
u Calorie intake can be reduced by reducing consumption of high energy dense foods, particularly
saturated fats, refined carbohydrate and some alcoholic drinks, as well as calorie restriction.
u Fat intake should be <30% of total energy intake.
u Foods with high fat content should be replaced with vegetables, fruit and cereal products.
u Increasing physical activity can make an important contribution and it is important that strategies for
promoting physical activity are offered and integrated into other initiatives that are ongoing (i.e. exercise on
prescription).
u Successful weight reduction requires sustained personal and family motivation, and long-term professional
support (see www.eatwell.gov.uk/healthydiet)8.
Drug Management of Obesity
Other interventions include anti-obesity medication, including inhibitors of intestinal fat absorption and those acting on the central nervous system to suppress appetite, to reduce food intake and increase thermogenesis19-20.
Guidelines currently recommend drug therapy be considered for those in obese people with one or more obesity
related disorders. However, most clinical trials have been of short duration and there is no assessment of these
drugs on long-term mortality. Weight regain is common when drug therapies are stopped.
Lifestyle Advice for Those at High Risk of DM
For those with IGT there is strong evidence that intensive diet and lifestyle interventions reduce the risk of DM.
In both the Finnish and the American studies, the intervention group were given individualised counselling to
achieve their lifestyle goals. After a median of 4 years, the Finnish Study showed a 58% reduction in risk of progression to T2DM in subjects with IGT21. Exactly the same result was seen in a multi-ethnic population in the
USA22. The Finnish Study has been followed for a further 3 years and there continued to be a 43% reduction in
relative risk of progression to diabetes. The benefits of lifestyle change were achieved in the intervention group
even after discontinuation of the intervention, with a 36% reduction in relative risk of developing diabetes over
the subsequent 3 years23.
042
u This highlights the importance of structured and targeted lifestyle interventions to people at high risk of
subsequent DM.
The main goals of this effective intervention were:
u Weight reduction of 5% or more
u Less than 30% of daily energy intake from fat
u Less than 10% of daily energy intake from saturated fat
u Fibre intake 15 grams per 1,000 Kilocalories or more
u Moderately intense physical activity of 30 minutes per day or more
Other Dietary Factors
Regular fish consumers appear to be at a lower risk of fatal CHD and RCTs show increased fish consumption
results in reductions in coronary and total mortality. There is some conflicting evidence on the benefits associated with increased consumption of omega 3 fats. Some studies had suggested that omega 3 fatty acids were
beneficial in preventing and treating CHD24. A meta-analysis of 48 RCTs and 26 cohort studies does not support
this25. In view of this uncertain effect and in order to avoid conflicting dietary advice, no change is recommended
from the advice given in the current dietary guideline (two 140g portions of fish, one of which should be a oily
fish, per week)26. Fish consumption may help to reduce intake of (saturated) fat from meat.
u All individuals are recommended to eat at least two portions of fish per week, one of which should be an oily fish2
Dietary Salt Intake
A meta-analysis of 28 trials on the effect of moderate salt reduction on blood pressure demonstrated that a
modest reduction in salt intake for four or more weeks has a significant effect on blood pressure in both hypertensive and normotensive individuals. A reduction in salt intake of 6g per day (100 mmol or 2.3g of sodium per
day) predicted a fall in blood pressure of 7.1/3.9 mmHg (p<0.001 for both systolic and diastolic) in hypertensive
patients and 3.6/1.7 mmHg in normotensive individuals (systolic: p<0.001; diastolic: p<0.005)27. The Food Standard Agency has recommended that adults should consume no more than 6g of salt per day (approximately
equivalent to one teaspoonful)28.
u People with hypertension should be advised to reduce their salt intake as much as possible to lower blood
pressure
u All individuals should aim to consume less than 6g of salt per day
Fruit and Vegetable Intake
Diets rich in fruit and vegetables tend also to be low in fat. Two systematic reviews of cohort studies examined
the benefits of fruit and vegetable consumption for the reduction of CHD risk. There is evidence from cohort
studies to support reduced CHD event rates from increased vegetable (risk ratio 0.77) and fruit (risk ratio 0.86)
intake in one review, and a 15% reduced relative risk of CHD in those consuming high levels of fruit and vegetables, in another29,30.
u Increased fruit and vegetable consumption is recommended to reduce cardiovascular risk for the entire
population
043
PART 1_Section 3
Omega 3 Fatty Acids
Antioxidant Vitamin Supplementation
Several systematic reviews of RCTs were identified that investigated the association between vitamin supplementation and prevention of CHD. One systematic review of 84 RCTs found that neither supplements of vitamin
E alone nor given with other agents yielded a statistically significant beneficial or adverse pooled relative risk for
all-cause mortality, cardiovascular mortality, fatal or non-fatal myocardial infarction in blood lipids31.
The US Preventive Services Task Force guideline investigated the evidence on the role of antioxidant supplementation in reducing the incidence of or progression to CHD. The guideline found little evidence that any single
vitamin supplementation (vitamin A, vitamin C, vitamin E, β-carotene), combined antioxidants or multivitamins
had benefit on primary or secondary prevention32.
Stanol Esters and Plant Sterols
Stanol esters and plant sterols are present in small amounts in normal diets, and can be supplemented using dietary products such as margarines and yogurt drinks. Two systematic reviews provide evidence that they can
reduce LDL cholesterol33,34. In the larger review of 41 RCTs of the effect on serum lipids, 2g per day supplements of stanol esters and plant sterols led to a 10% reduction in LDL cholesterol33. There was no benefit from
further dosage increases. The cost to the individual of this supplement has been estimated at £70 per year.34 As
yet, there is no evidence on whether these reductions in cholesterol translate in the longer term into reduction in
CVD, nor is there long term data (more than five years) on their safety.
Alcohol
Guidance should be the same as for the general population. Alcohol consumption ranging between 1-3 alcohol
units per day (1 unit equates to 80mrs of wine, 250mrs of normal strength beer and 30-50mls of spirits) is associated with the lowest all-cause mortality. Optimum consumption is lower for women than for men (recommendations are 14 units for women and 21 for men per week)1.
Promoting Physical Activity
A sedentary lifestyle is associated with increased vascular risk. In asymptomatic people, aerobic physical activity and cardio-respiratory fitness are associated in a dose-response fashion with a significant reduction in CVD
and all-cause mortality. Increased physical activity, whether at work or taken in leisure time, is associated with a
lower CHD risk in both men and women35. The greatest reduction in risk is between those with sedentary and
moderately active individuals. The benefits of physical activity on vascular outcomes is lost once physical activity is discontinued. Physical activity has an important contribution in both losing weight and preventing weight
gain, and has beneficial effects on blood pressure, increasing HDL cholesterol and reducing the risk of developing T2DM36. NICE has recently published guidelines on strategies to promote physical activity37. In general guidance should be given in line with the Chief Medical Officers Report 2004 and the NICE Guidance and this is in
line with the guidance for the general population37-38. This is summarised as:
u 30 minutes of moderate intensity physical activity at least 5 days a week
u Those with co-morbidity/or personal circumstances which mean they are unable to do this, should be
encouraged to exercise at their maximum safe capacity.
u Recommend types of activity which can be incorporated into everyday life i.e. brisk walking
u Any advice should take account of the persons needs, preference and circumstance.
A useful table of intensity and energy expenditure for common types of physical activity is found in the Appendix
page 89.
044
Hypertension
As BP rises, so does the risk of stroke, CHD and heart failure and CKD. Elevated BP is also associated with an
accelerated rate of decline of cognitive and renal function. The vascular risk associated with elevated blood
pressure is determined by both the level of BP and the presence of other risk factors. Data from many RCTs
provide compelling data and evidence of the effectiveness of anti-hypertensive therapy at reducing risk. Reduction in BP by an average of 12/6 mmHg can be expected to reduce stroke by 40% and CHD by 20%39. The absolute risk reduction is greatest in those at highest risk. In patients with diabetes and CKD lower targets for
blood pressure management are required. In CKD evidence has shown that lowering target BP may slow the
decline in kidney function in people that have moderate to high levels of proteinuria40. In people who have a high
rate of proteinuria (>1g in 24 hours) this effect was beneficial at a BP target of 125/75 mmHg. This was confirmed by a further meta-analysis41. However in CKD with lower levels or no proteinuria the evidence for lower
targets to preserve renal function is less clear42.
In DM a lower BP target is required because, the greater the blood pressure level, the greater the benefit in
terms of CVD events and there appears to be no threshold effect. Strict control of blood pressure is the most
important factor in preventing development of diabetes nephropathy and advanced renal failure43-45.
All people with persistently high BP ≥140/90, high/normal BP (135-139/85-89) or a family history of HT should
receive lifestyle advice to help reduce blood pressure and CVD risk. Lifestyle advice should continue, even when
drug therapy is initiated (Figure 8). Lower thresholds are recommended for subjects following a MI, stroke or
TIA, with established CKD and those with DM, where the intervention threshold is a systolic of >130 mmHg
and/or a diastolic of >80 mmHg43-45. Those who reach 80 years should remain on therapy if there is evidence of
CVD, target organ damage or other vascular disease such as DM. Optimal and audit standards for blood pressure target are outlined in Table 6.
Those with persistent BP ≥ 160/100 mmHg should be offered treatment regardless of other risk factors. An
audit standard of <150/90 should be considered as a minimum for all patients treated with hypertension and
should be <140/80 for those at highest risk. This is suggested by JBS-2 Guidance1.
u Figure 8. Intervention Thresholds for Blood Pressure
045
PART 1_Section 3
Interventions for Blood Pressure (BP)
Elevated BP 140/90 with a CVD risk 20% over 10 years and
/or target organ damage
Elevated BP with diabetes or CKD or
established atherosclerotic disease
Optimal1,2 (mmHg)
Audit Standard used by
JBS-2 (mmHg)1
<140/85
<150/90
<130/80
<140/80
u Table 6. Optimal and audit standard blood pressure targets
In terms of selection of particular drug therapy, many RCTs have been consistent in showing that BP lowering
based on various classes of drugs are effective at reducing complications and vascular morbidity and mortality.
There is long-standing evidence with diuretics and β-blockers, and recent studies have also confirmed the
safety and efficacy of ACE inhibitors, ARBs and calcium channel blockers46-50. Most clinical trials have shown
that patients require 2 or 3 blood pressure lowering drugs in order to achieve recommended BP targets. However, current practice in the UK suggests that almost two-thirds of treated patients receive mono-therapy and
less than 10% receive more than 2 drugs. This is reflected by the fact that less than half of patients with treated
hypertension have their blood pressure optimally controlled51.
The British Hypertension Society in its most recent guidelines has suggested the ABCD treatment algorithm to
advise and assist practitioners on logical sequencing and combinations of drug therapy in the treatment of hypertension (Figure 9).
u Figure 9. ABCD Treatment Algorithm for Hypertension52
* Beta Blockers are not a preferred initial treatment for hypertension but can be an alternative to A in patients < 55 years in whom A is
not tolerated or contraindication (includes women of child bearing potential)
046
Cholesterol and Lipid Lowering
Epidemiological evidence has shown that populations with higher cholesterol levels experience more atherosclerosis and CHD than populations with lower levels and the higher the level of cholesterol, the greater the risk of
coronary event53.
The focus on LDL cholesterol is because although HDL cholesterol is also inversely related to the risk of vascular
disease, and the total cholesterol to HDL ratio is used for vascular risk assessment, there is no particular treatment target for HDL cholesterol because HDL cholesterol is only altered modestly and not independently of
changes in other lipid parameters and there are, as yet, no drugs available which independently alter HDL cholesterol. Statins increase HDL cholesterol by about 3-10%. Fibrates increase HDL cholesterol and reduce
triglycerides, but have only a moderate effect on LDL cholesterol. A systematic review and meta-analysis of 58
RCTs of cholesterol lowering concluded that for 1 mmol reduction in LDL cholesterol there was a reduction in
coronary death and non-fatal MI of 11% in the first year, 24% in the second year and 33% in the third-fifth year,
and 36% in subsequent years54. Lipid assessment should be offered to all subjects from age 40 years1-3.
The primary action of statins is to lower LDL cholesterol with only small effects on HDL cholesterol or triglyceride
levels. A meta-analysis of 164 short term RCTs of lipid lowering by different statins showed absolute LDL cholesterol reduction associated with different doses of different statins. The reductions in LDL cholesterol are dosedependant and log-linear, so that with each doubling of dose of statin, LDL levels fall by approximately 6%55.
This meta-analysis showed that a reduction in LDL cholesterol of 1.6 mmol/l halves the risk of CHD events after
two years and that this reduction can be achieved with standard doses of some statins55.
The Benefits of Lowering Cholesterol for Cardiovascular Risk
Statins are central to lipid lowering therapy in the prevention of vascular events. Statins inhibit cholesterol synthesis in the liver, activating hepatocyte LDL receptors and increasing hepatic uptake of LDL from the circulation.
A meta analysis of lipid lowering in five randomised, placebo-controlled, double-blind trials included two trials in
patients without evidence of cardiovascular disease (n = 13,200) and three trials carried out in symptomatic patients (n = 17,617). Active treatment with statins was associated with a 34% relative risk reduction (95% CI 23%
to 43%; p <0.001) in major coronary events in the primary prevention trials and a 30% relative risk reduction
(95% CI 24% to 35%; p <0.001) in the secondary prevention trials. The mean reduction (weighted by sample
size) in TC, LDL cholesterol, and triglyceride levels was 20%, 28%, and 13%, respectively, and HDL cholesterol
was increased by an average of 5% among the five trials56.
047
PART 1_Section 3
As the concentration of total cholesterol and in particular LDL cholesterol increases, so does the risk of vascular
disease53. The relationship is continuous, and determined by the concentration of LDL cholesterol and that of
HDL cholesterol (inversely) and to a lesser extent by triglyceride concentration. The cholesterol/HDL ratio is incorporated into the risk assessment. However, the preferred target for lipid lowering treatment decisions is the
level of LDL cholesterol.
Statin Therapy in High Risk Individuals without Cardiovascular Disease2
u All adults over the age of 40 years who are assessed as having a ten year risk of having a first
cardiovascular event ≥20% should be considered for treatment with a statin (simvastatin 40 mg/day or a
drug of comparable effectiveness or acquisition cost2-3) following an informed discussion of risks and
benefits between the individual and a responsible clinician
u The level of CVD risk should be measured using a recommended CVD risk equation
u In individuals without established CVD, lifestyle measures to reduce cholesterol levels should be
encouraged, irrespective of the need for pharmacological treatment
u Secondary causes of dyslipidaemia should be considered and excluded before commencing lipid drug
therapy
Evidence from WOSCOPS and AFCAPS/TexCAPS indicates that the risk of major coronary events may be significantly reduced by standard doses of statin therapy57-58. A systematic review of economic evidence reported
that it is cost effective to give statins to individuals without evidence of CVD but with a ten-year 20% risk of CVD
with statins compared to providing standard diet and lifestyle measures2,59. The model made several simplifying
assumptions to conclude that such individuals could be identified with complete accuracy. It used an annual
cost for statins of about £320 per person (a weighted average of the drugs used in the pooled trials). The advent
of lower priced generic drugs has reduced the annual cost to under £502.
Statin Therapy in Individuals with Established CVD2
Individuals who are at high CVD risk, such as those with established CVD, will gain more benefit from aggressive
lipid lowering than individuals at lower absolute levels of risk. One systematic review reported that it is cost-effective to treat with a statin all individuals with CVD, compared to providing standard diet and lifestyle measures59. This was confirmed in a large trial of treatment with 40mg per day simvastatin in people with different
levels of coronary vascular risk60.
u All patients with established symptomatic atherosclerotic cardiovascular disease should be considered for
more intensive statin therapy following an informed discussion of risks and benefits between individual and
responsible clinician
u Patients should be advised to report unexplained muscle pains or other adverse effects promptly,
especially if associated with fever or malaise
u If such effects are mild, a different statin may be tried and/or the statin dose reduced after discussing the
risks with the patient
u If severe side effects are experienced statin therapy should be discontinued
048
Cholesterol Targets for Therapy in Patients with Established Cardiovascular Disease
(Secondary Prevention)
The JBS2 guideline states “there are no clinical trials which have evaluated the relative and absolute benefits of
cholesterol lowering to different total and LDL cholesterol targets in relation to clinical events”.1 Establishing a
cholesterol target for therapy is therefore an extrapolation from the apparent benefits indicated by major trials of
lipid lowering, while maintaining appropriate margins for safety, given that there are still no long term follow up
studies of statin therapy1.
Several guidelines have recommended titration of lipid lowering therapy to achieve LDL cholesterol levels less
than 2.5 mmol/l for patients at high cardiovascular risk1,61.
A systematic review of RCTs, cohort studies, and case control studies that examined the independent relationship between LDL cholesterol and major cardiovascular outcomes in patients with LDL cholesterol levels less
than 3.36 mmol/l found no clinical trial subgroup analysis, valid cohort or case control analyses suggesting that
the degree to which LDL cholesterol responds to statin independently predicts the degree of cardiovascular risk
reduction63. Although the review indicated that there was compelling evidence for the risk effectiveness of statin
therapy in lowering cholesterol in patients at high cardiovascular risk (regardless of their LDL cholesterol values)
it concluded that current clinical evidence does not demonstrate that lipid therapy should be titrated to achieve
proposed LDL cholesterol targets.64 While patients with established symptomatic cardiovascular disease should
be considered for intensive statin therapy, the long term safety and cost-effectiveness of such therapy has not
been established64.
In the SIGN guideline, the current NHS Scotland target for individuals at high cardiovascular risk is a total cholesterol of <5 mmol/l. This level is consistent with the Quality and Outcomes Framework65.
Reducing this target to 4.5 or 4.0 mmol/l would have major resource implications for NHS Scotland. Pending
further studies on mortality, safety and cost-effectiveness, the guideline development group suggests that current NHS Scotland targets are maintained, as the minimum standard of care, and the NICE Lipid Modification
Consultation also advocates this approach2-3.
Measuring Lipid Levels
It is important that the level of cholesterol incorporated into any risk assessment tool is that taken before drug
treatment was started, and this should always be used to estimate risk, not the cholesterol value on treatment.
LDL cholesterol can be calculated indirectly by measuring total cholesterol (TC), HDL cholesterol and triglycerides (TG) from a fasting venous blood sample and applying the Friedewald equation: LDL = TC-HDL(TG/2.2)66. This method is not suitable for individuals with TG levels > 5 mmol/l.
For greater accuracy fasting samples are required as HDL cholesterol and TG levels vary between fasting and
non-fasting states. HDL cholesterol is lower by 5% to 10% in the non-fasting state than in the fasting state and
TG levels are 20-30% higher.
Given the practical problems of routinely collecting fasting samples, non-fasting blood samples are generally collected for estimation of TC and HDL cholesterol67.
It may be practical to start with a non-fasting sample for total cholesterol and HDL cholesterol in terms of a comprehensive vascular assessment done in the context of population-based screening (Population Based Strategy).
However If the person is at high CVD risk, then a fasting sample is recommended at the initial assessment
(Record Based Strategy). Secondary causes of elevated lipids should be investigated. These include excessive
alcohol intake, undiagnosed or untreated DM, renal disease, liver disease and inadequately treated or undetected
hypothyroidism.
049
PART 1_Section 3
Current guidance from the Department of Health in England and Wales recommends that patients with established CHD should receive statins and dietary advice to lower serum cholesterol concentrations either to less
than 5 mmol/l (LDL cholesterol to below 3 mmol/l) or by 25% (30% for LDL cholesterol), whichever is greater62.
Management of Cholesterol in Special Groups
Subjects with diabetes are all considered to be at high CVD risk and should be offered a statin if aged 40 years
or more1-2. In subjects with DM aged between 18 and 39 the presence of;
u Retinopathy,
u Nephropathy,
u Poor glycaemic control,
u Elevated blood pressure,
u Raised total cholesterol of ≥ 6mmol/L
u Features of the Metabolic Syndrome
u Family history of premature CVD
are also indications for statin therapy1.
Antiplatelet Therapies
Aspirin or other platelet modifying drugs are recommended in all people with established atherosclerotic disease
and in those with DM, a dose of 75mg is advocated1-3. Aspirin is recommended for all those with T2DM who
are ≥ 50 years of age, and those at a younger age if they have had diabetes for more than 10 years or if they are
already receiving treatment for HT or have evidence of target organ damage, particularly retinopathy or
nephropathy. All those at high vascular risk (CVD risk ≥ 20% over ten years) should be considered for treatment
with aspirin 75, OD1-2.
In patients with CVD Clopidrogel should be considered in patients with hypersensitivity or intolerance in whom
aspirin causes unacceptable side effects2.
PART 1_Section 3 Reference List
1.
JBS 2: Joint British Societies' guidelines on prevention of cardiovascular disease in clinical practice. Heart 2005;91 Suppl 5:v1-52.
www.bcs.com/download/651/JBS2final.pdf
2. Scottish Intercollegiate Guidelines Network. Risk estimation and the prevention of cardiovascular disease: A national clinical guideline.
2007. http://www.sign.ac.uk/pdf/sign97.pdf
3. National Collaborating Centre for Primary Care. Cardiovascular risk assessment: the modification of blood lipids for the primary and
secondary prevention of cardiovascular disease - full guideline DRAFT. 2007. http://guidance.nice.org.uk/download.aspx?o=414903
4. National Institute for Clinical Excellence. Smoking Cessation: Brief interventions and referral for smoking cessation in primary care and
other settings. Public health intervention guidance 2006. http://guidance.nice.org.uk/PHI1/
5. National Institute for Clinical Excellence. TA039 Smoking cessation - bupropion and nicotine replacement therapy: Guidance. 2002.
http://www.nice.org.uk/TA039
6. NHS Health Scotland. Cardiovascular disease: a guide to primary prevention in Scotland. A report on behalf of the Heart Health National
Learning Committee. 2006. http://www.vhscotland.org.uk/library/misc/NHS-CVD%20Full%20Doc.pdf
7. Hooper L, Summerbell CD, Higgins JP, Thompson RL, Clements G, Capps N et al. Reduced or modified dietary fat for prevention of
cardiovascular disease. Cochrane.Database.Syst.Rev. 2004;CD002137.
8. Food Standards Agency. Advice on cardioprotective dietary changes. 2007. http://www.eatwell.gov.uk/
9. Jousilahti P, Tuomilehto J, Vartiainen E, Pekkanen J, Puska P. Body weight, cardiovascular risk factors, and coronary mortality. 15-year
follow-up of middle-aged men and women in eastern Finland. Circulation 1996;93:1372-9.
10. Despres JP. Health consequences of visceral obesity. Ann.Med. 2001;33:534-41.
11. Report of a WHO Consultation. Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and
classification of diabetes mellitus provisional report of a WHO consultation. Diabet.Med. 1998;15:539-53.
050
12. Alexander CM, Landsman PB, Teutsch SM, Haffner SM. NCEP-defined metabolic syndrome, diabetes, and prevalence of coronary heart
disease among NHANES III participants age 50 years and older. Diabetes 2003;52:1210-4.
13. Alberti KG, Zimmet P, Shaw J. Metabolic syndrome--a new world-wide definition. A Consensus Statement from the International
Diabetes Federation. Diabet.Med. 2006;23:469-80.
14. Mulrow CD, Chiquette E, Angel L, Cornell J, Summerbell C, Anagnostelis B et al. Dieting to reduce body weight for controlling
hypertension in adults. Cochrane.Database.Syst.Rev. 1998;CD000484.
15. Neter JE, Stam BE, Kok FJ, Grobbee DE, Geleijnse JM. Influence of weight reduction on blood pressure: a meta-analysis of randomized
controlled trials. Hypertension 2003;42:878-84.
16. Dattilo AM,.Kris-Etherton PM. Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis. Am.J Clin.Nutr.
1992;56:320-8.
17. Anderson JW,.Konz EC. Obesity and disease management: effects of weight loss on comorbid conditions. Obes.Res. 2001;9 Suppl
4:326S-34S.
18. O'Meara S, Glenny AM, Wilson C, Melville A, Sheldon TA. Effective management of obesity. Qual.Health Care 1997;6:170-5.
19. National Institute for Clinical Excellence. Orlistat for the treatment of obesity in adults (TA22). 2002. http://guidance.nice.org.uk/TA22
20. National Institute for Clinical Excellence. The clinical effectiveness and cost effectiveness of sibutramine for obesity.(TA31). 2001.
http://guidance.nice.org.uk/TA31
22. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA et al. Reduction in the incidence of type 2 diabetes
with lifestyle intervention or metformin. N.Engl.J Med. 2002;346:393-403.
23. Lindstrom J, Ilanne-Parikka P, Peltonen M, Aunola S, Eriksson JG, Hemio K et al. Sustained reduction in the incidence of type 2
diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study. Lancet 2006;368:1673-9.
24. Bucher HC, Hengstler P, Schindler C, Meier G. N-3 polyunsaturated fatty acids in coronary heart disease: a meta-analysis of
randomized controlled trials. Am.J Med. 2002;112:298-304.
25. Hooper L, Thompson RL, Harrison RA, Summerbell CD, Moore H, Worthington HV et al. Omega 3 fatty acids for prevention and
treatment of cardiovascular disease. Cochrane.Database.Syst.Rev. 2004;CD003177.
26. Food Standards Agency. Health diet:nutrition essentials: fish and shellfish. 2006.
http://www.eatwell.gov.uk/healthydiet/nutritionessentials/fishandshellfish/
27. He FJ,.MacGregor GA. Effect of modest salt reduction on blood pressure: a meta-analysis of randomized trials. Implications for public
health. J Hum.Hypertens. 2002;16:761-70.
28. Food Standards Agency. Science on salt. 2006. http://www.salt.gov.uk/science_on_salt.html
29. Anderson JW, Hanna TJ, Peng X, Kryscio RJ. Whole grain foods and heart disease risk. J Am.Coll.Nutr. 2000;19:291S-9S.
30. Law MR,.Morris JK. By how much does fruit and vegetable consumption reduce the risk of ischaemic heart disease: response to
commentary. Eur.J Clin.Nutr. 1999;53:903-4.
31. Shekelle PG, Morton SC, Jungvig LK, Udani J, Spar M, Tu W et al. Effect of supplemental vitamin E for the prevention and treatment of
cardiovascular disease. J Gen.Intern.Med. 2004;19:380-9.
32. Morris CD,.Carson S. Routine vitamin supplementation to prevent cardiovascular disease: a summary of the evidence for the U.S.
Preventive Services Task Force. Ann.Intern.Med. 2003;139:56-70.
33. Katan MB, Grundy SM, Jones P, Law M, Miettinen T, Paoletti R. Efficacy and safety of plant stanols and sterols in the management of
blood cholesterol levels. Mayo Clin.Proc. 2003;78:965-78.
34. Law M. Plant sterol and stanol margarines and health. BMJ 2000;320:861-4.
35. US Department of Health and Human Services. Physical Activity and Health:a report of the Surgeon General. Atlanta, Geoargia: US
Department of Health and Human Services, Centres for Disease Control and Prevention, National Centre for Chronic Disease Prevention
and Health Promotion. 1996.
36. Boule NG, Haddad E, Kenny GP, Wells GA, Sigal RJ. Effects of exercise on glycemic control and body mass in type 2 diabetes mellitus:
a meta-analysis of controlled clinical trials. JAMA 2001;286:1218-27.
37. National Institute for Clinical Excellence. Four commonly used methods to increase physical activity: brief interventions in primary care,
exercise referral schemes, pedometers and community-based exercise programmes for walking and cycling. Public health intervention
guidance. 2006. http://www.nice.org.uk/download.aspx?o=299528
051
PART 1_Section 3
21. Tuomilehto J, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H, Ilanne-Parikka P et al. Prevention of type 2 diabetes mellitus by
changes in lifestyle among subjects with impaired glucose tolerance. New England.Journal of Medicine 2001. 344;1343-50.
38. Department of Health. On the state of the public health: Annual report of the Chief Medical Officer. 2004.
http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/AnnualReports/DH_4086602
39. Blood Pressure Lowering Treatment Trialists' Collaboration. Effects of different blood-pressure-lowering regimens on major cardio
vascular events: results of prospectively-designed overviews of randomised trials. Lancet 2003;362:1527-35.
40. Buckalew VM, Jr., Berg RL, Wang SR, Porush JG, Rauch S, Schulman G. Prevalence of hypertension in 1,795 subjects with chronic
renal disease: the modification of diet in renal disease study baseline cohort. Modification of Diet in Renal Disease Study Group. Am.J
Kidney Dis. 1996;28:811-21.
41. Jafar TH, Stark PC, Schmid CH, Landa M, Maschio G, De Jong PE et al. Progression of chronic kidney disease: the role of blood
pressure control, proteinuria, and angiotensin-converting enzyme inhibition: a patient-level meta-analysis. Ann.Intern.Med.
2003;139:244-52.
42. Wright JT, Jr., Bakris G, Greene T, Agodoa LY, Appel LJ, Charleston J et al. Effect of blood pressure lowering and antihypertensive drug
class on progression of hypertensive kidney disease: results from the AASK trial. JAMA 2002;288:2421-31.
43. Schrier RW, Estacio RO, Esler A, Mehler P. Effects of aggressive blood pressure control in normotensive type 2 diabetic patients on
albuminuria, retinopathy and strokes. Kidney Int. 2002;61:1086-97.
44. Williams B. The unique vulnerability of diabetic subjects to hypertensive injury. J Hum.Hypertens. 1999;13 Suppl 2:S3-S8.
45. Estacio RO, Jeffers BW, Gifford N, Schrier RW. Effect of blood pressure control on diabetic microvascular complications in patients with
hypertension and type 2 diabetes. Diabetes Care 2000;23 Suppl 2:B54-B64.
46. Brown MJ, Palmer CR, Castaigne A, de Leeuw PW, Mancia G, Rosenthal T et al. Morbidity and mortality in patients randomised to
double-blind treatment with a long-acting calcium-channel blocker or diuretic in the International Nifedipine GITS study: Intervention as a
Goal in Hypertension Treatment (INSIGHT). Lancet 2000;356:366-72.
47. Psaty BM, Lumley T, Furberg CD, Schellenbaum G, Pahor M, Alderman MH et al. Health outcomes associated with various
antihypertensive therapies used as first-line agents: a network meta-analysis. JAMA 2003;289:2534-44.
48. Hansson L, Lindholm LH, Ekbom T, Dahlof B, Lanke J, Schersten B et al. Randomised trial of old and new antihypertensive drugs in
elderly patients: cardiovascular mortality and morbidity the Swedish Trial in Old Patients with Hypertension-2 study. Lancet
1999;354:1751-6.
49. Hansson L, Lindholm LH, Niskanen L, Lanke J, Hedner T, Niklason A et al. Effect of angiotensin-converting-enzyme inhibition compared
with conventional therapy on cardiovascular morbidity and mortality in hypertension: the Captopril Prevention Project (CAPPP)
randomised trial. Lancet 1999;353:611-6.
50. Hansson L, Hedner T, Lund-Johansen P, Kjeldsen SE, Lindholm LH, Syvertsen JO et al. Randomised trial of effects of calcium
antagonists compared with diuretics and beta-blockers on cardiovascular morbidity and mortality in hypertension: the Nordic Diltiazem
(NORDIL) study. Lancet 2000;356:359-65.
51. Primatesta P, Brookes M, Poulter NR. Improved hypertension management and control: results from the health survey for England 1998.
Hypertension 2001;38:827-32.
52. National Institute for Clinical Excellence. Hypertension: management of hypertension in adults in primary care. Clinical Guidelines (CG34).
2006. http://www.nice.org.uk/CG034
53. Stamler J, Wentworth D, Neaton JD. Is relationship between serum cholesterol and risk of premature death from coronary heart disease
continuous and graded? Findings in 356,222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT). JAMA
1986;256:2823-8.
54. Law MR, Wald NJ, Rudnicka AR. Quantifying effect of statins on low density lipoprotein cholesterol, ischaemic heart disease, and
stroke: systematic review and meta-analysis. . BMJ 2003; 326:1407-8.
55. Hebert PR, Gaziano JM, Chan KS, Hennekens CH. Cholesterol lowering with statin drugs, risk of stroke, and total mortality. An overview
of randomized trials. JAMA 1997;278:313-21.
56. LaRosa JC, He J, Vupputuri S. Effect of statins on risk of coronary disease: a meta-analysis of randomized controlled trials. JAMA
1999;282:2340-6.
57. Downs JR, Clearfield M, Weis S, Whitney E, Shapiro DR, Beere PA et al. Primary prevention of acute coronary events with lovastatin in
men and women with average cholesterol levels: results of AFCAPS/TexCAPS. Air Force/Texas Coronary Atherosclerosis Prevention
Study. JAMA 1998;279:1615-22.
58. Shepherd J, Cobbe SM, Ford I, Isles CG, Lorimer AR, Macfarlane PW et al. Prevention of coronary heart disease with pravastatin in men
with hypercholesterolemia. West of Scotland Coronary Prevention Study Group. N.Engl.J Med. 1995;333:1301-7.
59. Ward S, Lloyd JM, Pandor A, Holmes M, Ara R, Ryan A et al. A systematic review and economic evaluation of statins for the prevention
of coronary events. Health Technol.Assess. 2007;11:1-178.
052
60. Mihaylova B, Briggs A, Armitage J, Parish S, Gray A, Collins R. Cost-effectiveness of simvastatin in people at different levels of vascular
disease risk: economic analysis of a randomised trial in 20,536 individuals. Lancet 2005;365:1779-85.
61. National Heart, Lung and Blood Institute. Third Report of the National Cholesterol Education Program Expert Panel on Detection,
Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Final Report. National Institute of Health. 2002.
62. Department of Health. National Service Framework for Coronary Heart Disease. 2000.
http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_4094275
63. Hayward RA, Hofer TP, Vijan S. Narrative review: lack of evidence for recommended low-density lipoprotein treatment targets: a solvable
problem. Ann.Intern.Med. 2006;145:520-30.
64. Cannon CP, Steinberg BA, Murphy SA, Mega JL, Braunwald E. Meta-analysis of cardiovascular outcomes trials comparing intensive
versus moderate statin therapy. J Am.Coll.Cardiol. 2006;48:438-45.
65. NHS Scotland Information and Statistics Division. Quality and Outcomes Framework. Revisions to the QOF for 2006/7. Revision to the
GMS Contract 2006/7. Delivering Investment in General Practice. 2006. http://sehd.scot.nhs.uk/pca/PCA2006(M)08Ann.pdf
66. Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of
the preparative ultracentrifuge. Clin.Chem. 1972;18:499-502.
PART 1_Section 3
67. National Heart, Lung and Blood Institute. Recommendations on lipoprotein measurement. National Institute of Health. 1995.
053
054
PART 1_Section 4
Implications and Public Health Perspective
Issues for Primary Care Trusts and Directors of Public Health
Cardiovascular disease is the commonest preventable cause of mortality in the developed world and there is a
wide range of both population and individual interventions that could potentially reduce the burden of cardiovascular disease.
An effective strategy to reduce population risk needs to both reduce overall population risk (by reducing smoking rates, changing diets and increasing physical activity) - “shifting the curve” - as well as identifying individuals
at increased risk who could benefit from specific individual interventions.
There is now a comprehensive set of guidance for assessment and management of overall cardiovascular disease and its risk factors in the general population1-4.
It has been suggested that vascular risk assessment should be offered to adults aged from 40 years1-3. As part
of a comprehensive public health approach to cardiovascular risk reduction, there needs to be a review of current activity, as well as an assessment of both the potential resource implications and potential benefits of additional activity, including the potential impact on health inequalities. The additional benefit will depend on the
extent to which these activities are already underway and this will vary between practices. Any risk reduction
programme needs a robust and detailed strategy for evaluation and audit.
Review of Current Cardiovascular Risk Reduction Activities
This should include both population/community level activities and primary care activity and will identify gaps
and variation in provision that can be addressed within any Vascular Risk Reduction Programme.
Population activities, such as smoking, healthy eating and physical activity programmes should be reviewed with
respect to both coverage and impact. Although many of these programmes involve wider partnership working,
the NHS can set an example by introducing healthy eating policies on NHS premises and developing NHS
transport plans to encourage walking and cycling.
It should also include general practice level assessment of current activity, using QOF and/or local audit data
where available, and including data on recording of and values recorded for:
u
u
u
u
u
u
u
u
ethnicity
smoking
BMI
blood pressure
cholesterol/lipid profile
blood glucose
appropriate prescription of aspirin, statins, anti-hypertensives (as indicated by risk factor information)
access to lifestyle interventions
An audit can establish the extent to which individuals with risk factors have already been identified, had appropriate blood tests and been started on appropriate treatments. Comparison within and between practice populations will identify variations in risk and in risk assessment and risk management activity.
055
PART 1_Section 4
The evidence base for cardiovascular risk assessment and multiple risk factor intervention in general populations
is less comprehensive and includes the findings of the OXCHECK trial, the British Family Heart and a subsequent systematic review and meta-analysis5-7. Overall, the investment of major resources required for relatively
small changes in risk factors in the general population led to an initial emphasis on secondary prevention and
targeting largely individuals with major clinical risk factors (diabetes and hypertension) for risk reduction.
Identification of Resource Implications, Costs and Benefits
Assessing Costs/Resource Implications
The potential costs to the NHS of providing risk assessment to specific population groups should be considered
before any additional activity is undertaken. The costs will depend on the number of people offered risk assessment and the number of people identified as needing follow up and further treatment. The costs will include
u Costs of risk assessment including staff training, administrative costs of identifying eligible/high risk
individuals and organising risk assessment
u Costs of blood testing –fasting lipid profiles and fasting glucose, glucose tolerance testing (which will not
be routinely available in all practices)
u Costs of behavioural interventions for those who need support to change lifestyle factors and of follow up
and treatment of all those with treatable risk factors
u Costs of audit
One of the major costs of risk reduction will be the costs of follow up for all those identified at high risk or with
abnormal test results and so these do need to be carefully considered alongside the costs of risk assessment.
Assessing Potential Benefits
The cost effectiveness of risk assessment is entirely dependent on whether as a result of risk assessment, costeffective interventions are introduced earlier than they would be otherwise.
Evidence-based guidelines have already been produced by NICE and SIGN including for management of diabetes and hypertension and many of the pharmacological interventions available for managing cardiovascular
risk factors, including smoking cessation, have been demonstrated to be cost effective2,3,4,8-10. It is therefore
possible to use audit data to estimate how many additional people might be treated with specific pharmacological interventions as a result of risk assessment. If overall appropriate prescribing increases as a result of any programme and risk factor levels fall in the practice population, the magnitude of change is an indicator of the
potential benefit. Attempting to quantify the relative costs and relative benefits of different risk assessment
strategies will be helpful in identifying which practices/communities and which population group to target initially.
Assessing Potential Harm
Risk assessment can have the well-recognised negative effects of ‘disease-labelling’ in those identified with specific clinical risk factors (hypertension, diabetes, IGT or IFG) or ‘false reassurance’ in those at lower cardiovascular risk who would still benefit from lifestyle change. This is difficult to quantify, but it is worth considering how a
programme can maximise the proportion of those assessed who gain some evidence-based benefit from assessment, for example smoking cessation advice, to counter balance the potential to do more harm than good.
Reducing Inequalities
There is potential to use routine information sources and audit data to target resources in communities at higher
risk in order to reduce inequalities as well as reduce the overall burden of cardiovascular disease.
This requires PCTs to
u Identify communities and population groups at increased risk of cardiovascular disease and diabetes
u Raise local awareness of the potential to reduce risk through both population-wide initiatives (physical
activity, healthy eating, smoking cessation) and individual risk assessment and clinical intervention
(management of hypertension, lipids, diabetes)
u Target support for general practices with the greatest unmet need for risk reduction
u Use routine clinical management data to target treatment, for example look at QOF CHD scores verses CHD
mortality rates to identify practices who appear to be providing below standard care. This may highlight practices
with the most scope for improvement and allow targeted use of financial incentives provided by QOF
056
Establishing Mechanisms for Evaluation and Audit
There needs to be development of a structure and process for audit of both current and future activity, which
brings together information on both ad hoc and systematic screening, and to ensure that data is collected to
avoid duplication of activity. This is in particular regard to lipid and glucose blood testing.
If a new programme is to be introduced, an evaluation of population changes in risk factor levels, particularly if it
is possible to compare practices introducing new activities with those who have not introduced those activities.
This will allow an assessment of whether the programme is likely to produce the expected benefits in terms of
measurable risk reduction.
Introducing routine audit of risk assessment activity will assist practices in incrementally improving the recording
of risk factors and in ensuring that where abnormal test results or significant overall risk is recorded that all the
appropriate follow up and treatment has occurred.
Other Issues
Screening Personnel
Healthcare assistants can be recruited and trained to offer a risk assessment and health promotion advice to
people who attend for screening. Further work is needed to assess the effectiveness of health promotion and
risk reduction intervention offered to individuals by healthcare assistants. An example Job Description with required competencies from the Skills and Knowledge framework is shown in the SOP Section pages 145-147.
In the DHDS paper based systems were unpopular, and ultimately proved to be unsuitable. Practice systems
are likely to be appropriate, but consistency in recording and coding information on risk factors, test results and
diagnostic testing using locally developed system templates need to be better developed. An example of a
template to record the outcome of a vascular assessment is shown in the SOP Section page 109.
Routine risk assessment will become increasingly feasible as general practices continue to develop routine collection and recording with consistent coding of risk factors. In addition to age, this is required for body mass
index, hypertension, ethnicity and smoking status. Other risk factors such as family history and waist circumference may be of value, particularly in terms of self-assessment of vascular risk.
PART 1_Section 4 Reference List
1. JBS 2: Joint British Societies' guidelines on prevention of cardiovascular disease in clinical practice. Heart 2005;91 Suppl 5:v1-52.
www.bcs.com/download/651/JBS2final.pdf
2. Scottish Intercollegiate Guidelines Network. Risk estimation and the prevention of cardiovascular disease: A national clinical guideline.
2007. http://www.sign.ac.uk/pdf/sign97.pdf
3. National Collaborating Centre for Primary Care. Cardiovascular risk assessment: the modification of blood lipids for the primary and
secondary prevention of cardiovascular disease - full guideline DRAFT. 2007. http://guidance.nice.org.uk/download.aspx?o=414903
4. National Institute for Clinical Excellence. Hypertension: management of hypertension in adults in primary care. Clinical Guidelines (CG34).
2006. www.nice.org.uk/CG034
5. Effectiveness of health checks conducted by nurses in primary care: final results of the OXCHECK study. Imperial Cancer Research
Fund OXCHECK Study Group. BMJ 1995;310:1099-104.
6. Family Heart Study Group. Randomised controlled trial evaluating cardiovascular screening and intervention in general practice: principal
results of British family heart study. BMJ 1994;304:313-20.
7. Ebrahim S,.Smith GD. Systematic review of randomised controlled trials of multiple risk factor interventions for preventing coronary heart
disease. BMJ 1997;314:1666-74
8. National Institute for Clinical Excellence. Smoking Cessation: Brief interventions and referral for smoking cessation in primary care and
other settings. Public health intervention guidance. 2006. http://guidance.nice.org.uk/PHI1/
9. National Institute for Clinical Excellence. TA039 Smoking cessation - bupropion and nicotine replacement therapy: Guidance. 2002.
http://www.nice.org.uk/TA039
10. National Institute for Clinical Excellence. Four commonly used methods to increase physical activity: brief interventions in primary care,
exercise referral schemes, pedometers and community-based exercise programmes for walking and cycling. Public health intervention
guidance. 2006. http://www.nice.org.uk/download.aspx?o=299528
057
PART 1_Section 4
Data Recording
058
PART 2_Section 1
Implementation of Vascular Risk Assessment
Programme; Broad Overview
PART 2_Section 1
Record Based - Existing Disease Registers
u Figure 10. ’Record Based’ Strategy (Existing Disease Register) for Vascular risk Assessment
Procedure 1; Ensure current disease registers for LVD, Stroke/TIA CHD and DM registers are;
u As complete as possible
u That the optimal implementation of the current recommendations occurs
u That all on these registers (except those on DM register already) should be offered annual
screening for DM, as these subjects are at high risk for T2DM, but do not require CVS risk scoring as they
already have established CVD
u That all new patients diagnosed with DM as a result of the overall strategy are updated on to the Diabetes Register
In this context, as patients often have planned visits, it is suggested that a fasting plasma glucose (FPG) is
measured with a cut-off of 6 mmol/l. In both SA and White European populations, this will give a sensitivity of
>80% and will result in less than 10% of subjects requiring an OGTT. As it is assumed that both patients on
these disease registers will be offered optimal lifestyle advice, the need and justification for an addition of benefits of detecting patients with IGR is less of an issue.
Patients could be given the choice of having a fasting glucose done along with their cholesterol and renal function, either before their assessment visit, or a fasting or random glucose could be sent on the day of the visit.
u Use FPG to screen for T2DM (if Random Glucose used, use the same cut-off)
u Offer OGTT to those with ≥ 6 mmol/l on FPG (See page 32)
u < 10% will require OGTT if this strategy is used (based on FPG, more required if Random Glucose is used)
059
Subjects should be informed that there is a reasonable likelihood, i.e. 1 in 10, that they may require a confirmatory test, that the test is being done to look for undiagnosed diabetes, and if this is found then their targets for
therapy for blood pressure may change, and that they may require additional screening of eyes, feet and kidney
function. Procedure 1 is summarised in Algorithm 1
u Algorithm 1. ‘Record Based’ Strategy Procedure 1
060
What the Practice Needs to Have in Place
List of Required Standard Operating Procedures (SOP’s) for procedure 1 with examples of all in the SOP Section
u Search Strategy
u Inclusion/Exclusion Criteria
u Invitation Letter
u DNA procedure
u OGTT letter (if required)
u What to expect from the visit
u Procedure for OGTT – what to expect (patient)
u Procedure for OGTT (HCP)
u Venepuncture
p96
p98
p99
p105
p109
p107
p110
p117
p118
PART 2_Section 1
A worked example of this procedure with numbers involved in a typical practice is shown in Table 7.
u Table 7. ‘Record Based’ Procedure 1 Worked Example
061
Limiting assessment to those at high risk is only likely to be feasible if risk information can be obtained without
patients being invited to attend the surgery and if the criteria are understood and accepted by the practice staff.
It is important and practical to use age, BMI and hypertension which are already recommended to be recorded
on registers as a starting point for such a record-based risk assessment programme.
Record Based – Procedure 2 ‘At Risk’ Registers
To offer all of those on existing vascular risk registers (to include those Hypertension Obesity and CKD Registers)
– a vascular assessment visit. Each individual register does not include a comprehensive assessment to allow
CVD risk score, or a comprehensive assessment of lifestyle factors to allow targeted intensive lifestyle intervention and screening for undiagnosed T2DM and CKD.
u Figure 11. ‘Record Based’ Strategy (at Risk Register) for Vascular Risk Assessment
It is suggested that the initial focus might be on the hypertension register which, from the QOF data, is the most
complete. Vascular assessment could be offered to all adults on these registers. Patient already on a risk register (currently the Hypertension, Obesity Register, and CKD and those with a measured and recorded BMI of >
30 mg/kg2, as not all will be recorded on the Obesity register) should be invited for a comprehensive vascular
risk assessment.
062
Clinical Assessment of Vascular Risk
This assessment should include a record of;
Age and gender
Ethnicity (for recording see SOP Section)
Smoking habit (for recording see SOP Section)
Record for Family history of CHD (to include history of premature cardiovascular disease,
i.e. angina, stroke or MI in men <55 years and women <65 years)
u Record for FH of DM in a first degree relative
u Diabetes Risk Score (For example the Leicester Diabetes Risk Score)
u
u
u
u
See questionnaire template to collect this data before the visit
p107
p107
p108
p108
p82-83
p107
u Measurement of weight (including calculation of BMI, weight in kg, height in metres, BMI calculated
as kg/m2) (see SOP Section pages 117-118)
u Waist circumference: indicate central obesity: >94cms in men and >80 in women in White
Europeans, and 90cms and 80cms in SA populations (See SOP Section page 115)
u BP (see SOP Section page 121)
u Blood tests (fasting) sent to laboratory for lipid profile and glucose (eGFR for those on HT register)
Patients should be invited using an invitation letter that describes what to expect from their visit.
Blood tests could be done prior to their vascular assessment so that results are available to the patient and
healthcare professional, or could be done at the time of the vascular assessment with results communicated at
a follow-up visit. The procedure is summarised in Algorithm 2
u Algorithm 2. ‘Record Based’ Strategy Procedure 2
063
PART 2_Section 1
At the visit;
List of Additional SOPs for Procedure 2 with Examples of all in SOP Section
u Measurement of Glucose
u Measurement of Lipids
u Measurement of eGFR (for those on HT/CKD Register)
u Collection of samples and transfer to the Laboratory
u Pre-Visit Questionnaire
u Ethnicity Record
u Smoking History
u Family History of CHD and DM
u BP
u WC
p126
p125
p113
p107
p107
p107
p108
p121
p115
u Weight
u Height
u BMI
u Recording results on IT system
u Individual care plan
u Management plan
u Equipment List
A worked example of this procedure with numbers involved in a typical practice is shown in Table 8
u Table 8. ‘Record Based’ Procedure 2 Worked Example
064
p117
p114
p118
p133
p109
p127
Population-based screening
This is suggested as the second phase of an overall vascular risk assessment strategy. All subjects on the practice register who are not on a disease register covered by the record based approach (CHD, DM, LVD, CKD HT
Obesity), will be included. An example of population based screening in a structured and systematic way could
start with patients offered this on their 50th birthday for the first year and then extended to those on their 40th
birthday.
It will be important to ensure that certain, already higher risk groups (for example those from BME groups or from
deprived areas) respond to invitations for screening, otherwise this approach may inadvertently widen health inequalities. Practices need to guard against this by monitoring uptake and where uptake is low but risk/need is
high they will need to use other approaches to improve uptake in these groups/geographical areas. This may require more innovative approaches with full use of the multi disciplinary team, social services and community facilities.
Everybody, regardless of their fasting glucose level, may be at future risk of diabetes particularly in those who have a
fasting or random glucose ≥5.0 mmol/L. This should be explained to the patients. Those with a FINDRISC score of
≥ 12 may have higher risk of DM and vascular disease, and would benefit from lifestyle intervention (intensive lifestyle
intervention for those ≥ 15). This is based on data from North America and Finland where an intensive lifestyle intervention reduces the risk of diabetes by two-thirds.1-2 The principal components of such a programme are well understood and include 5 key lifestyle targets as previously described. For summary of the procedure see Algorithm
3. (For further explanation of possible approaches to identify those with impaired glucose regulation see pages
34-35)
A worked example of this procedure with numbers involved in a typical practice is shown in Table 9.
065
PART 2_Section 1
Patients should receive an invitation letter which will clearly explain to them the reason that they are being invited
and what to expect from the visit. Also the practice should encourage people to book for such an Assessment
using posters in the surgery (see SOP Section p105 for example). Opportunistic screening should be encouraged
and can be facilitated by computer prompts on records of eligible patients in their 40th and 50th year who may
attend the surgery for other reasons. Patients should have the option of attending for a fasting blood test which
will include assessment of lipid profile and glucose prior to their planned appointment, or be given the option of
attending on the day and having the assessment done at the same time. For opportunistic testing a random
blood test for lipids and glucose is acceptable but will need to be repeated in some patients (according to SOPs)
Patients should be given clear feedback in terms of the results of the investigations, which should not be indicated as either positive or negative. The gradient of risk should be explained.
u Algorithm 3. Population Based Strategy
u Table 9. Population Based Strategy Worked Example
066
Self Assessment
A self-assessment tool is being developed around the concept of the FINDRISC. The Leicester Diabetes questionnaire could be used to identify those who should be offered a blood test for diagnosis of impaired glucose
regulation or an intensive lifestyle programme. Until further work is available, the FINDRISC offers some potential
in assessment of those who need diagnostic testing (≥12) and those who should be offered intensive lifestyle intervention (≥15). The vascular assessment programme may require lifestyle and behavioural intervention not
based on the level of blood glucose or CVD risk score but on the presence of risk factors such as increased
BMI, waist circumference, positive family history and poor lifestyle and dietary habits such as is used in Finland
with the FINDRISC. It can be used as a simple way to engage patients in assessing their own risk and also
used to sign post subjects for further assessment3 (see page 33).
See algorithm 4 for an example of how this strategy could work.
PART 2_Section 1
The whole area of self assessment and vascular risk needs further development, e.g. to include a question regarding smoking status.
u Algorithm 4. Self Assessment Approach
067
Sporadic Activities
When looking at any sporadic activity, it is important that the organisation liaise with the appropriate members of
the local healthcare team, as well as the clinical biochemistry service. The Public Health Department within the
local primary care organisation may be a useful first point of contact. There should be consultation regarding
the choice of testing method, and clear referral pathways to primary care should be agreed. There is already a
national advertised programme regarding screening for diabetes in Lloyds Pharmacy, using finger-prick blood
tests.
Whilst these are beyond the remit of the programme we have given general guidance regarding risk assessment
and triggers for further assessment and intervention in the comprehensive list of Standard Operating Procedures
(SOP’s).
It is important that any sporadic activity undertaken adheres to clinical governance principles. These include
having clear lines of responsibility and accountability for the overall quality of clinical care, comprehensive programme of quality improvement activity, clear policies aimed at managing risk, procedures for all professional
groups to identify and remedy poor performance.
Regarding sporadic activities it is likely, for example, that pharmacies may have an important role in terms of
being involved in sporadic activities involved with the risk reduction programme. For example, the Royal Pharmaceutical Society of Great Britain has issued clear guidance with regard to, for example, screening for undiagnosed diabetes.5 There is clear guidance regarding the equipment, premises where this should be undertaken,
and examples of quality assurance programme as well as outlining the code of ethics and clear Standard Operating Procedures for testing of body fluids5.
Regarding recommended training, in this case they suggest that pharmacists and pharmacy technicians who
are involved in testing must be suitably trained in the procedure to be followed and in the advice to be given to
patients.
The training should be in the following areas:
u Developing and working within Standard Operating Procedures
u Testing (this includes the completion of any training programmes provided by the equipment
suppliers to ensure competence in the use of equipment and interpretation of test results)
u Quality assurance arrangements
u Referral criteria and procedure
u Feedback to patients (advice giving explanation of the probability of disease or risk in relation to
the test results)
u False negatives (why they can occur)
u Safe handling of sharps
u Record keeping
u Giving consistent lifestyle advice
u Reinforcing the person’s desire to take care of themselves
u Medicines management in issues related to vascular risk
u Clinical governance and liability issues
u Insurance
It is important that any organisation involved in sporadic activities adheres to similar best practice.
068
PART 2_Section 1 Reference List
1. Tuomilehto J, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H, Ilanne-Parikka P et al. Prevention of type 2 diabetes mellitus by
changes in lifestyle among subjects with impaired glucose tolerance. N.Engl.J.Med. 2001;344:1343-50.
2. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA et al. Reduction in the incidence of type 2 diabetes with
lifestyle intervention or metformin. N.Engl.J Med. 2002;346:393-403.
3. Lindstrom J,.Tuomilehto J. The diabetes risk score: a practical tool to predict type 2 diabetes risk. Diabetes Care 2003;26:725-31.
4. Kroenke K, Spitzer RL, Williams JB. The PHQ-9: validity of a brief depression severity measure. J Gen.Intern.Med. 2001;16:606-13.
PART 2_Section 1
5. The Royal Pharmaceutical Society of Great Britain. RPS e-PIC References on: Diagnostic testing in community pharmacy. 2007.
www.rpsgb.org.uk/pdfs/rpsepicdiagtest.pdf
069
070
PART 2_Appendix
Comparison of Software Available for a Population Based CVD Risk Assessment Strategy
Oberoi Consulting Ltd
u Features (see table on page 074)
CHD risk tool based on the Framingham equation and a CVD risk tool based on BHS guidelines.
Stand alone system, partially integrated.
Practice populations based approach.
Ranks all age-appropriate patients (32-74) in a practice by their Framingham risk score.
Creates a list which can be exported to excel for further analysis.
Excludes patients with pre-existing CVD (MI, stroke etc).
Includes patients already on treatment for hypertension and basis management on latest recording of risk
factors but provides ‘worst case’ CVD risk score based on previous highest values of
recorded risk factors (BP & cholesterol).
Acknowledges any missing risk factors in the calculation.
Allows easy comparison of change in CVD risk as a result of recent changes in risk factors.
Has not been peer reviewed
Cost approx. £500 per practice
Impossible to use opportunistically for individual patients as requires separate screen to be open for
individual patient record to be accessed.
It does not recognise patients who have already been risk assessed and have a risk score READ coded from
a consultation say a week previously.
Details obtained from Oberoi Consultancy Website1.
EMIS
u Features (see table on page 074)
Integrated Framingham risk score currently CHD but evidently CVD risk score is being phased in.
Can provide an estimated risk score for individual patients when information such as smoking
status and cholesterol are missing by using population averages.
u Limitations
EMIS systems has a search function but it is not possible to follow one set of patients from start to finish
comparing differences at two different time points as it brings different populations each time it is run.
Search can identify those who have had risk assessment (READ coded) using integrated risk
equation. At risk patient search limited to those with underlying risk factors only as cannot
systematically risk score practice at population level.
Smoking status is based on last recorded status (problem with actual risk if recently stopped).
Uses last 2 BP readings and uses average – not appropriate for treated hypertensive patients as pretreatment BP should be used2,3.
071
PART 2_Appendix
u Limitations
E-nudge
u Features (see table on page 074)
Developed in collaboration with EMIS as part of an RCT.
Integrated within clinical system
Prompts clinician when individual patient may need risk assessment based on recorded risk
factors and also identifies which risk factors need modification if at high risk.
Assumes diabetes status as positive in those with no record of diabetes and no record of a
normal glucose result in the last three years when estimating CVD risk score (prompt for screening for
diabetes). If risk score is high then such a patient is categorised under the ‘missing data’ group until glucose
measurement is recorded. If still not on diabetes register, risk will then be calculated using negative diabetes
status. Framingham risk score is never calculated on a patient known to have diabetes.
Ex-smokers considered as smokers unless stopped for over a year when calculating CVD risk score.
Allows for opportunistic and practice population screening strategy.
As it is integrated regularly updated lists are available for practice population risk assessment.
u Limitations
May under-estimate risk in controlled hypertensive patients but these would not necessarily be a priority
group initially.
Structure of the algorithm used to create the software will be published in the medical literature and will allow
any software company to duplicate it but is currently not available.
u The e-Nudge Trial – baseline data collected June-September 2006
Aggregated data
Total over 50 population
Proportion in Group 1 (%)
Proportion in Group 2 (%)
Proportion in Group 3 (%)
Proportion in Group 4 (%)
Proportion in Group 5 (%)
Proportion in Group 6 (%)
Group 1:
Group 2:
Group 3:
Group 4:
Group 5:
Group 6:
38137
8.92
26.50
5.96
0.46
0.12
2.78
Patients of all ages with existing CVD or diabetes, whose BP/cholesterol outside QOF targets
Patients not known to have CVD or diabetes and whose risk profile is incomplete but estimated
CVD risk >20% using assumed values
Patients not known to have CVD or diabetes and <75yrs with CVD risk >20%.
Patients not known to have CVD or diabetes and >75yr old.
Patients with possible undiagnosed diabetes on the basis of at least one previous high blood
glucose record
Patients with CVD but no diabetes, who have had no blood glucose measurement in the last
three years
For further information see 4,5
072
Sandwell
u Features
Interrogates clinical system and creates a list which can be exported to excel.
Excluded patients on CHD register, or with CVD and those on BP treatment in the pilot project (but this can
be modified).
u Limitations
PART 2_Appendix
Improvement in management seen where nurses are employed with the specific task to follow-up and
manage patients. As yet, no evidence from comparative practices in that providing a list of ‘at risk’ patients
modifies professional behaviour.
Intellectual property issues not resolved yet for integrated version (currently in discussion with iSOFT).
For further information and Excel version allowing individual patient assessment, can be downloaded from
the following site (but cannot be integrated into clinical system):
http://www.pcpoh.bham.ac.uk/publichealth/cardiovascular/index.htm6,7
073
Individual patients
Can systemically risk score Prac- Can systemically risk score PracCan systemically risk score Practice population
tice population
tice population
Individual patients
Population searches based on
risk factors only
Population
targeted
074
See text
Risk assessment of individual
patients
Activity READ coded
Can search for previous calculated risk scores but cannot
systemically risk score
practice population
Free
Strengths and
Special
features
Limitations
Cost
See text
Not integrated
Can interrogate clinical system
(iSOFT)
£500
Not integrated, stand alone system
Provides ʻworst caseʼ CVD risk
score based on previous
recorded risk factors.
Can interrogate a number of clinical
software systems (EMIS/iSOFT/).
5/10 CHD risk
5/10 CVD risk
* Uses population averages when risk factors not present to create an estimated risk score
≠ Assumes diabetes status positive when no record or no blood glucose result record in last 3 years in those whose estimated CVD risk is particularly sensitive to this missing data.
† Ex-smokers considered as smokers unless stopped for over a year
± Assumes risk factor negative if no record
See text
Prompts opportunistic screening
(automatic screen alerts)
Identifies those with abnormal
blood glucose
Highlights missing risk factors
Activity READ coded
Fully integrated
Integration with
clinical system
Fully integrated (EMIS only)
Estimated and actual 10 year CVD
10 year CVD risk
risk score
Estimated and Actual 10 year
CHD/ CVD risk score
Calculated Risk
Sex
Age 32-74 years
Systolic BP
Diastolic BP
Cholesterol (total, LDL and HDL)
Smoking status
Diabetes status
Risk factors
included:
Sex
Age 35-74 years
Systolic BP recorded in the last
year*
Cholesterol (total & HDL)*
Smoking status±
Diabetes status±
ECG-LVH±
Sex
Age <75 years
Systolic BP (average of last three
readings) *
Cholesterol (Total & HDL) *
Smoking status†
Diabetes≠
ECG-LVH±
Framingham
Sex
Age 30-74 years
Systolic BP (last two reading
averages) *
Cholesterol (Total & HDL)*
Smoking status±
Diabetes±
ECG-LVH±
Framingham
Framingham
Oberoi Consulting Ltd1
Framingham
E-nudge (Warwickshire University)4,5 Sandwell model 6,7
Equation used
GP clinical systems eg EMIS
Comparison of Software Available for a Population Based CVD Risk Assessment Strategy
Screening for Diabetes - Recent Data from Screening Studies in Leicester
The STAR (Screening Those At Risk) Study (Study 1) was designed to provide information regarding the logistics
and best methods for screening for T2DM and IGT in a mixed ethnic population in the UK: It was a multimethod, multi-disciplinary approach regarding the utility of different strategies of screening. Inclusion criteria
were White European subjects aged between 40 and 75 years, and South Asian subjects aged between 25
and 75 years.
The Study involved 17 practices in Leicestershire of mixed urban and rural character, with some city practices
having a high South Asian population. All subjects gave informed consent, and underwent 75 gram OGTT
done in standardised conditions. There was standardised health assessment including anthropometric measures, questionnaires, full biochemical data and collection of data to allow calculations of both the Cambridge Diabetes Risk Score and the FINDRISC8-9. We have full information on 3,418 subjects.
For the purpose of this handbook we provide information regarding the sensitivity and specificity of a two-stage
screening approach for diabetes based on looking at hypertension and obesity. The STAR Study is reported as
part of a MD thesis by Dr Jenny Tringham11.
Study 1: n = 3418 Adults (33.3% SA)
Study 2: n = 2813 (30% SA)
1) Results of two staged approach using HT/BMI then FPG
Applying the Study 1 derived screen to the Study 2 study South Asians to detect T2D:
Discrimination of score, with first stage derived from hypertension status and BMI for predicting T2DM, where
second stage is: fasting blood glucose ≥ 5.5mmol/l
Cutpoint
for BMI*
All pass
1st stage
Sens
(%)
95.7
99.9
Spec
(%)
75.6
78.9
OGTT
(%)
25.2
78.1
72.1
22.1
28.6
1.40
≥20
95.7
78.1
99.9
75.9
72.4
79.2
25.0
21.8
28.3
1.40
≥21
95.7
78.1
99.9
75.9
72.4
79.2
25.0
21.8
28.3
1.40
≥22
95.7
78.1
99.9
76.4
72.9
79.6
24.5
21.4
27.9
1.39
≥23
91.3
72.0
98.9
76.9
73.4
80.0
24.0
20.9
27.3
1.47
≥24
91.3
72.0
98.9
77.8
74.4
80.9
23.1
20.1
26.4
1.45
≥25
87.0
66.4
97.2
79.5
76.2
82.5
21.5
18.5
24.7
1.51
≥26
78.3
56.3
92.5
81.8
78.6
84.7
19.1
16.3
22.2
1.67
≥27
69.6
47.1
86.8
83.6
80.6
86.4
17.1
14.4
20.1
1.88
≥28
69.6
47.1
86.8
85.8
82.9
88.4
15.1
12.6
18.0
1.81
≥29
69.6
47.1
86.8
86.9
84.0
89.4
14.2
11.7
16.9
1.77
≥30
65.2
42.7
83.6
88.0
85.2
90.4
13.0
10.7
15.7
1.88
95% CI
95% CI
95% CI
NND
Sens = Sensitivity, Spec = Specificity, OGTT = proportion of those screened continuing to OGTT,
NND = Number needed to diagnose. * if HT absent; HT is equivalent to +6.4 units BMI)
All text and tables © University of Leicester
075
PART 2_Appendix
ADDITION - Leicester (Study 2)10 - which is currently being conducted in 24 practices across Leicestershire.
These are different practices to those in the STAR Study, for the purpose of this report we have complete
cleaned data on 2,813 subjects.
Applying the Study 1 derived screen to the Study 2 study South Asians to detect T2D:
Discrimination of score, with first stage derived from hypertension status and BMI for predicting Type 2 diabetes,
where second stage is: fasting blood glucose ≥ 6.0mmol/l
Cutpoint
for BMI*
All pass
1st stage
Sens
(%)
95.7
99.9
Spec
(%)
92.6
94.5
OGTT
(%)
9.8
78.1
90.3
7.7
12.2
1.13
≥20
95.7
78.1
99.9
92.7
90.5
94.6
9.7
7.6
12.1
1.13
≥21
95.7
78.1
99.9
92.7
90.5
94.6
9.7
7.6
12.1
1.13
≥22
95.7
78.1
99.9
92.7
90.5
94.6
9.7
7.6
12.1
1.13
≥23
91.3
72.0
98.9
92.9
90.6
94.8
9.4
7.4
11.8
1.19
≥24
91.3
72.0
98.9
92.9
90.6
94.8
9.4
7.4
11.8
1.19
≥25
87.0
66.4
97.2
93.1
90.8
94.9
9.1
7.1
11.5
1.25
≥26
78.3
56.3
92.5
93.5
91.3
95.3
8.4
6.5
10.7
1.39
≥27
69.6
47.1
86.8
93.8
91.7
95.6
7.9
6.0
10.1
1.58
≥28
69.6
47.1
86.8
94.6
92.6
96.2
7.2
5.4
9.3
1.56
≥29
69.6
47.1
86.8
94.9
92.9
96.5
6.9
5.1
9.0
1.55
≥30
65.2
42.7
83.6
95.5
93.6
97.0
6.2
4.5
8.2
1.65
95% CI
95% CI
95% CI
NND
Sens = Sensitivity, Spec = Specificity, OGTT = proportion of those screened continuing to OGTT,
NND = Number needed to diagnose. * if HT absent; HT is equivalent to +6.4 units BMI)
2) Results of two staged approach using HT/BMI then FPG
Applying the Study 1 derived screen to the Study 2 study White Europeans to detect T2D:
Discrimination of score, with first stage derived from hypertension status and BMI for predicting Type 2 diabetes,
where second stage is: fasting blood glucose ≥ 5.5mmol/l
Cutpoint
for BMI*
All pass
1st stage
Sens
(%)
90.9
97.5
Spec
(%)
75.6
77.4
OGTT
(%)
25.1
78.3
73.6
23.3
27.0
1.50
≥20
90.9
78.3
97.5
75.8
73.9
77.7
24.9
23.1
26.8
1.50
≥21
90.9
78.3
97.5
75.8
73.9
77.7
24.9
23.1
26.8
1.50
≥22
90.9
78.3
97.5
76.0
74.1
77.8
24.7
22.9
26.6
1.50
≥23
88.6
75.4
96.2
76.6
74.7
78.4
24.1
22.3
26.0
1.53
≥24
88.6
75.4
96.2
77.0
75.1
78.8
23.7
22.0
25.6
1.52
≥25
86.4
72.6
94.8
78.0
76.1
79.8
22.8
21.0
24.6
1.55
≥26
81.8
67.3
91.8
79.4
77.6
81.2
21.3
19.6
23.1
1.63
≥27
79.5
64.7
90.2
81.1
79.4
82.8
19.6
17.9
21.3
1.65
≥28
75.0
59.7
86.8
83.2
81.5
84.8
17.5
15.9
19.2
1.72
≥29
75.0
59.7
86.8
85.0
83.4
86.5
15.8
14.3
17.4
1.67
≥30
68.2
52.4
81.4
86.7
88.2
88.2
14.0
12.6
15.6
1.82
95% CI
95% CI
95% CI
NND
Sens = Sensitivity, Spec = Specificity, OGTT = proportion of those screened continuing to OGTT,
NND = Number needed to diagnose. * if HT absent; HT is equivalent to +6.4 units BMI)
All text and tables © University of Leicester
076
Applying the Study 1 derived screen to the Study 2 study White Europeans to detect T2D:
Discrimination of score, with first stage derived from hypertension status and BMI for predicting Type 2 diabetes,
where second stage is: fasting blood glucose ≥ 6.0mmol/l
All pass
1st stage
Sens
(%)
84.1
93.4
Spec
(%)
92.2
93.3
OGTT
(%)
9.2
69.9
90.9
8.0
10.5
1.31
≥20
84.1
69.9
93.4
92.2
91.0
93.3
9.2
8.0
10.5
1.31
≥21
84.1
69.9
93.4
92.2
91.0
93.3
9.2
8.0
10.5
1.31
≥22
84.1
69.9
93.4
92.2
91.0
93.3
9.2
8.0
10.5
1.31
≥23
81.8
67.3
91.8
92.4
91.1
93.5
9.0
7.8
10.3
1.35
≥24
81.8
67.3
91.8
92.4
91.1
93.5
9.0
7.8
10.3
1.35
≥25
79.5
64.7
90.2
92.7
91.4
93.8
8.6
7.5
9.9
1.39
≥26
75.0
59.7
86.8
93.0
91.7
94.0
8.3
7.1
9.5
1.47
≥27
72.7
57.2
85.0
93.2
92.0
94.2
8.0
6.9
9.3
1.52
≥28
68.2
52.4
81.4
93.4
92.3
94.5
7.6
6.6
8.9
1.62
≥29
68.2
52.4
81.4
94.0
92.9
95.0
7.1
6.1
8.3
1.61
≥30
63.6
47.8
77.6
94.4
93.3
95.4
6.7
5.6
7.8
1.72
95% CI
95% CI
95% CI
NND
Sens = Sensitivity, Spec = Specificity, OGTT = proportion of those screened continuing to OGTT,
NND = Number needed to diagnose. * if HT absent; HT is equivalent to +6.4 units BMI)
Using cut-off of plasma venous glucose of 6mmol/l reduces number of OGTTs required from ~20% to less than 10%.
Sensitivity ~80% (87%~ in SA population) detecting T2DM if BMI cut off 25kg/m2, sensitivity - 63-68% for ≥ BMI 30kg/m2
u A two stage procedure using BMI (>25kg/m2) and the presence of hypertension in both South Asian
and White European populations has a sensitivity of between 80-86% with only 7-9% requiring OGTT
u FPG cut off should be >6mmol/l to detect undiagnosed diabetes
u This approach will not detect the majority of cases of impaired glucose regulation (IGR) see page 31
All text and tables © University of Leicester
077
PART 2_Appendix
Cutpoint
for BMI*
Development of the Leicester Diabetes and Pre-diabetes Risk Score
Screening for Type 2 diabetes and IGR (otherwise known as Pre-diabetes) in the population might consist of three
stages. Stage 1 would consist of an initial screen using only information readily available to a general practice, or
to a person assessing their own risk. People who scored above a specified cutpoint would progress to Stage 2
and attend to have their FPG measured. Those with sufficiently high values would be invited for an OGTT - to be
followed, if necessary, with a second OGTT - after which a positive or negative diagnosis would be made.
We compared the implications for sensitivity, specificity and resource use of three possible approaches to the first
stage of screening as suggested above:
u use of the FINDRISC test, the latest version to include information on family history of diabetes
u use of a new ‘prototype’ Leicester Diabetes and PDM risk score developed here for illustration only
u having no separate Stage 1, and instead invite the entire population group to have their FPG tested
The ‘prototype’ Leicester Diabetes and Pre-diabetes risk score was derived from data from the STAR cross-sectional population-based study carried out in Leicester 2002-2005 in which OGTT diagnoses were made on all participants, using logistic regression modelling. The characteristics initially considered for inclusion in the model
were: age (ranging from 40 to 75 years), sex, ethnicity (either South Asian or white European), measures of obesity, frequency of physical exercise, frequency of fruit and vegetables in the diet, whether there was a 1st degree
family history of diabetes and the IMD index of deprivation derived from the postcode.
Obesity was assessed both as body mass index and as waist circumference - body mass index was assessed as
quintiles calculated separately for each of the two ethnic groups, and waist circumference was assessed as quintiles calculated separately for each combination of ethnic group and sex. The variables in the model other than
obesity were tested for an ‘interaction’ to judge whether any relation they had to the presence of undiagnosed
T2DM might differ between the ethnic groups, but these were not found to be statistically significant.
The deprivation index was taken out of the model due to being non-significant, but as the score was developed in
a relatively homogeneous cohort it may be included when we validate the tool in a larger more heterogeneous population.
The resulting risk score is shown in the table below.
variable
level
age
40-44
45-54
55-64
65-
rounded
score
0
4
7
10
Gender and Ethnicity
WC (cm)
0
2
4
7
BMI (kg/m2)
0
3
5
7
0
3
0
4
Previous HT Treatment
1st degree FH of DM
All text and tables © University of Leicester
no
yes
no
yes
SA Male
6
SA Male
<88
88-97
98-102
>103
SA
<23.8
23.8-25.6
25.7-30.5
>30.6
078
Sa Female
4
Sa Female
<82
82-92
93-99
>100
WE
<24.3
24.3-26.6
26.7-32.1
>32.2
WE Male
1
WE Male
<90
90-101
102-107
>108
WE Female
0
WE Female
<81
81-94
95-103
>104
The score could be made easier to use by replacing the use of quintiles for body mass index with a specific number of points assigned for each combination of ethnicity and BMI group (e.g. 12-14 kg/m2, 15-17 kg/m2, etc ), and
correspondingly for waist circumference, and this is illustrated in the example shown on pages 82-83.
Further work that will be needed in order to further develop a Diabetes and PDM risk score that can be provided
for use in public health will include validation on other population datasets, possibly also using the same modelling
approach of other datasets to examine the consistency of model coefficients, more complete examination for the
more complex ‘interaction’ effects and, if practical, the systematic examination of what information can be assumed from the fact that certain items of information are not recorded for that individual by the general practice (or
are not answered by the user). An example of the current prototype is shown on pages 82-83.
We have used this with a cut off score of 19 to determine who should proceed to a fasting glucose test and com-
PART 2_Appendix
pare using this approach to the FINDRISC and a strategy using FPG for all.
All text and tables © University of Leicester
079
Comparison of Strategies to Detect DM and (Pre-diabetes or Impaired Glucose Regulation)
Using FPG in all, or ‘Pre-Screening’ with either FINDRISC or the Leicester Diabetes and
PDM Risk Score
Strategy with FPG for all
Overall prevalence of
DM and PDM
Stage 1 screen
People going on
to have FPG
Stage 2 screen
People going on
to have OGTT
FPG for all
FPG for all
FPG for all
361 / 1919 = 18.8%
361 / 1919 = 18.8%
361 / 1919 = 18.8%
(none)
(none)
(none)
1919 = 100%
1919 = 100%
1919 = 100%
FPG ≥ 5.0 mmol/l
FPG ≥ 5.5 mmol/l
FPG ≥ 6.0 mmol/l
Sensitivity:
327 / 361 = 90.6%
Specificity:
690 / 1558 = 44.3%
Overall sensitivity*:
327 / 361 = 90.6%
Sensitivity:
269 / 361 = 74.5%
Specificity:
1288 / 1558 = 82.7%
Overall sensitivity*:
269 / 361 = 74.5%
Sensitivity:
205 / 361 = 56.8%
Specificity:
1542 / 1558 = 99.0%
Overall sensitivity*:
205 / 361 = 56.8%
1195 / 1919 = 62.3%
539 / 1919 = 28.1%
221 / 1919 = 11.5%
Results for screening for pre-diabetes (including diabetes), using various FPG cut-points, when there is no initial
screen - based on STAR data, for South Asians and white Europeans, aged 40 - 75 years (In 1919 subjects
with complete FINDRISC Data). *Overall sensitivity of a staged approach to detect both DM and PDM.
Strategy using ‘Prototype’ Leicester Diabetes and Pre-diabetes Risk Score
Overall prevalence
Stage 1 screen
People going on
to have FPG
Stage 2 screen
People going on
to have OGTT
FPG if new score ≥ 19
FPG if new score ≥ 19
361 / 1919 = 18.8%
Sensitivity =
247 cases / 361 = 68.4%,
Specificity =
986 non-cases / 1558 = 63.3%
361 / 1919 = 18.8%
Sensitivity =
247 cases / 361 = 68.4%,
Specificity =
986 non-cases / 1558 = 63.3%
819 / 1919 = 42.7%
819 / 1919 = 42.7%
FPG ≥ 5.0 mmol/l
FPG ≥ 5.5 mmol/l
Sensitivity:
226 / 247 = 91.5%
Specificity:
223 / 572 = 39.0%
Sensitivity:
189 / 247 = 76.5%
Specificity:
438 / 572 = 76.6%
Overall sensitivity*:
226 / 361 = 62.6%
Overall sensitivity*:
189 / 361 = 52.4%
575 / 819 = 70.2% of stage 2
575 / 1919 = 30.0% overall
323 / 819 = 39.4% of stage 2
323 / 1919 = 16.8% overall
Results for screening for pre-diabetes (including diabetes), using various FPG cut-points, when the initial screen
is ‘new score ≥ 19’ - based on STAR data, for South Asians and White Europeans, aged 40 - 75 years (In 1919
subjects with complete FINDRISC Data)
* Overall sensitivity of staged approach to detect both DM and PDM
All text and tables © University of Leicester
080
FPG if FINDRISC ≥ 12
FPG if FINDRISC ≥ 12
361 / 1919 = 18.8%
Sensitivity =
220 cases / 361 = 60.9,
Specificity =
1006 non-cases / 1558 = 64.6%.
361 / 1919 = 18.8%
Sensitivity =
220 cases / 361 = 60.9,
Specificity =
1006 non-cases / 1558 = 64.6%.
People going on
to have FPG
772 / 1919 = 40.2%
772 / 1919 = 40.2%
Stage 2 screen
FPG ≥ 5.0 mmol/l
FPG ≥ 5.5 mmol/l
Sensitivity:
204 / 220 = 92.7%
Specificity:
221 / 552 = 40.0%
Overall sensitivity*:
204 / 361 = 56.5%
Sensitivity:
168 / 220 = 76.4%
Specificity:
438 / 552 = 79.3%
Overall sensitivity*:
168 / 361 = 46.5%
535 / 772 = 69.3% of stage 2
535 / 1919 = 27.9% overall
282 / 772 = 36.5% of stage 2
282 / 1919 = 14.7% overall
Overall prevalence
Stage 1 screen
People going on
to have OGTT
Results for screening for pre-diabetes (including diabetes), using various FPG cut-points, when the initial screen
is ‘FINDRISC ≥ 12’ - based on STAR data, for South Asians and white Europeans, aged 40 - 75 years (In 1919
subjects with complete FINDRISC Data)
* Overall sensitivity of staged approach to detect both DM and PDM
u For a summary of these strategies see page 080
All text and tables © University of Leicester
081
PART 2_Appendix
Strategy using FINDRISC
Example of Prototype Leicester Diabetes and Pre-diabetes Risk Score*
* This is a prototype and is not subject to external validation or pilot work. It is likely to
change as a result of further developmental work and is shown as an example only
Prototype © University of Leicester
082
PART 2_Appendix
Prototype © University of Leicester
083
Intensity and Energy Expenditure for Common Types of Physical Activity
Energy Expenditure
Activity
Intensity
Intensity (METS)
(Kcal equivalent, for a
person of 60kg doing the
activity for 30 minutes)
Ironing
light
2.3
69
Cleaning and dusting
light
2.5
75
Walking - strolling, 2mph
light
2.5
75
Painting/decorating
moderate
3.0
90
Walking - 3mph
moderate
3.3
99
Hoovering
moderate
3.5
105
Golf - walking, pulling clubs
moderate
4.3
129
Badminton - social
moderate
4.5
135
Tennis - doubles
moderate
5.0
150
Walking - brisk, 4mph
moderate
5.0
150
Mowing lawn walking, using power-mower
moderate
5.5
165
Cycling - 10-12mph
moderate
6.0
180
Aerobic dancing
vigorous
6.5
195
Cycling - 12-14mph
vigorous
8.0
240
Swimming slow crawl, 50 yards per-minute
vigorous
8.0
240
Tennis - singles
vigorous
8.0
240
Running - 6mph
(10 minutes/mile)
vigorous
10.0
300
Running - 7mph
(8.5 minutes/mile)
vigorous
11.5
345
Running - 8mph
(7.5 minutes/mile)
vigorous
13.5
405
084
085
* AUC = Area under the curve
PPV = Positive Predictive Value
NPV = Negative Predictive Value
PART 2_Appendix
N/A
(Park, Griffin et al.
2002)16
KORA Survey14
British Birth Cohort
Study17
External& Cross
-validation on 1,208 &
2,874 subjects
Temporal Validation
on
4586 subjects12
External
IGLOO study13
Australian Study
Validation of
(Franicosi et al. 2005)
(Glumer, Borchthe risk
KORA Survey14
Johnsen et al. 2005)15
score
Internal
Validation
Performance
Cross Validation
Sensitivity 77%
Specificity 55%
AUC 71%
Sensitivity 77%
Specificity 72%
PPV -11.3%
NPV 98.6%
AUC 80%
Sensitivity 76%
Specificity 72%
PPV 11%
AUC 80%
Sensitivity 77%
Specificity 66%
PPV 7%
AUC 80%
External & cross
validation
Multivariate
analysis
Logistic
regression
Univariate &
multivariate
regression
Multivariate
logistic regression
Analysis
Cohort of
7,915 subjects
Sample
Population based
sample of 1,077 plus
additional cases from
41 practices
Population based
random sample of
3,250 subjects
Population based
random sample of
4,435 subjects
ARIC (clinical
model)
Danish Risk
Questionnaire15
FINDRISC12-15
Cambridge Risk
Score14,16,17
DIABETES RISK SCORES
KORA Survey
(Rathman, Martin
et al. 2005)14
Cross Validation &
Temporal Validation
Sensitivity 77%
Specificity 55%
PPV 8%
AUC 80%
Logistic
regression
Population based
sample of
1,112 subjects
Symptom Risk
Questionnaire14
Mohan et al. (2007)18
External & Cross
Validation
Sensitivity 76.6%
Specificity 59.9%
PPV 9.4%
NPV 97.9%
AUC 73%
Logistic
regression
Population based
cohort of
10,003 subjects
Indian Score18
Comparison of Various Diabetes Risk Scores
PART 2_Appendix Reference List
1. Oberoi Consultancy. http://www.oberoi-consulting.com. 2007.
2.
JBS 2: Joint British Societies' guidelines on prevention of cardiovascular disease in clinical practice. Heart 2005;91 Suppl 5:v1-52.
www.bcs.com/download/651/JBS2final.pdf
3. National Institute for Clinical Excellence. Hypertension: management of hypertension in adults in primary care. Clinical Guidelines (CG34).
2006. www.nice.org.uk/CG034
4. E-Nudge Trial. http://www2.warwick.ac.uk/fac/med/research/hsri/research/cardio/e-nudge/. 2007.
5. Holt TA, Thorogood M, Griffiths F, Munday S. Protocol for the 'e-Nudge trial': a randomised controlled trial of electronic feedback to
reduce the cardiovascular risk of individuals in general practice [ISRCTN64828380]. Trials 2006;7:11.
6. Marshall T. Estimating the value of information in strategies for identifying patients at high risk of cardiovascular disease.Inform.Prim.Care
2006;14:85-92.
7. Marshall T. The use of cardiovascular risk factor information in practice databases: making the best of patient data. Br.J Gen.Pract.
2006;56:600-5.
8. Griffin SJ, Little PS, Hales CN, Kinmonth AL, Wareham NJ. Diabetes risk score: Towards earlier detection or type 2 diabetes in general
practice. Diabetes/Metabolism Res.Rev. 2000;16:164-71.
9. Lindstrom J,.Tuomilehto J. The diabetes risk score: a practical tool to predict type 2 diabetes risk. Diabetes Care 2003;26:725-31.
10. Davies MJ, Khunti K, Griffin, S., Wareham, N., and Farooqi, A. ADDITION Leicester - part of the ADDITION Europe Study: A randomised
trial of the cost effectiveness of screening and intensive multi-factorial intervention for Type 2 diabetes. 2007.
11. Tringham, J. R. Strategies for the early detection of type 2 diabetes in an at risk population MD University of Leicester. 2006.
12. Saaristo T, Peltonen M, Lindstrom J, Saarikoski L, Sundvall J, Eriksson JG et al. Cross-sectional evaluation of the Finnish Diabetes Risk
Score: a tool to identify undetected type 2 diabetes, abnormal glucose tolerance and metabolic syndrome. Diab.Vasc.Dis.Res.
2005;2:67-72.
13. Franciosi M, De Berardis G, Rossi MC, Sacco M, Belfiglio M, Pellegrini F et al. Use of the diabetes risk score for opportunistic screening
of undiagnosed diabetes and impaired glucose tolerance: the IGLOO (Impaired Glucose Tolerance and Long-Term Outcomes
Observational) study. Diabetes Care 2005;28:1187-94.
14. Rathmann W, Martin S, Haastert B, Icks A, Holle R, Lowel H et al. Performance of screening questionnaires and risk scores for
undiagnosed diabetes: the KORA Survey 2000. Arch.Intern.Med. 2005;165:436-41.
15. Glumer C, Borch-Johnsen K, Colagiuri S. Can a screening programme for diabetes be applied to another population? Diabet.Med.
2005;22:1234-8.
16. Park PJ, Griffin SJ, Sargeant L, Wareham NJ. The performance of a risk score in predicting undiagnosed hyperglycemia. Diabetes Care
2002;25:984-8.
17. Thomas C, Hypponen E, Power C. Type 2 Diabetes Mellitus in Midlife Estimated From the Cambridge Risk Score and Body Mass Index.
Arch.Intern.Med. 2006;166:682-6.
18. Mohan V, Sandeep S, Deepa M, Gokulakrishnan K, Datta M, Deepa R. A diabetes risk score helps identify metabolic syndrome and
cardiovascular risk in Indians - the Chennai Urban Rural Epidemiology Study (CURES-38). Diabetes Obes.Metab 2007;9:337-43.
086
u SECTION 1.1 Search & Invitation Strategy for Record Based Approach
Search Used for New Vascular Risk Assessment Programme
Template for Identification and Search – Record Based Procedure 1
Template for identification and search – Record Based Procedure 2
Inclusion/Exclusion criteria - record based
Initial Invitation letter – record based using existing disease register (procedure 1)
Initial Invitation letter - record based using ‘at risk’ registers (procedure 2)
089
090
091
092
093
094
u SECTION 1.2 Search & Invitation Strategy for Population Based Approach
Template for identification and search – population-based strategy
Inclusion/Exclusion criteria - population based
Initial invitation letter to screening on 50th or 40th birthday
Initial invitation protocol - for population and starting with those aged 50 yrs or 40 yrs
Second invitation (reminder) protocol
Second invitation letter (reminder)
095
096
097
098
099
100
u SECTION 2 Information Sheets and Practice Posters
Patient Information Leaflet - What to Expect at your Appointment
Patient Information Leaflet 2 - Why Should I Attend?
OGTT letter - Invitation for Patient
OGTT letter- What to Expect
Sample Poster for Population Based Strategy - Invitation
Sample Poster for Population Based Strategy - What to Expect
101
102
103
104
105
106
u SECTION 3 Collection of Clinical Data
Pre-visit Questionnaire
Risk Assessment Patient Results Outcome Sheet
107
109
u SECTION 4 Clinical Protocols and Measurements
OGTT procedure for Healthcare Professionals
Venepuncture
Collection of Samples and Transfer to the Laboratory
Height measurement
Waist circumference
Self Measurement of Waist Circumference
Weight
BMI
Patient Guide to BMI
Arm circumference
Blood pressure (JBS Guidance)
Blood pressure (using OMRON or similar electronic device)
What is meant by fasting
Measurement of blood glucose and diagnosis of Diabetes
111
112
113
114
115
116
117
118
119
120
121
122
123
124
087
PART 2_SOP
PART 2_SOP
Standard Operating Procedures
u SECTION 4 Clinical Protocols and Measurements (cont)
Measurement of lipids
Appropriate action for Ketones in urine
Equipment needed for clinic
125
126
127
u SECTION 5 Risk Assessment
Calculating CVD Risk Score
CVD Risk Prediction Charts
CVD Risk Score Adjustment for Other Risk Factors
What is Your Risk; Risk Factors You Can Change.
Example of a Care Plan
128
129
131
132
133
u SECTION 6 Patient Information Sheets
Cardiovascular Health Risk Assessment
Physical Activity for Health
Smoking - A Summary
Healthy Eating
Five Choices to Help You Stay Healthy
Cholesterol
134
137
138
139
142
143
u SECTION 7 Other
Employing Health Care Assistants in General Practice
Health Care Assistant Job Description
Reference List
145
147
148
088
Search used for new vascular risk assessment programme
Identification of Patients; An Example
Example for Search performed on EMIS LV
The administrator will identify, using the Practice EMIS Computer System (or whichever system is used), patients
who are eligible for vascular risk assessment. These patients will fall within the following groups:
w ST – Search & statistics
w B – Patient searches
w A – Build and perform new search
w A – On today’s practice population
w Add a feature
w 1. Age
w Upper Limit = 74 – enter
w Lower Limit = 40 – enter
w A – Shared
w Return
w Are features correct – enter ‘Y’
w Give search a name: vascular assessment. - enter
w Save under ‘One-Off Search File’.
w The system will ask if you want to run the search – enter ‘Y’ for yes.
Escape out of this section, until you get the screen which indicates the name of the Surgery in the top left-hand
corner.
089
PART 2_SOP
1) Build a Search on patients aged 40 - 74
‘How to’ identify appropriate patients for assessment
Template for identification and search: Record Based; Procedure 1
Search Strategy
Template for identification – Record-based strategy using the existing disease registers - (procedure 1)
Search for all patients aged from 18 years up to 74 years (up to 74yrs, 11mths, 30 days) (lower age limit 18
years)
From those in ‘1’ above search for patients on the following registers;
w LVF
w Stroke/TIA
w CHD
The criteria should be ‘included’
Call this ‘List A’
Exclude any patients on the Diabetes register
Call this ‘List B’
From ‘List B’ exclude any patients with a blood glucose record of ≤ 6mmol or an HbA1c ≤ 6% in the past 15/12
Call this ‘List C’
List C are those people who will need a FPG test done at the Vascular Assessment or earlier along with cholesterol & eGFR
090
‘How to’ identify appropriate patients for assessment
Template for identification and search: Record Based; Procedure 2
Search Strategy
Template for identification – Record-based strategy using ‘at risk’ registers (obesity/hypertension/CKD) - procedure 2
u All adults aged 25 (up to 24yrs, 11mths, 30 days) to 74 (up to 74yrs, 11mths, 30 days)
Call this ‘List A’
u From ‘List A’ exclude patients on any or all of the following registers;
w LVF
w Stroke/TIA
w CHD
w Diabetes
u From ‘List B’ search for patients with the following criteria;
w
w
w
Hypertension
Obesity
CKD
Call this ‘List C’
These are the people who will receive a ‘Vascular Assessment’ invitation letter.
091
PART 2_SOP
Call this ‘List B’
Inclusion/Exclusion criteria - record based
Record-based using existing disease register (procedure 1):
u Inclusion;
w Strategy for diabetes screening for patients on the LVD, stroke, TIA and CHD register: all Adults
aged 18 - 74 will be offered annual screening for diabetes in the form of a fasting plasma glucose, and
screening for chronic kidney disease (eGFR).
u Exclusion:
w If there is already a record of a plasma glucose of < 6 mmol/l within the past 15 months (or an
w
w
HbA1c ≤ 6%).
At the clinician’s discretion, for example, poor prognosis due to other co-morbidities which
makes screening inappropriate.
If the patient expresses a wish not to have the test done
Record-based screening using at risk register (procedure 2):
u Inclusion;
w All those on the CKD, Hypertension or Obesity register and all those with BMI > 30 kg/m2:
w Aged 25-74 years
u Exclusion:
w Those who have recorded that they have removed their consent to be contacted for vascular
risk assessment.
w Those who, according to the clinician, have severe co-morbidities which means vascular
assessment is inappropriate.
092
Initial Invitation letter – record based using existing disease register (procedure 1):
For those on LVD, stroke/TIA and CHD registers:
SAMPLE LETTER
ry
Anyt
ge
n Sur
ow
As you know the practice invites you for a regular check-up. As part of your check-up we
will now be including a screening test for diabetes. This is because diabetes has been
shown to be more common in people with established vascular disease, including a history
of stroke and/or heart attack. Therefore we would like option 1: for you to attend fasting
approximately 7-10 days before your planned visit to have your fasting blood test done, and
when we send the blood test to check your cholesterol and kidney function we will also
include a blood glucose or option 2: we would like you to attend fasting on the day of your
visit so that we can send, in addition to your cholesterol level and kidney function, a blood
test to screen for diabetes.
9 times out of 10 we will be able to tell on the initial fasting blood glucose whether you have
diabetes or whether this is very unlikely. However, one in ten times we will need to do a
second test to confirm this. If you need a second test this is nothing to worry about, but it
does take a little longer. You will be informed of the need for a second test within two weeks
of your visit.
Please do not hesitate to get in touch should you have any queries, by calling 0123456.
The enclosed sheet tells you how to prepare for your visit.
With kind regards,
Yours sincerely,
093
PART 2_SOP
Dear Mr Bloggs:
Initial Invitation letter - record based using ‘at risk’ register (procedure 2):
SAMPLE LETTER
ry
Anyt
ge
n Sur
ow
Dear Mr Bloggs
VASCULAR ASSESSMENT VISIT
We would like to invite you to attend the surgery for a check-up. This is because as part of our
practice’s commitment to the health of patients people who we have identified who may be at
higher risk of developing vascular diseases including diabetes, heart disease and kidney disease have been selected to have a general check up. I enclose an information sheet that explains exactly what will be involved in this check-up, and would encourage you to attend. If you
cannot make this appointment please contact the surgery on 0123456 to
arrange another time.
Yours sincerely,
94
‘How to’ identify appropriate patients for assessment
Template for identification and search – population based strategy
Search Strategy; an example
Template for identification – population-based
u Identify all those aged between 40 (up to 39yrs, 11mth, 30 days) and 74 (74 yrs, 11mths, 30 days)
Call this ‘Step 1’
The criteria should be ‘excluded’ as we want to exclude people already on any of the registers.
Call this ‘Step 2’
Patients in ‘Step 2’ are invited, for example starting with people having their 50th birthday in that year and then
as a second ‘wave’ people from their 40th Birthday depending on the predicted workload.
The interval between assessments, if CVD Risk is low at first, is likely to be not less than 5 years.
95
PART 2_SOP
u From ‘Step 1’ exclude all those on the following registers;
w Hypertension
w CHD
w TIA/Stroke
w CKD
w Obesity
w Diabetes
Inclusion/Exclusion criteria – population based
u Inclusion:
w
All adults aged between 40 and 74 should be offered a risk assessment this may start from the year of
their 40th birthday.*
u Exclusion:
w
w
*
Those who have recorded that they have removed their consent to be contacted for vascular risk
assessment.
Those who, according to the clinician, have severe co-morbidities which means vascular assessment is
inappropriate.
40 years old is the age currently suggested by recent guidelines1-2. However local services will need to
decide how long they will implement such a programme. For example start with patients that are aged 50
years old or over first.
96
Initial invitation letter to screening on 50th or 40th birthday
SAMPLE LETTER
ry
Anyt
ge
n Sur
ow
Dear Mr Bloggs
Now that you have reached this milestone, we would like to invite you to X for a general
check-up of your health. We note from our records that you have not had a health check
including measurement of your blood pressure, cholesterol levels etc., and as part of our
practice’s commitment to the health of patients, we now see this as an important part of the
preventative health care.
I enclose a sheet that gives you information on what to expect at this appointment. If you
have any further questions, please call 0123456, and someone will be able to help you.
We look forward to hearing from you.
Yours sincerely,
97
PART 2_SOP
Congratulations on your recent birthday. The doctors and staff at Blooming Health Medical
Centre would like to wish you a very Happy Birthday.
Initial invitation protocol – for population and starting with those aged 50yrs or 40yrs
Initial invitation
u 1. At the beginning of each month perform a search to find anyone with a 50th (or 40th) birthday during the
next month. i.e. First week in January search for patients with 50th birthday in February.
u 2. Make a note on the calendar to send invitation ‘birthday card’ 2-3 days before the due date.
u 3. Ensure that PIL and ‘What to expect at your clinic appointment’ are enclosed with invitation letter
u 4. When patient calls for appointment make the blood test appointment first, entering ‘reason’ – Vascular
Assessment - followed by the screening appointment 10 days later to ensure blood results are back.
u 5. Enter ‘reason for appointment’ – Vascular Assessment OR enter on to a pre-booked clinic.
98
Second invitation (reminder) protocol
No response to first and second invitations protocol
u 1. At beginning of each month check on diary for preceding month for patients who had 1st
reminder letter. If patient has not booked an appointment or DNA’d for second time put entry on
to patient record ‘DID NOT ATTEND VASCULAR ASSESSMENT AT AGE 50’ (OR AGE 40).
Use the ‘patient diary’ to enter the next due date for re-call.
Second invitation
u 2. At beginning of month check on diary to see who was due for appointment during preceding
month. I.e then check the patient’s diary to ensure they attended or have an appointment booked.
w Ideally telephone to make another appointment.
w Confirm appointment by post enclosing PIS and ‘What to expect…’ leaflet
w Write to the patient using 2nd reminder letter also enclosing PIS and ‘what to expect…’
w If patient contacts to decline invitation but would like to be invited in the future UPDATE RECORD
w If patient states they do not wish to be contacted UPDATE RECORD
99
PART 2_SOP
u 3. If patient has not booked an appointment or DNA’d;
Second invitation letter (reminder)
SAMPLE LETTER
No response to first and second invite
ry
Anyt
ge
n Sur
ow
Dear Mr Bloggs
You may remember that I wrote to you on your recent birthday to invite you to come along
to our (clinic title). I notice that we haven’t heard from you.
I would encourage you to come along as soon as possible for this important health check. This
will give you peace of mind and if we do detect anything out of the ordinary we can start to deal
with it before it becomes too serious. The appointment will only take (about 30 minutes) and
with our flexible clinic times we can usually find a time that is convenient for you.
Of course, if you wish to decline this time but would like to be invited in future please let us
know.
With kind regards
100
Patient Information Leaflet - What to Expect at Your Appointment
What to expect at your
(clinic name) appointment
u Please allow 30 minutes for your appointment
u Bring along any medication you are currently taking
u If you have not had a fasting blood test prior to this appointment please
attend fasting (fasting means nothing to eat or drink apart from water for at
least 8 hours)
u Wear comfortable, non-restrictive clothing
u Your blood pressure will be taken 3 times throughout the appointment, so
that we can get an ʻaverageʼ reading
u We will measure your height and weight
u We will measure your waist
u We will discuss:
w Your blood test results
w Your lifestyle – diet, exercise, smoking etc
w Family history of heart disease and/or diabetes
In some patients (about 1 in 10) a follow-up visit is required for additional
blood tests, e.g. to be certain whether someone does or does not have
diabetes. You will be informed about this within 2 weeks of your visit
We will test your urine with a test strip. If necessary we may ask you to do
another urine sample to send off to the hospital for further tests (if we
suspect infection for example)
Anytown Surgery
101
PART 2_SOP
u Please bring along the enclosed questionnaire which should take
no more than 10-15 minutes to complete
Patient Information Leaflet 2 - Why Should I Attend?
Why is it important that I attend this appointment?
You have been invited to come along as you are now in the age range that maybe at an increased risk of high blood pressure, heart disease, stroke, kidney disease or diabetes. We
would hope to delay the onset or minimise the risk of complications of these diseases by inviting you to attend this appointment.
Initial appointment for a blood test
When you contact the surgery to make your appointment for (insert clinic title) you will be
asked to make an appointment for a fasting blood test. We will be checking for cholesterol, and
kidney function and in some people, glucose. This test should be approximately 7 – 10 days
before your screening appointment. At this initial appointment you will be given a urine bottle.
Please use this to bring a sample to your screening appointment.
What happens at my screening appointment?
Your appointment will be with the Health Care Assistant or Practice Nurse and will take around
15-30 minutes. He/she will measure your height and weight, take your blood pressure and test
your urine. You will also have a discussion about your lifestyle (diet, exercise, smoking status
etc.) and family history of heart disease and diabetes. Please feel free to ask any questions or
raise concerns that you may have.
The Nurse or Health Care Assistant will also discuss the results of your blood test. If necessary
he/she may ask you to see the doctor. Don’t worry, your results may be outside the desired
range and the doctor may wish to do some further tests but this will be discussed fully with
you.
All the outcomes of the appointment will be discussed with you and recorded for you to take
away.
Will I have to come back again?
In some patients (about 1 in 10) a follow-up visit is required for additional blood tests, e.g. to be
certain whether someone does or does not have diabetes. You will be informed about this
within 2 weeks of your visit.
Provided all the tests are within the desired range we will not need to follow-up this appointment. If, however, something is a little out of the ordinary we will follow the National guidelines
to give you the best care we can.
You will be recalled for your next vascular review appointment after approximately 5 years but
this will depend on the outcome of the initial visit.
u
Please bring a urine sample to your main screening appointment
102
OGTT Letter - Invitation to Patient
SAMPLE LETTER
ry
Anyt
ge
n Sur
ow
You recently attended the surgery for your vascular risk assessment. The sample that was
sent for the measurement of blood sugar is above the normal range and therefore we need
to perform a second test to confirm whether or not you have diabetes. This is nothing to
worry about, and we enclose a patient information sheet to tell you how to prepare for this
test.
Option 1:
Please find enclosed a date and time for the appointment for the test. If this is inconvenient,
please ring on (insert number)
Option 2:
Please ring on (insert number) to arrange a convenient time and date for the test to be done,
or if you have any queries.
Yours sincerely,
103
PART 2_SOP
Dear Mr Bloggs
OGTT Letter- What to Expect
Patient Information Leaflet - Oral Glucose Tolerance Test
Why should I have this test?
Sometimes we check the level of glucose in blood by a ʻfinger-prick testʼ or on a single test sent
to the laboratory. However, this is not an accurate way of detecting or diagnosing diabetes.
If you have a test that is specifically designed to diagnose diabetes and have prepared properly
for the test, following our guidelines, we can get a much more accurate diagnosis.
How long does it take?
We ask you to allow 2 1/2 hours from arrival to departure
What should I do before having the test?
The test will be carried out early in the morning, usually around 8.30 – 9.00 a.m.
Do not have any food or drink from midnight the night before. So, if your test is at 8.30a.m.
on February 1st you should not eat or drink from 11.59p.m. (Midnight) January 31st.
You may have water. Please do not smoke during this time.
What about my medication?
You should take your medication as normal unless it should be taken with food. If you need
to eat something immediately before or after taking your medication please wait until after
the test to take your tablets. Please check with your doctor if you are unsure about this.
What will happen during the test?
u You should arrive promptly for your appointment. The Practice Nurse or Health Care
Assistant will check that you have had nothing to eat or drink since midnight and then she/he
will take the first blood sample from your arm.
u You will then be asked to drink your Lucozade.
u After drinking the Lucozade you will be asked to sit in the waiting-room. Please feel free to
bring a book or some other quiet activity as you will now have to wait for 2 hours. We ask
that you do not leave the surgery as any form of exercise during these two hours may give a
false reading when we take the final blood sample. Do not eat or drink anything else.
u After 2 hours you will have another blood sample taken from your arm
u You are now free to go or you may eat your snack and have a drink before you leave.
After 7-10 days (option please telephone for the results of your test or your results will be
sent to you).
Please remember to bring along a snack for after the test if you want one.
Anytown Surgery
104
Sample Poster for Population Based Strategy - Invitation
Is it your
40th or 50th
Birthday this year?
PART 2_SOP
If so,
congratulations!
Now you have reached
this milestone we would
like to invite you for a
Vascular Risk check
(includes blood pressure,
cholesterol level and alot more)
Anyt
ry
105
n Sur
ow
ge
Please speak to your GP
or Practice Nurse for details
or make an appointment at
reception
Sample Poster for Population Based Strategy - What to Expect
Interested in Attending a
Vascular Risk Assessment Visit?
What to expect at your visit
u
Please allow 30 minutes for your appointment
u
Bring along any medication you are currently taking
u
Please bring along the enclosed questionnaire which should take no
more than 10-15 minutes to complete
u
If you have not had a fasting blood test prior to this appointment
please attend fasting (fasting means nothing to eat or drink apart from
water for at least 8 hours)
u
Wear comfortable, non-restrictive clothing
u
Your blood pressure will be taken 3 times throughout the
appointment, so that we can get an ‘average’ reading
u
We will measure your height and weight
u
We will measure your waist
u
We will discuss:
w Your blood test results
w Your lifestyle – diet, exercise, smoking etc
w Family history of heart disease and/or diabetes
In some patients (about 1 in 10) a follow-up visit is required for additional blood tests, e.g.
to be certain whether someone does or does not have diabetes. You will be informed
about this within 2 weeks of your visit
We will test your urine with a test strip. If necessary we may ask you to do another urine
sample to send off to the hospital for further tests (if we suspect infection for example)
Anytown Surgery
106
Pre-Visit Questionnaire
Pre-Visit Questionnaire for Vascular Risk Assessment
(please complete this and bring along with you to your appointment)
Name:
Male
/
Female
/
Health Questionnaire - Please tick (✔) the box that best describes your ethnic origin
WHITE
CHINESE
White British
Chinese
White Irish
Any other
Any other white background
MIXED
BLACK OR BLACK BRITISH
White and Black Caribbean
Caribbean
White and Black African
African
White and Asian
Any other black background
Any other mixed race
ASIAN OR ASIAN BRITISH
Indian
Pakistani
Bangladeshi
Any other Asian background
Smoking Status
Non-smoker
Yes
Ex-smoker
Yes
Date stopped smoking
Current smoker
Yes
How many used to smoke per day?
How many per day?
Do you currently take any medication?
Yes
No
If ʻyesʼ, please enter details below: (or bring a list of your medicines)
Name of Medication
© University of Leicester
Reason for use
107
PART 2_SOP
Sex:
Date of Birth:
Family History
Diabetes (type if known, for example type 1 or type 2)
Which family member and at what age
Number of 1st degree relatives with diabetes (mother, father, brother or sister)
Parent or sibling with diabetes
Yes
Problem (Stroke or Peripheral Vascular Disease) Age Which family member
Does anyone in your family have Heart Disease? (angina or heart attack) Yes
If yes, please enter details below
Problem
Age
No
Which family member
Do you have any 1st degree relatives with diabetes (mother, father, brother or sister) who had/has
angina, stroke or a heart attack aged less than 55 years and male or 65 years and female:
Yes
No
Do you usually have daily at least 30 minutes of physical activity at work and/or during leisure time
(including normal daily activity)?
Yes
No
How often do you eat vegetables or fruit?
Every day
Not every day
Have you ever been found to have high blood glucose (eg in a health examination, during an
illness, during pregnancy)?
Yes
© University of Leicester
No
108
Risk Assessment - Patient Results Outcomes Sheet
Date
Personal Details
Name:
Home Address:
/
Female
/
No
SCORE
NOTES
Weight
kg
Height
m
BMI
kg/m2
Waist Circumference
Smoker
if > 30 update of
obesity register
cm
Yes / No / Ex
Total Cholesterol
offer smoking cessation
if current smoker
mmol/l
Triglyceride
Blood Pressure
mmHg
eGFR
mls/m2
CVD Risk Score
%
if > 150/90 place
on HT register
if < 60mls/1.73m2
place on CKD register
if > 20% offer place
on CHD register
(Specify which
DM Risk Score score was used)
FPG
mmol/l
OGTT Outcome (if relevant)
mmol/l
N/IGT/IFG/DM
ENSURE RESULTS UPDATED IN PRACTICE TEMPLATE AND DATE RECORDED
© University of Leicester
109
PART 2_SOP
Sex:
Male
Date of Birth:
Fasting:
Yes
Smoking Status
Non-smoker
Yes
Ex-smoker
Yes
Date stopped smoking
Current smoker
Yes
How many used to smoke per day?
How many per day?
Does your patient currently take any medication? (or update computer medical list)
Yes
No
Medication Type
Reason for use
Tick (✔) Name of Medication
ACE – Inhibitor
Alpha Blocker
ARB
Beta-blockers
Calcium Channel Blockers
Diuretics/Thiazides
Aspirin
Lipid Lowering – Statin
Lipid Lowering – Fibrate
Metformin
Sulphonylurea
Glitazone
Prandial Glucose Regulator
Steroids
Please state whether Steroids are oral, injected or inhaled: Oral
Injected
Inhaled
Thyroid/Anti-Thyroid
Others
Family History
Diabetes (ask which type)
Which family member and at what age
Number of 1st degree relatives with diabetes (mother, father, brother or sister)
Patient or sibling with diabetes
Yes
Patient and sibling with diabetes
Yes
Does the patient have a family history of Heart Disease? Yes
If yes, please enter details below
Problem
Age
Which family member
Other Measurements
Height
Weight
© University of Leicester
.
m
.
Waist Measurements
kg
110
No
cm
OGTT procedure for Health Care Professionals (HCPs)
u 1. Prepare blood bottle and syringe following Health & Safety and Clinical Governance guidelines.
For blood glucose measurement a yellow 2.7 fluoride bottle is required
u 2. Perform venepuncture and label the blood bottle with time taken and patient details. Complete
blood test request form according to local guidelines
u 3. Ask patient to drink Lucozade (394ml of current preparation) within 5 minutes (or use an
equivalent source of 75gms of anhydrous glucose). Note time subject starts the Lucozade.
u 4. Patient should sit in the waiting-room for 2 hours. Advise the patient not to leave the surgery as
any form of exercise can have a detrimental effect on the test
u 5. After precisely 2 hours from subject starting to drink the Lucozade take the second blood test
and again, label the bottle including timing of sample (i.e. second in series) and complete blood test request
form according to local guidelines
111
Venepuncture
Guidance on Venepuncture
The subject attending for vascular assessment should expect venepuncture and be prepared (i.e. fasting)
Venepuncture is not always straightforward and, since assessment sessions run smoothly only when adhering
to tight time-lines, we must manage situations where there is difficulty. This plan aims to ensure that:
u Subjects do not undergo multiple attempts at venepuncture
u Venepuncture difficulties do not cause delay for other subjects
The allocated Health Care Professional (HCP) including Health Care Assistant (HCA) (or ‘screener’) may take up
to two attempts at venepuncture with each subject at each timepoint. If blood samples are not collected after
two attempts, the ‘screener’ will request assistance from a suitably-qualified colleague, who may or may not be
part of the Screening Team for that session i.e. the Practice Nurse or GP allocated to cover the assessment session. Provided the subject is agreeable, the colleague may take up to two attempts to collect blood samples. If
samples are still not obtained, venepuncture will be abandoned and the subject will be invited to attend another
assessment session.
In addition to basic venepuncture training (see training manual for details of dates, venues etc.) further training or
supervised practice is always available and anyone who feels they would benefit from these should discuss with
their Line Manager.
112
PART 2_SOP
u Ensure best practice, for example handwashing, is implemented
Collection of Samples and Transfer to the Laboratory
u Check whether the patient is fasting- if not- proceed but record non-fasting on form and on patient record
(unless for OGTT in which case rebook appointment)
u Check on clinical system or blood test request form what blood tests are needed
u Prepare appropriate blood bottles
u Invite patient into clinic room. Check details – name address, D.O.B etc.
u Take blood following practice guidelines
u Label samples and send to lab for processing
u Give patient a urine bottle for next appointment reminding them to bring it with them next time.
stressed that glucose preservatives do not totally prevent glycolysis. If whole blood is used, the sample
should be kept at 0-4 °C or centrifuged immediately, or assayed immediately – WE RECOMMEND PLASMA
SAMPLES FOR ASSESSMENT OF BLOOD GLUCOSE
113
PART 2_SOP
u Glucose concentrations should not be determined on serum unless red cells are immediately removed,
otherwise glycolysis will result in an unpredictable under-estimation of the true concentrations. It should be
Height measurement
The height should be measured with the base plate on a firm and level surface, preferably with a perpendicular
surface to ensure the measure is vertical.
u Ask the subject to remove their shoes and stand on the base plate with their back to the measure.
u If the subject has a ponytail or other hair dressing that may effect the result, ask them to remove it.
u Tell them to stand as tall and straight as possible with feet together and arms held loosely at the side and
shoulders relaxed (to avoid lordosis).
u The head should be placed in the Frankfurt Plane, such that an imaginary line joining the upper margin of the
external auditory meatus and the lower border of the eye is horizontal. (Ensure that subject is looking straight
ahead with back of head against the back plate. i.e. head not tilted up or down)
u Lower the head plate so that it gently rests on the highest part of the subjects head. Press down to flatten
hair.
u Read the height measurement from where the arrow points to on the measure to the nearest (cm).
114
Waist circumference
u This should be measured over bare skin, or light clothing.
u Ask the subject to stand with their arms by their sides and to relax, not to deliberately hold stomach in or out,
looking straight ahead.
u If possible, kneel or sit on a chair to the side of the subject.
u Palpate the lower rib margin (coastal margin) and the iliac crest and mark half way between the two points.
This is the level the measurement of waist circumference should be taken.
u The measuring tape should be placed horizontally on the circumference and you should check that it is not
kinked or twisted, this is best done by looking sideways on. As well as checking the front, peer round the
subjects back to inspect their left side. The tape should rest on the skin, not indent it. Do not pull too tight.
u Take the reading at the end of expiration.
u Add this data to the template
Central obesity is present if the waist circumference is >102 cms (40.2”) in men and 88cms (34.5”) in women.
For the Asian population, lower values of waist circumference are more appropriate: >90cms (35.4”) in men and
80cms (31.4”) in women.
115
PART 2_SOP
u Measure to the nearest (cm)
Self-Measurement of Waist Circumference
Waist Circumference Measurement Guide3
Operating D-Loop tape measure:
u 1) Pull out the tape measure end, with the cm side face up
u 2) Pull the tape measure around your waist so the numbers are upside down
u 3) When both ends of the tape measure meet, attach the open side to the notch and press the white
button underneath to tighten the tape
Measuring the waist circumference:
u 1) Find your bottom rib
u 2) Find the top of the hip bone
u 3) Place the tape half way between your bottom rib and the top of your hip bone
u 4) Read and note your waist circumference measurement
Bottom Rib
Waist
Hip Bone
Bottom
Rib
Hip
Bone
116
Weight
The participant should remove their shoes and coat and heavy outerwear for this test .
u Ensure scales have been calibrated / serviced within the specified time range
u Set scale to ‘0’
u Ask patient to step on scales
u Wait for weight to register properly
PART 2_SOP
u Record weight (usually in kg) in practice template and in patient record booklet
117
BMI - Body Mass Index kg/m2
The body-mass index is used to assess if a person’s weight lies within the healthy weight range for their particular height. The index is calculated by dividing body weight (kg) by the square of body height (m) for example, if
height is 165cm and weight 70kg, body-mass index will be 70/(1.65 x 1.65), or 25.7. Or use chart below to estimate BMI
118
Patient Guide to BMI - Body Mass Index
A healthy weight range is based on a measurement known as the Body Mass Index (BMI). This can be determined if you know your weight in Kilograms and your height in Metres. Frame sizes vary, and it is difficult for any
simple measurement to establish a person’s frame. It is more accurate to recommend a weight range rather
than a specific weight for a given height.
You can calculate your BMI in 3 ways:
u You can use an automatic calculator via the internet, where there are both imperial and metric
versions available.
u You can calculate your BMI manually yourself, by following these three steps:
w Work out your height in Metres, and multiply the number by itself, e.g. if your height is 1.6,
then 1.6 X 1.6 = 2.56.
w Measure your weight in Kilograms.
w Divide this by the answer to question 1. For example, you might be 1.6 Metres tall and weigh 65
Kilograms. The calculation would then be 1.6 X 1.6 = 2.56. BMI would be 65 ÷ 2.56 = 25.4.
PART 2_SOP
u If you know your height in metres (or in feet and inches) and your weight in kilograms (or in pounds), you can
calculate your BMI by using the chart below.
119
Arm circumference
u Ask the subject to stand with their arm hanging at the side.
u The tip of the acromion (point of shoulder) is palpated and marked.
u With the subject’s arm flexed at 90o, the olecranon (tip of elbow) is palpated.
u Put the tape measure on the mark on the shoulder and drop it down to the tip of the elbow, by the side of the
arm.
u Read the exact distance as if you had drawn an imaginary horizontal line from the bottom part of the elbow
to the tape.
u Mark a point on the arm half way between the acromion and olecranon. This marks the level that the
circumference should be taken. (See diagram)
u Ask the subject to relax their arm
u Apply the tape around the arm at the level marked.
u Ensure the tape is horizontal all the way around.
u The tape should rest on the skin but not indent it, do not pull it too tight.
u Read the tape to the nearest 0.1cm.
u Complete this information in the template.
Acromion
Olecranon
Measure at midpoint
between acromion
and olecranon
120
Blood Pressure - taken from JBS Guidance4
Blood pressure measurement by standard mercury sphygmomanometer or semi-automated device
u Use a properly maintained, calibrated, and validated device
u Measure sitting blood pressure routinely: standing blood pressure should be recorded in elderly and diabetic
people
u Remove tight clothing, support arm at heart level, ensure hand relaxed, and avoid talking during the
measurement procedure
Use cuff of appropriate size
Lower mercury column slowly (2 mm/s)
Read blood pressure to the nearest 2 mm Hg
Measure diastolic as disappearance of sounds (phase V)
Take the mean of at least two readings; more recordings are needed if notable differences between initial
measurements are found
u Do not treat on the basis of an isolated reading
u
u
u
u
u
It is important to note that ambulatory blood pressure monitoring or home blood pressure targets are usually
lower than clinic readings and therefore thresholds and targets should be adjusted downward by 10/5mm of
mercury. Therefore, for self-measurement of blood pressure, ≥135/85 should be considered to be in the hypertensive range.
Seated blood pressure recordings are generally sufficient, but standing blood pressure should be measured in
elderly or diabetic patients to exclude postural hypotension.
The average of 2 readings, each of several visits, should be used to guide the decision to treat.
121
PART 2_SOP
Measurements should be made under standardised conditions using accurate validated and well-maintained
monitors with an appropriate cuff-size. Further information at www.bhsoc.org5
Blood pressure (using OMRON or similar electronic device)
u Before taking blood pressure complete the template to say which arm was used (Left or Right).
u In order to choose the right cuff size first of all measure the upper arm circumference. (See SOP: Arm
circumference)
u Choose the appropriate cuff size for the subject depending on the arm circumference.
Normal size cuff = 22-32cms
Large cuff = 32-42cms
u Apply the cuff to the upper arm of the subject ensuring the tube is placed over the artery.
u Secure the cuff using the Velcro.
u Ensure the patient is not talking whilst the BP is being measured and make sure their legs are not crossed.
u Press the ‘on’ button
u Press the ‘start’ button
u The cuff will inflate and deflate giving a reading that should be entered into the template.
u The subject should be given 5 minutes rest between blood pressure readings.
u The blood pressure should be repeated a further 2 times.
u Insert all readings on to template, calculating the ‘average’ using the last 2 readings.*
*To calculate ‘average’ of
130/90 and 125/85
1. Add 130 + 125 = 155. Divide by 2 = 127.5 (round up to nearest whole figure) =128
2. Add 90 + 85 = 175. divide by 2 = 87.5 (round up to nearest whole figure) = 88
Average BP reading = 128/88
122
What is meant by fasting
PART 2_SOP
Fasting, which means that you should have nothing to eat or drink
apart from water, from 10pm the night (preferably for least 10 hours)
before the test.
123
Measurement of blood glucose and diagnosis of Diabetes
* Blood glucose alone (with cut off of 5.0 mmol/l or above) is an unreliable means of diagnosis of IGR (IGT or
IFG). Other measures of risk assessment are required (For example diabetes self-assessment score see
pages 87-88)
124
Measurement of Lipids
u Total cholesterol and HDL cholesterol can usually be measured in the non-fasting state.
u However, in all of those in whom there is higher risk, i.e. those on hypertension or obesity registers, should
have a fasting lipid profile.
u Blood should be drawn after at least a 10 hour fast, and the lipid profile should include the total cholesterol,
triglyceride, HDL cholesterol and, where available, a direct measurement of LDL cholesterol.
u When the LDL cholesterol cannot be measured directly, it can be estimated. LDL cholesterol = total
cholesterol minus HDL cholesterol minus (triglycerides/2.2). This formula should not be used in non-fasting
individuals or if the plasma triglycerides are higher than 4 mmol/L and it is less reliable in patients with
diabetes.
u Monitoring lipids in the non-fasting state may underestimate the LDL cholesterol level.
u It is important to note that at the time of an acute event, particularly a MI, cholesterol and LDL cholesterol
may fall. A lipid profile done within 24 hours of the onset of symptoms may give a reasonable indication of
total cholesterol and HDL. However, this will still usually be an underestimate. It is important to repeat the
fasting lipid profile 8-12 weeks after the event, even if a statin has been commenced, to determine whether a
person has familial dyslipidaemia and to assess whether the person has achieved their total and LDL
cholesterol targets.
u Other laboratory baseline measures done at the time of initiation of treatment include muscle enzymes
including creatinine phosphokinase (CK) and liver function tests including ALT or AST. If both CK and liver
function tests are normal, repeat routine measurement of these tests is not usually indicated unless
symptoms develop.
125
PART 2_SOP
u Lipid analysis should be done in the laboratory participating in the National Quality Control scheme.
Appropriate action for Ketones in urine
u Moderate or more ketones in the urine with any degree of glucose may indicate evolving type 1 diabetes.
This needs to be reported ON THE DAY OF SCREENING.
u After 40 secs, if see ++ GLUCOSE and ++KETONES together = contact doctor
u It is the responsibility of the medical professional in charge to be aware of and act upon the urine dipstick
results.
u A capillary glucose estimation or an urgent laboratory glucose test should also be performed and
reported with the abnormal urine result.
126
Equipment needed for clinic
u 1. Urine test strips
u 2. Blood pressure monitor (electronic – Omron or similar, manual sphygmomanometer) duly calibrated
and quality tested
u 3. Scales – electronic or manual, duly calibrated and quality tested
u 4. Height measure
u 5. Tape measure (for waist)
u 6. Access to computer and patient clinical system (EMIS or similar)
u 7. Record booklet / sheet for patient
PART 2_SOP
u 8. Relevant lifestyle/diet/stop smoking booklets
127
Calculating CVD Risk Score
The following patients should not have a CVD risk calculated as they are of sufficiently high risk to justify intensive intervention without formal risk assessment.
These include people with;
u Established atherosclerotic vascular disease, including PAD, CHD and stroke or TIAs,
u Persistently elevated blood pressure of >160/100 or when target organ damage is already present
u Those with a total cholesterol of HDL ratio >6,
u Those with either type 1 or type 2 DM
u Those with established CKD
u Those with familial hypercholesterolaemia.
Risk score should not be used with patients ≥ 75 years old
The information collected should be used to calculate the vascular risk score using the preferred CVD risk score
as advocated by NICE or SIGN guidance.1,2,4
Age Group: The risk should be estimated for the person’s current age. In the younger age group, the risk will
be overestimated because the chart is based on age at 49 and 59 years.
Sex: It is important to consider the separate charts for men and women.
Smoking habit: An assessment of lifetime tobacco exposure is required
Blood pressure should be measured according to the British Hypertension Society Guidelines.5
The risk score should be adjusted appropriately taking into account (see page 137 for adjustment of CVD score)
u ethnicity multiply the score by a factor of 1.4
u triglyceride levels, raised triglyceride of >1.7 mmol/L multiply by a factor of 1.3
u for IGR (if known impaired glucose regulation (IGR) as defined by IGT or IFG but not DM multiply the score by
factor of 1.5
u family history of premature CVD (multiply score by 1.3)
For CVD vascular risk of >20% over 10 years, it is defined as high risk and justifies targeted lifestyle intervention
and appropriate use of anti-thrombotic, antihypertensive and lipid lowering therapy. Other factors which should
be assessed during the vascular assessment which are not included in the vascular risk prediction chart are
obesity, low HDL, raised triglycerides and women with premature menopause.
The physician and healthcare professional should always use clinical judgement by taking into account other risk
factors before reaching a final decision about the person’s overall CVD risk, and their need for intensive lifestyle
and pharmacological intervention.
128
Cardiovascular Risk Prediction Charts (an example from JBS-2)4
How to use the Cardiovascular Risk Prediction Charts for Primary Prevention
These charts are for estimating cardiovascular disease (CVD) risk (non-fatal myocardial infarction and stroke,
coronary and stroke death and new angina pectoris) for individuals who have not already developed coronary
heart disease (CHD) or other major atherosclerotic disease. They are an aid to making clinical decisions about
how intensively to intervene on lifestyle and whether to use antihypertensive, lipid lowering and anti-platelet
medication, but should not replace clinical judgement.
u The use of these charts is not appropriate for patients who have existing diseases which already
put them at high risk such as:
u The charts should not be used to decide whether to introduce antihypertensive medication when blood
pressure is persistently at or above 160/100mmHg or when target organ damage due to hypertension is
present. In both cases antihypertensive medication is recommended regardless of CVD risk. Similarly the
charts should not be used to decide whether to introduce lipid-lowering medication when the ratio of serum
total to HDL cholesterol exceeds 6. Such medication is usually indicated regardless of estimated CVD risk.
u To estimate an individual’s absolute 10-year risk of developing CVD choose the chart for his or her gender,
lifetime smoking status and age. Within this square identify the level of risk according to the point where the
coordinates for systolic blood pressure and the ratio of total cholesterol to high density lipoprotein (HDL)
cholesterol meet. If no HDL cholesterol result is available, then assume this is 1.0mmol/litre and the lipid
scale can be used for total cholesterol alone.
u Higher risk individuals (red areas) are defined as those whose 10-year CVD risk exceeds 20%, which is
approximately equivalent to the coronary heart disease risk of > 15% over the same period.
u The chart also assists in identifying individuals whose 10-year CVD risk is moderately increased in the range
10-20% (orange areas) and those in whom risk is lower than 10% over 10 years (green areas).
u Smoking status should reflect lifetime exposure to tobacco and not simply tobacco use at the time of
assessment. For example, those who have given up smoking within 5 years should be regarded as current
smokers for the purposes of the charts.
u The initial blood pressure and the first random (non-fasting) total cholesterol and HDL cholesterol can be
used to estimate an individual’s risk. However, the decision on using drug therapy should generally be based
on repeat risk factor measurements over a period of time.
u Men and women do not reach the level of risk predicted by the charts for the three age bands until they
reach the ages 49, 59 and 69 respectively. The charts will overestimate current risk most in the under 40s.
Clinical judgement must be exercised in deciding on treatment in younger patients. However, it should be
recognised that blood pressure and cholesterol tend to rise most and HDL cholesterol decline most in
younger people already with adverse levels. Left untreated, their risk at the age 49 years is likely to be higher
than the projected risk shown on the age-under-50-years chart. From age 70 years CVD risk, especially for
men, is usually > 20% over 10 years and the charts will underestimate true total CVD risk.
129
PART 2_SOP
w Coronary heart disease or other major atherosclerotic disease;
w Familial hypercholesterolaemia or other inherited dyslipidaemias;
w Renal dysfunction including diabetic nephropathy
w Type 1 and 2 diabetes mellitus
u These charts (and all other currently available methods of CVD risk prediction) are based on groups of people
with untreated levels of blood pressure, total cholesterol and HDL cholesterol. In patients already receiving
antihypertensive therapy in whom the decision is to be made about whether to introduce lipid-lowering
medication, or vice versa, the charts can only act as a guide. Unless recent pre-treatment risk factor values
are available it is generally safest to assume that CVD risk is higher than that predicted by current levels of
blood pressure or lipids on treatment.
u CVD risk is also higher than indicated in the charts for:
w
w
w
w
Those with a family history or premature CVD or stroke (male first-degree relatives and <55 years and
female first-degree relatives ages <65 years)
Those with raised triglyceride levels (1.7mmol/l)
Women with premature menopause;
Those who are not yet diabetic, but have impaired fasting glycaemia (6.1-6.9 mmol/l) or impaired
glucose tolerance (2 hour glucose > 7.8 mmol/li but <11.1 mmol/l in an OGTT
u The charts have not been validated in ethnic minorities and in some may underestimate CVD risk. For
example, in people originating from the Indian subcontinent it is safest to assume that the CVD risk is
higher than predicted from the charts.
u An individual can be shown on the chart the direction in which his or her risk of CVD can be reduced by
changing smoking status, blood pressure, or cholesterol, but it should be borne in mind that the estimate of
risk is for a group of people with similar risk factors and that within that group there will be considerable
variation in the risk. It should also be pointed out in younger people that the estimated risk will generally not
be reached before the age of 50, if their current blood pressure and lipid levels remain unchanged. The
charts are primarily to assist in directing intervention to those who typically stand to benefit most.
Non Diabetic Men
Images © University of Manchester
Non Diabetic Women
130
CVD Risk Score Adjusting for other factors
Calculate CVD Risk Score According to SOP
CVD Score
No ScoreYes
= Adjusted
✔
%x
South Asian Ethnicity
Score
Add 1
TOTAL
1.5
+1
2.5
Score
Add 1
TOTAL
+1
1.8
0.4
TG > 1.7 mmol/l
✔
0.3
Family History of CHD (see definition)
✔
0.3
IGR (IGT or IFG)
✔
0.5
ADD TOTAL b
2.5
Example
No
Yes
South Asian Ethnicity
✔
-
TG > 1.7 mmol/l
✔
-
Family History of CHD (see definition)
✔
0.3
IGR (IGT or IFG)
✔
0.5
ADD TOTAL b
CVD Score
© University of Leicester
12
%x
1.8
0.8
= 21.6%
131
PART 2_SOP
CVD Risk Score = 12%
What is Your Risk - Risk Factors you Can Change
BMI
40+
!
100
99
98
97
BP Systolic
120
140
160
180
!
BP Diastolic
70
80
90
100+
!
Total Cholesterol
3.5
4.0
5.0
6.0
!
Smoking
CVD Risk Score
Diabetic Risk Score*
Glucose (FPG)
© The DESMOND Collaborative 2007
<2
3
Less
than 10
10 to 20
10 - 18
0 to 9
<5.0
5.5 - 6.0
132
!
>4
PASSIVE
SMOKER
NON SMOKER
109
109
106
106
109
105
105
108
104
104
108
103
103
107
102
102
107
101
101
100
99
98
97
96
96
27.5
30
23
25
LDL
108
107
106
105
104
103
102
101
100
99
98
95
97
94
95
Greater risk
95
94
93
92
91
90
89
88
87
86
85
84
83
82
81
80
79
78
77
76
75
74
96
93
94
92
91
90
93
92
91
90
89
88
87
86
85
84
83
82
81
80
79
78
77
76
75
74
73
South Asian
White European
Greater risk
Greater risk
Ideal Increased
risk
73
South Asian
Male Waist
Circumference (cm)
72
Female Waist
Circumference (cm)
72
Ideal Increased risk
89
88
87
86
85
84
83
82
81
80
79
78
77
76
75
74
73
Male Waist
Circumference (cm)
72
Ideal Increased risk
SMOKER
!
More
than 30
!
19 or more
!
20 to 30
6.1 - 6.9
+7
!
* Using prototype Leicester Diabetes & Pre-diabetes
Risk Score (see pages 82 and 83)
Example of a Care Plan
Score
My BMI is
Agreed Action
kg/m2
My waist circumference is
cm
My total cholesterol level is
mmol/l
My blood pressure is
mmHg
My CVD risk score is
%
My diabetes risk score is
My physical activity level is
Changes that I may need
to make to my diet
© University of Leicester
133
PART 2_SOP
My smoking status is
Cardiovascular Health Risk Assessment
UK guidelines recommend that all people aged 40 or more should have a routine cardiovascular risk assessment.1,2 A 'risk factor calculator' is commonly used by doctors and nurses to assess the risk of you developing a cardiovascular disease such as: heart attack, angina, stroke, and peripheral vascular disease.
Treatment is recommended if you are at high risk.
What is cardiovascular disease?
Cardiovascular diseases are diseases of the heart or blood vessels that are caused by atheroma. Patches of
atheroma are like small fatty lumps that develop within the inside lining of arteries (blood vessels). Atheroma is
also known as 'hardening of the arteries'. A patch of atheroma makes an artery narrower, which can reduce the
blood flow through the artery. Sometimes blood clots form over a patch of atheroma. Depending on the site of
the atheroma the diseases that it causes include heart attack, angina, stroke, and peripheral vascular disease.
Who should have their cardiovascular health risk assessed?
u All adults aged 40 or more.
u Adults of any age who have:
w A strong family history of early cardiovascular disease. This means if you have a father or
brother who developed heart disease or a stroke before they were 55, or in a mother or sister
before they were 65.
w A first degree relative (parent, brother, sister, child) with a serious hereditary lipid disorder. For
example, familial hypercholesterolaemia or familial combined hyperlipidaemia. These diseases
are uncommon.
If you already have a cardiovascular disease or diabetes then you do not need to be screened. This is because
you are already known to be in the high risk group.
What does the screening involve?
A doctor or nurse will ask if you have any current lifestyle risk factors that increase your risk of developing a cardiovascular disease. These include: smoking, obesity, a poor diet, lack of physical activity, and drinking a lot of
alcohol. You will then have a blood test to check your blood cholesterol and glucose (sugar) level. Your blood
pressure will be measured. A score is calculated based on several of these risk factors, your age and sex. An
adjustment to the score is made for certain other risk factors such as strong family history and ethnic origin.
What does the assessment score mean?
You are given a score as a % chance. So, for example, if your score is 30% this means that you have a 30%
chance of developing a cardiovascular disease within the next 10 years. This is the same as saying a 30 in 100
chance (or a 3 in 10 chance). In other words, in this example, 3 in 10 people with the same risk factors that you
have will develop a cardiovascular disease within the next 10 years. Note: the score cannot say if you will be one
of the three. It cannot predict what will happen to each individual person. It just gives you the odds.
You are said to have a:
u High risk - if your score is 20% or more. (That is, a 2 in 10 chance or more of developing a
cardiovascular disease within the next 10 years.)
u Moderate risk - if your score is 10-20% (between 1 in 10 and 2 in 10 chance).
u Low risk - if your score is less than 10% (less than a 1 in 10 chance).
134
Who should be treated to reduce their cardiovascular health risk?
Treatment to reduce the risk of developing a cardiovascular disease is usually offered to people with a high risk.
That is:
u People with a risk assessment score of 20% or more. That is, if you have a 2 in 10 chance or more of
developing a cardiovascular disease within the next 10 years
u People with an existing cardiovascular disease (to lower the chance of it getting worse, or of developing a
further disease).
u People with diabetes. If you have diabetes, the time that treatment is started to reduce cardiovascular risk
depends on factors such as: your age, how long you have had diabetes, your blood pressure, and if you
have any complications of diabetes.
u People with certain kidney disorders.
What treatments are available to reduce the risk?
u Drug treatment to lower your cholesterol level, usually with a statin drug. No matter what your current
cholesterol level, drug treatment is advised. The aim is to reduce the level by 25% or to get the level under 5
mmol/l* - whichever is the biggest reduction. See leaflet called 'Cholesterol' for details.
u Drug treatment to lower blood pressure if your blood pressure is high. This is even if your blood pressure is
just mildly high. See leaflet called 'High Blood Pressure' for details.
u A daily low dose of aspirin - depending on your age and other factors. Aspirin helps to prevent blood clots
from forming on patches of atheroma. See leaflet called 'Aspirin to Prevent Blood Clots' for details.
u Where relevant, to encourage you to tackle lifestyle risk factors. This means to:
w stop smoking if you smoke.
w eat a healthy diet.
w keep your weight and waist in check.
w take regular physical activity.
w cut back if you drink a lot of alcohol.
You may be offered a referral to specialist services. For example, to a dietician to help you to lose weight and eat
a healthy diet, to a specialist 'stop smoking clinic', or to a supervised exercise programme.
What if I am at moderate or low risk?
If you are not in the high risk category, it does not mean you have no risk - just a lesser risk. Drug treatment is
not usually prescribed. However, you may be able to reduce whatever risk you do have even further by any relevant changes in lifestyle (as described in the above paragraph).
Some people with a moderate risk buy a low dose statin drug from a pharmacy to lower their cholesterol level.
(Statin drugs are available on prescription and funded by the NHS if your risk is high. However, you need to buy
them if your risk is not in the high category.)
© EMIS and PIP 2006 Updated: July 2006 PRODIGY Validated7
* Amended to be in line with recent National Guidance1,2
135
PART 2_SOP
If you are at high risk
If you are at high risk of developing a cardiovascular disease then drug treatment is usually advised along with
advice to tackle any lifestyle issues. This usually means:
Physical Activity for Health
The benefits of doing regular physical activity include a reduced risk of: heart disease, stroke, bowel cancer,
breast cancer, osteoporosis, and obesity. In addition, many people feel better in themselves. Regular physical
activity helps you to control your weight, and is also thought to help ease stress, anxiety, and depression.
How much physical activity should I take?
To gain health benefits you should do at least 30 minutes of moderate physical activity, on most days (at least
five days per week).
u 30 minutes per day is probably the minimum to gain health benefits. However, you do not have to do this all
at once. For example, cycling to work and back 15 minutes each way adds up to 30 minutes. Try to increase
the amount to 40-60 minutes per day if you can.
w For people who need to manage their weight and are at risk of putting on weight and becoming
obese, it should be for 45-60 minutes.
w For people who have been obese, or are still obese and have lost weight, it should be for 60-90
minutes.
w For older people, the above recommendations still apply, depending on ability.
w Children should get at least one hour a day of moderate physical activity.
u Moderate physical activity means that you get warm, mildly out of breath, and mildly sweaty. It does not have
to be intense. However, some evidence suggests that the more vigorous the physical activity, the better for
health - particularly for preventing heart disease.
u On most days. You cannot 'store up' the benefits of physical activity. You need to do it regularly.
What sort of physical activity?
Anything that makes your heart rate increase, and makes you at least mildly out of breath. For example: brisk
walking, jogging, swimming, cycling, dancing, badminton, tennis, etc. You can even use normal activities as part
of your physical activity routine. For example, fairly heavy housework, DIY, or gardening can make you mildly out
of breath and mildly sweaty. Consider a brisk walk to work or to the shops instead of using a car or bus, etc.
What are the health benefits of physical activity?
Heart disease and stroke
On average, the risk of developing heart disease such as angina or a heart attack is reduced by about a third in
people who are regularly physically active compared to those who are not. You are also less likely to have a
stroke. Physical activity is good for the heart muscle, but it also reduces some 'risk factors' for heart disease
and stroke. For example, on average, blood pressure, cholesterol, and body weight are lower in people who are
regularly physically active compared with those who are not.
If you already have heart disease, regular physical activity is usually advised as an important way to help prevent
the heart disease from getting worse.
Weight control
Physical activity helps to burn off excess fat. Regular physical activity combined with a healthy diet is the best
way of losing excess weight, and to maintain a healthy body weight.
Osteoporosis
Regular physical activity helps to prevent osteoporosis ('thinning of the bones'). The pulling and tugging on the
bones by the muscles stimulates bone-making cells which strengthens the bones. (The benefits of doing regular
physical activity include a reduced risk of: heart disease, stroke, bowel cancer, breast cancer, osteoporosis, and
obesity. In addition, many people feel better in themselves. Regular physical activity helps you to control your
weight, and is also thought to help ease stress, anxiety, and depression.)
136
Cancer
Regular physical activity roughly halves the chance of developing cancer of the colon (bowel cancer). There is
also evidence that breast cancer is less common in women who are regularly physically active.
Mental health
Physical activity is thought to help ease stress, and improve general well-being and self-esteem. Regular physical activity can also help to ease anxiety and depression. It can also help to make you sleep better. (But do the
activity during the daytime or early evening, not near to bed time.)
Older people
If you are over 70, you are less likely to fall and be injured if you are regularly physically active.
u Injury, sprains, and sometimes more serious injuries, are a risk if you do some types of activity such as
competitive sports. You can cut down the risk of injury by always warming up before any vigorous activity,
and by wearing the correct footwear.
u Endurance sports such as marathon running can cause stress fractures, fatigue, and cause menstrual
periods to stop in some women.
u Sudden death sometimes occurs in people who are doing some physical activity. This is rare if you are used
to moderate physical activity. It is more likely to occur if you do not usually do much physical activity, but then
do a sudden bout of vigorous activity such as an intense game of squash. However, even in this situation,
sudden death is uncommon.
If you gradually build up to do regular moderate physical activity, the potential health gains greatly outweigh the
small risks involved.
Some other points about physical activity
u If you have a condition that concerns you about physical activity, then see a doctor before starting a physical
activity programme. However, there are few reasons why physical activity may be harmful. A common wrong
belief is that physical activity may be "bad for the heart". On the contrary, physical activity is good for most
people with heart disease.
u If you are not used to physical activity, it is best to gradually build up the level of activity.
u One of the biggest obstacles is the uphill battle to become fit. Many people feel that the first few attempts at
physical activity are quite a struggle. Do not get disheartened. You are likely to find that each time it becomes
easier and more enjoyable.
u Try and keep physical activity high on your list of priorities. If one kind of activity becomes boring, try
switching to other types to maintain the health benefits.
u Some people set their goals too high. For example, aiming for a marathon run. This may take too much time,
you may lose enthusiasm, and physical activity may become a drudge. Beware of this pitfall.
u Physical activity is not just for young 'sporty' types. It is never too late to start to gain the benefits, no matter
how old or unfit you are.
The bottom line: realistically, walking is likely to be the activity chosen by many people. But, this is fine as brisk
walking is an excellent moderate physical activity. One report about physical activity stated: "The bottom line walking two miles a day can cut the risk of death by half".
Note: The British Heart Foundation and the Countryside Agency are running a 'Walking The Way
To Health' initiative to encourage people who do little physical activity to walk more in their own
neighbourhoods. For more information: Tel: 01242 533258 Website www.whi.org.uk
© EMIS and PIP 2005 Updated: July 2006 PRODIGY Validated8
See Page 089 in Appendix for Table of Physical Activity Intensity and Energy Expenditure
137
PART 2_SOP
Are there any risks with physical activity?
Smoking - A Summary
Stopping smoking can make a big difference to your health. See your practice nurse if you want to give up,
but are finding it difficult. This is a brief summary about smoking. If you prefer there are other more detailed
leaflets about smoking.
Why is smoking so bad?
Smoking is the greatest cause of early death in the UK. If you smoke, it is not just that you are likely to die earlier.
Smoking-related diseases such as lung cancer, heart disease, emphysema, and chronic bronchitis can cause
distressing symptoms, often for several years before death.
In addition, asthma, other lung diseases, Raynaud's phenomenon, and osteoporosis are often made worse by
smoking. Male smokers have an increased chance of becoming impotent in middle age (due to the damaging
effect of smoking on the blood vessels). Also, on average, children who live with smokers have more illnesses
than children who live in a smoke-free home.
Some tips which may help you to stop smoking
u Set a date for stopping, and stop completely. (Some people prefer the idea of cutting down gradually.
However, research has shown that if you smoke less cigarettes than usual, you are likely to smoke more of
each cigarette, and nicotine levels remain nearly the same. Therefore, it is usually best to stop once and for all
from a set date.)
u Tell everyone that you are stopping. Friends and family often give support and help.
u Get rid of ashtrays, lighters, and all cigarettes.
u Be prepared for some withdrawal symptoms. When you stop smoking, you are likely to get symptoms such
as: feeling sick, headaches, anxiety, being irritable, craving, and just feeling awful. These symptoms are
caused by the lack of nicotine that your body has been used to. They tend to peak after 12-24 hours,
and then gradually ease over 2-4 weeks.
u Be aware of situations in which you are most likely to want to smoke (for example, the pub). Try changing
your routine for the first few weeks.
u Take one day at a time. Mark off each successful day on a calendar. Look at it when you feel tempted to
smoke, and tell yourself you don't want to start all over again.
u Be positive. Tell people that you don't smoke. You will smell better. After a few weeks you should feel better,
taste your food more, and cough less. You will have more money.
u Food. Some people worry about gaining weight when they give up smoking as the appetite may improve. Be
prepared for an increase in appetite, and try not to increase fatty or sugary foods as snacks. Try sugar-free
gum and fruit instead.
u Don't despair if you fail and have a cigarette. You don't have to start smoking again. Examine the reasons
why you felt it was more difficult at that particular time, and try again. On average, people who eventually stop
smoking have made 3 or 4 previous attempts.
u Nicotine Replacement Therapy (NRT) can help if withdrawal symptoms are troublesome. You can get nicotine
gum, sprays, patches, tablets, lozenges, and inhalers. Using one of these roughly doubles your chance of
stopping smoking if you really want to stop. A pharmacist, GP, or practice nurse can advise.
u A medicine called bupropion (trade name 'Zyban') is another option. It also roughly doubles your chance of
stopping smoking if you really want to stop. It helps reduce the symptoms of nicotine withdrawal. It may be
prescribed by your GP.
Further help and information
Quit - a charity to help people stop smoking. Quitline: 0800 00 22 00 Web: www.quit.org.uk
NHS smoking helpline: 0800 169 0 169 and website www.givingupsmoking.co.uk
© EMIS and PIP 2005 Updated: August 2005 PRODIGY Validated9-11
138
Healthy Eating
A healthy diet helps to prevent, or reduce the severity of, diseases such as heart disease, stroke and diabetes. A healthy diet may also help to reduce the risk of developing some cancers. Also, a main way of combating obesity and overweight is to eat a healthy diet. This leaflet gives the principles of a healthy diet.
Eat plenty of starchy foods (complex carbohydrates)
Starchy foods such as bread, cereals, potatoes, rice, and pasta, together with fruit and vegetables, should provide the bulk of most meals. Some people wrongly think that starchy foods are 'fattening'. In fact, they contain
about half the calories than the same weight of fat. (However, it is easy to add fat to some starchy foods. For example, by adding butter to jacket potatoes or bread, or by adding oil to potatoes to make chips, etc.)
Also, starchy foods often contain a lot of fibre (roughage). When you eat starchy foods, you get a feeling of fullness (satiety) which helps to control appetite. Tips to increase starchy foods include:
Eat plenty of fruit and vegetables
Is is recommended that we eat at least five portions, and ideally 7-9 portions, of a variety of fruit or vegetables
each day. If you eat a lot of 'fruit and veg', then your chance of developing heart disease, a stroke, or bowel
cancer are reduced. In addition, 'fruit and veg':
u contain lots of fibre which help to keep your bowels healthy. Problems such as constipation are less
likely to develop.
u contain plenty of vitamins and minerals, which are needed to keep you healthy.
u are naturally low in fat.
u are filling but are low in calories.
One portion of fruit or vegetables is roughly equivalent to one of the following.
u One large fruit such as an apple, pear, banana, orange, or a large slice of melon or pineapple.
u Two smaller fruits such as plums, kiwis, satsumas, clementines, etc.
u One cup of small fruits such as grapes, strawberries, raspberries, cherries, etc.
u Two large tablespoons of fruit salad, stewed or canned fruit in natural juices.
u One tablespoon of dried fruit.
u One glass of fresh fruit juice (150ml).
u A normal portion of any vegetable (about two tablespoons).
u One dessert bowl of salad.
Some tips on how to increase fruit and vegetables in your diet include:
u Try some different types which you have not tried before. The variety of tastes and textures may be
surprising. Juices, frozen, canned, and dried varieties all count.
u Try adding chopped bananas, apples, or other fruits to breakfast cereals.
u Aim to include at least two different vegetables with most main meals. Do not over-boil vegetables.
Steaming, stir-frying, or lightly boiling are best to retain the nutrients.
u Always offer fruit or fruit juice to accompany meals.
u Try new recipes which include fruit. For example, some curries or stews include fruit such as dried apricots.
u Have fruit based puddings. Fruit with yoghurt is a common favourite.
u How about cherry tomatoes, carrot sticks, dried apricots, or other fruits as part of packed lunches? A
banana sandwich is another idea for lunch.
u Fruit is great for snacks. Encourage children to snack with fruit rather than with sweets.
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PART 2_SOP
u For most meals, include generous portions of rice, pasta, baked potatoes, or bread.
u For more fibre, choose wholemeal bread. When baking, use at least 1/3 wholemeal flour.
u If you have cereals for breakfast, choose porridge, high fibre cereals, or wholemeal cereals (without sugar coating).
u Have tea breads, and plain or fruit scones, instead of sugary cakes and biscuits.
Eat plenty of fibre (roughage)
Fibre is the part of food that is not digested. It is filling, but has few calories. It helps the bowels to move regularly, which reduces constipation and other bowel problems. Fibre may also help to lower your cholesterol level.
Starchy foods, and fruit and vegetables contain the most fibre. So the tips above on starchy foods and fruit and
vegetables will also increase fibre. Have plenty to drink when you eat a high fibre diet (at least 6-8 cups of fluid a
day).
Eat protein foods in moderation
Meat, fish, nuts, pulses, chicken, and similar foods are high in protein. You need a certain amount of protein to
keep healthy. However, most people eat more protein than is necessary. Beware, some meats are also high in
fat. Choose poultry such as chicken, or lean meat. Also, many meat based recipes include creamy or fatty
sauces which are high in calories.
Fish. There is some evidence that eating oily fish helps to protect against heart disease. Oily fish include: herring,
sardines, mackerel, salmon, fresh tuna (not tinned), kippers, pilchards, trout, whitebait, anchovies and swordfish.
It is probably the 'omega-3 fatty acids' in the fish oil that helps to reduce the build up of atheroma (furring of the
arteries) which causes angina and heart attacks. Aim to eat at least two portions of fish per week, one of which
should be oily.
Do not eat too much fat
A low-fat diet helps to reduce the chance of developing diseases such as heart disease and stroke. It will also
help you to reduce weight. The total amount of fat should be low. Also, the type of fat is important. You should
not have much saturated fat such as butter, lard, dripping, and unspecified margarine. Unsaturated fats are better such as corn oil, sunflower oil, olive oil, and low fat spreads. Tips to reduce fat in your diet include the following.
u Whenever possible, do not fry food. It is better to grill, bake, poach, barbecue, or boil food. If you do fry, use
unsaturated oil. Drain the oil off the food before eating.
u Choose lean cuts of meat, and cut off any excess fat.
u Avoid adding unnecessary fat to food. For example, use low fat spreads, spread less butter or margarine on
bread, measure out small portions of oil for cooking, etc.
u Watch out for hidden fats that are in pastries, chocolate, cakes, and biscuits.
u Have low-fat milk, cheeses, yoghurts, and other dairy foods rather than full-fat varieties.
u Avoid cream. Use low fat salad cream, or low-fat yoghurt as a cream substitute.
Do not have too many sugary foods and drinks
Sugary foods and drinks are high in calories, and too much may cause weight gain. It isn't just the amount of
sugar that may be bad. Eating small amounts of sugary foods (sweets etc) too often is bad for teeth. Tips include:
u
u
u
u
u
Try not to add sugar to tea, coffee, and breakfast cereals. Your taste for sweetness often changes with time.
Use artificial sweeteners only if necessary.
Reduce sugar in any kind of recipe. Use fruit as an alternative to add sweetness to recipes.
Try sugar-free drinks. Give children water as their main drink.
If you eat chocolate or sweets, try and keep the quantity down. Eating them as part of a meal, and then
brushing your teeth, is better than between meals as snacks.
140
Do not eat too much salt
Too much salt increases the risk of developing high blood pressure. Government guidelines recommend that we
should have no more than 5-6 grams of salt per day. (Most people in the UK currently have more than this.) If
you are used to a lot of salt, try to gradually reduce the amount that you have. Your taste for salt will eventually
change. Tips on how to reduce salt include:
u
u
u
u
Use herbs and spices to flavour food rather than salt.
Limit the amount of salt used in cooking, and do not add salt to food at the table.
Choose foods labelled 'no added salt'.
As much as possible, avoid processed foods, salt-rich sauces, take-aways, and packet soups
which are often high in salt.
Keep alcohol within the recommended limits
u Men should drink no more than 21 units of alcohol per week (and no more than four units in any
one day).
u Women should drink no more than 14 units of alcohol per week (and no more than three units in
any one day).
u Pregnant women - the amount that is safe is not known, so many women have little or no alcohol
when they are pregnant.
What is a unit of alcohol?
One unit of alcohol is 10 ml (1 cl) by volume, or 8 g by weight, of pure alcohol. For example:
u One unit of alcohol is about equal to:
w Half a pint of ordinary strength beer, lager, or cider (3 to 4% alcohol by volume), or
w A small pub measure (25 ml) of spirits (40% alcohol by volume), or
w A standard pub measure (50 ml) of fortified wine such as sherry or port (20% alcohol by volume).
u There are one and a half units of alcohol in:
w A small glass (125 ml) of ordinary strength wine (12% alcohol by volume), or
w A standard pub measure (35 ml) of spirits (40% alcohol by volume).
Further information
British Nutrition Foundation www.nutrition.org.uk
© EMIS and PIP 2005 Updated: July 2006 PRODIGY Validated12
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There is some evidence that drinking 1-2 units of alcohol per day may help to protect against heart disease. But,
drinking above the recommended limits can lead to serious problems. For example, drinking heavily can damage the liver, brain, stomach, pancreas, and heart. It can also cause high blood pressure. Also, alcohol contains
a lot of calories, and too much can cause weight gain.
Five Choices to Help You Stay Healthy
A healthy diet helps to prevent, or reduce the severity of, diseases such as heart disease, stroke and diabetes. A healthy diet may also help to reduce the risk of developing some cancers. Also, a main way of combating obesity and overweight is to eat a healthy diet. This leaflet gives the principles of a healthy diet.
What can I do to help stay healthy?
You should not smoke
If you smoke, stopping smoking is often the single most effective thing that you can do to reduce your risk of future illness. The risk to health falls rapidly as soon as you stop smoking (but takes a few years before the increased risk reduces completely). If you find it hard to stop smoking, then see your practice nurse for help.
Medication may be advised to help you to stop.
Do some regular physical activity
Anything that gets you mildly out of breath and a little sweaty is fine. For example: jogging, heavy gardening,
swimming, cycling, etc. A brisk walk each day is what many people do - and that is fine. However, it is thought
that the more vigorous the activity, the better. To gain most benefit you should do at least 30 minutes of physical
activity on most days. Two shorter bursts is thought to be just as good. For example, two 15 minute bouts of
activity at different times in a day.
Eat a healthy diet
Briefly, a healthy diet means:
u AT LEAST five portions, and ideally 7-9 portions, of a variety of fruit and vegetables per day.
u THE BULK OF MOST MEALS should be starch-based foods (such as cereals, wholegrain bread, potatoes,
rice, pasta), plus fruit and vegetables.
u NOT MUCH fatty food such as fatty meats, cheeses, full-cream milk, fried food, butter, etc. Use low fat,
mono-, or poly-unsaturated spreads.
u INCLUDE 2-3 portions of fish per week. At least one of which should be 'oily' (such as herring, mackerel,
sardines, kippers, pilchards, salmon, or fresh tuna).
u If you eat meat it is best to eat lean meat, or poultry such as chicken.
u If you do fry, choose a vegetable oil such as sunflower, rapeseed or olive oil.
u Try not to add salt to food, and limit foods which are salty.
Try to lose weight if you are overweight or obese
You don't need to get to a perfect weight. If you are overweight you can gain great health benefits by losing 510% of your weight. This is often about 5-10 kg. (10 kg is about one and a half stone.)
Don't drink too much alcohol
A small amount of alcohol is usually fine, but too much can be harmful. Men should drink no more than 21 units
per week (and no more than 4 units in any one day). Women should drink no more than 14 units per week (and
no more than 3 units in any one day). One unit is in about half a pint of normal strength beer, or two thirds of a
small glass of wine, or one small pub measure of spirits.
Do you want more detail?
See you practice nurse if you want further advice or help on any of the above. Also, there is a more detailed
leaflet for each of the topics listed above. There is also another leaflet called 'Preventing Cardiovascular Diseases' which is more detailed.
© EMIS and PIP 2006 Updated: July 2006 PRODIGY Validated13
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Cholesterol
You will usually be advised to take a statin drug to lower your cholesterol level if you have a high risk of developing a cardiovascular disease such as heart disease or stroke. As a rule, no matter what your cholesterol
level is, then lowering the level reduces your risk. UK guidelines recommend that all people aged 40 or more
should have a cholesterol blood test as part of a routine cardiovascular risk assessment.1-2
What is cholesterol?
Cholesterol is a lipid (fat chemical) that is made in the liver from fatty foods that we eat. A certain amount of cholesterol is present in the bloodstream. You need some cholesterol to keep healthy. Cholesterol is carried in the
blood as part of particles called lipoproteins. There are different types of lipoproteins, but the most relevant to
cholesterol are:
What are atheroma and cardiovascular diseases?
Patches of atheroma are like small fatty lumps that develop within the inside lining
of arteries (blood vessels). Atheroma is also known as 'atherosclerosis' and 'hardening of the arteries'. Patches of atheroma are often called 'plaques' of atheroma.
Over months or years, patches of atheroma can become larger and thicker. So, in
time, a patch of atheroma can make an artery narrower, which can reduce the
blood flow through the artery. For example, narrowing of the coronary (heart) arteries with atheroma is the cause of angina.
Sometimes a blood clot (thrombosis) forms over a patch of atheroma, and completely blocks the blood flow.
Depending on the artery affected, this can cause a heart attack, a stroke, or other serious problems.
Cardiovascular diseases are diseases of the heart (cardiac muscle) or blood vessels (vasculature). However, in
practice, when doctors use the term 'cardiovascular disease' they usually mean diseases of the heart or blood
vessels that are caused by atheroma.
In summary, cardiovascular diseases that can be caused by atheroma include: angina, heart attack, stroke, transient ischaemic attack (TIA), and peripheral vascular disease. In the UK, cardiovascular diseases are a major
cause of poor health and the biggest cause of death.
What factors affect the level of blood cholesterol?
In most people, your cholesterol level reflects the amount of fat that you eat. This is not the full story as different
people who eat the same amount of fat can make different amounts of cholesterol. However, in general, if you
eat less fat your cholesterol level is likely to go down.
In some people a high cholesterol level is due to another condition. For example, an underactive thyroid gland,
obesity, drinking a lot of alcohol, and some rare kidney and liver disorders can raise the cholesterol level.
In some people a very high level of cholesterol runs in the family due to an inherited genetic problem with the
way cholesterol is made. One example is called familial hypercholesterolaemia.
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Low density lipoproteins carrying cholesterol - LDL cholesterol. This is often referred to as 'bad cholesterol' as it
is the one mainly involved in forming atheroma. Atheroma is the main underlying cause of various cardiovascular
diseases (see below). Usually, about 70% of cholesterol in the blood is LDL cholesterol, but the % can vary from
person to person.
High density lipoproteins carrying cholesterol - HDL cholesterol. This is often referred to as 'good cholesterol' as
it may actually prevent atheroma formation.
Risk factors
Everybody has some risk of developing atheroma which then may cause one or more cardiovascular diseases.
However, certain 'risk factors' increase the risk. Risk factors include:
u Lifestyle risk factors that can be prevented or changed:
w Smoking.
w Lack of physical activity (a sedentary lifestyle).
w Obesity.
w An unhealthy diet.
w Excess alcohol.
u Treatable or partly treatable risk factors:
w Hypertension (high blood pressure).
w High cholesterol blood level.
w High triglyceride (fat) blood level.
w Diabetes.
w Kidney diseases that affect kidney function.
u Fixed risk factors - ones that you cannot alter:
w A strong family history. This means if you have a father or brother who developed heart disease or a
stroke before they were 55, or in a mother or sister before they were 65.
w Being male.
w An early menopause in women.
w Age. The older you become, the more likely you are to develop atheroma.
w Ethnic group. For example, people who live in the UK with ancestry from India, Pakistan, Bangladesh,
or Sri Lanka have an increased risk.
However, if you have a fixed risk factor, you may want to make extra effort to tackle any lifestyle risk factors that
can be changed.
Note: Some risk factors are more 'risky' than others. For example, smoking and a high cholesterol level cause a
greater risk to health than obesity. Also, risk factors interact. So, if you have two or more risk factors, your health
risk is much more increased than if you just have one. For example, a middle aged male smoker who has high
blood pressure and a high cholesterol level has a high risk of developing a cardiovascular disease such as a
heart attack before the age of 60.
What is a 'high' cholesterol level?
The following levels are generally regarded as desirable
u Total cholesterol (TC) - 5.0 mmol/l or less. However, about 2 in 3 adults in the UK have a total cholesterol
level of 5.0 mmol/l or above.
u Low-density lipoprotein (LDL) cholesterol after an overnight fast: 3.0 mmol/l or less.
u High-density lipoprotein (HDL) cholesterol: 1.2 mmol/l or more.
u TC/HDL ratio: 4.5 or less. That is, your total cholesterol divided by your HDL cholesterol. This reflects the fact
that for any given total cholesterol level, the more HDL, the better.
As a rule, the higher the cholesterol level, the greater the risk to health.
However, your level of cholesterol has to be viewed as part of your overall cardiovascular health risk. The cardiovascular health risk from any given level of cholesterol can vary, depending on the level of your HDL cholesterol,
and on other health risk factors that you may have.
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Employing Health Care Assistants in General Practice
There is a current drive to employ health care assistants (HCAs) within general practice; this is a new development for many practices.
This paper aims to guide practice nurses and their colleagues through the principles of implementing good employment practice, an effective training framework and making appropriate use of HCAs. If effective processes
and systems are in place the employment of HCAs in general practice should enhance patient care.
“The acquisition of a Vocational Qualification is not a permit to practice, but merely identifies the holder as competent to undertake a range of duties in a care environment. Decisions as to who should do what, remain with
the manager (registered nurse or other professional).” Storey (2002)
When HCAs are appropriately trained, assessed, supervised as required, supported and updated their contribution to patient care as a member of the team should ensure that both patients and the practice benefit.
There should be a formal arrangement for a health care professional to supervise the HCA on a regular basis.
Supervision, including observation should include time built into the workload.
Standards of care must not be compromised, and the patient must be made aware of the qualifications of the
staff member who is delivering their care or treatment.
HCAs must be an integral, valued member of the General Practice team and wider PCO organisations, which
have a culture of life-long learning and good employment practice, meeting the recommendations of Improving
Working Lives15.
It is recommended that all HCAs should undertake a nationally recognised qualification in care, such as National
Vocational Qualifications/Scottish Vocational Qualifications or equivalent. Any role development e.g. from receptionist to HCA must be undertaken within an approved framework of training, assessment, supervision and update. Any person who trains, assesses and updates HCAs must be competent in the skill, and be an accredited
trainer and assessor. Records must be kept of training undertaken, with dates and names/signatures of those
concerned.
All HCAs should be aware that they are accountable to the patient for any errors they may make, through civil
law, and to their employer, through their contract. The RN, or other professional, is however accountable for the
appropriate delegation of any task or duty. The HCA cannot be professionally accountable as they are currently
unregulated, apart from in social care settings.
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HCAs are trained in a particular role, but do not have a professional registration. They undertake simple clinical
procedures that have been taught and delegated, such as venepuncture, ECG recording, weighing, as well as a
range of support functions such as re stocking clinical areas.
They work at all times within defined protocols and procedures and should not be placed in a position where
they are required to make clinical judgements.
HCAs should always be directly accountable to a registered health care professional and should have regular
supervision and assessment of competence.
Careful consideration should be given to the education program for HCAs: in addition to clinical skills, their initial
preparation should include:
u Communication, including dealing with upset or aggressive patients
u Confidentiality
u Record keeping and IT systems
HCAS must not enter into consultations with patients unsupervised. They must be made aware of their limitations.
Accountability and the registered nurse
u You are personally accountable for ensuring that you promote the interests and dignity of each patient and
client and respond to their need for care.
u You remain accountable for the delegation of the work, for ensuring that the person who does the work is
able to do it. . .
u “. . .Such delegation must not compromise existing care but must be directed to meeting the needs and
serving the interests of patients and clients”.
(NMC Code of Professional Conduct, 2004)
GPs, practice managers and practice nurses planning to employ HCAs will need to either draw on the services
of an already approved local S/NVQ assessment centre. This is most likely to be the local Primary Health Care
organisation, or hospital. It is recommended that registered nurses within the practice undertake a VQ assessor
qualification.
Principles of Delegation
The Registered Nurse must ensure that:
u The primary motivation for delegation is to serve the interests of the patient
u Delegation is appropriate
u Always assess the needs of the patient – their needs should define ‘who does what’.
u The level of experience, competence, role of the person to whom the task is delegated is appropriate
u The level of supervision is appropriate
u They do not delegate to junior colleagues tasks and responsibilities beyond their level of skill and experience
u Appropriate assessment, planning, implementation and evaluation of the delegated role
u Communication related to the delegated role is in a manner understandable to the person to
whom the role is being delegated
u The level of supervision and feedback is appropriate to the task delegated
u Rigorous protocols clearly define the HCA’s role within a clinical activity.
u These protocols should be updated regularly.
u The registered practitioner should ensure their own competency in any delegated tasks
u The competency of the HCA to deliver specific delegated clinical activities must be assessed prior to
delegation and reviewed at regular intervals (6-12 monthly)
References15-18
146
Health Care Assistant Example Job Description
Title:
Health Care Assistant
Base:
Accountable to: The post holder will be employed by the partners of the Practice and as such will be account
able to them via the Practice Manager
Responsible to:
Hours of Duty:
Contract:
Job Purpose:
To provide an efficient auxiliary nursing service to the practice population, assisting the Nurses
and GP’s within the professional competencies of the post holder.
DUTIES AND RESPONSIBILITIES:
u 2. Correctly sterilise medical equipment to the required standard.
u 3. Correctly send patient samples to the laboratory on a daily basis.
u 4. Correctly monitor usage of sharps bins in all clinical rooms and replacing when required and preparing for
collection by clinical waste contractor.
u 5. Correctly restock all clinical rooms and ensure medical equipment inventory is maintained for each room.
u 6. Monitoring of stock levels of vaccines in all fridges and relaying stock requirements to Admin.
u 7. Correctly monitoring temperature of vaccine fridges and reporting readings beyond normal limits to
Practice Nurse Co-ordinator and Practice Manager.
u 8. Correctly carry out electro-cardio graphs (ECG’s) according to Practice protocols as required.
u 9. Correctly carry out blood pressure measurement according to Practice protocols as required.
u 10. Correctly carry out spirometry tests according to Practice protocols as required.
u 11. Take a positive and active role in audit, informing the Practice Nurse Co-ordinator of any problems.
u 12. Training and education - Attend both in-house and external training courses whenever required, to
develop skills.
u 13. Ensure the Minor Ops Room is kept clean and tidy between visits from cleaning staff, with the aim of
maximising efficiency at all times and minimising H&S incidents/accidents.
u 14. Open up premises at the start of day, when required.
u 15. Such other appropriate duties consistent with the nature and grading of the post which may be allocated,
as the situation dictates, by the Practice Manager or the Partners.
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u 1. Correctly perform phlebotomy clinics and home tests when required.
Reference List
1. National Collaborating Centre for Primary Care. Cardiovascular risk assessment: the modification of blood lipids for the primary and
secondary prevention of cardiovascular disease - full guideline DRAFT. 2007. http://guidance.nice.org.uk/download.aspx?o=414903
2. Scottish Intercollegiate Guidelines Network. Risk estimation and the prevention of cardiovascular disease: A national clinical guideline.
2007. http://www.sign.ac.uk/pdf/sign97.pdf
3. Despres JP, Lemieux I, Prud'homme D. Treatment of obesity: need to focus on high risk abdominally obese patients. BMJ.
2001;322:716-20.
4.
JBS 2: Joint British Societies' guidelines on prevention of cardiovascular disease in clinical practice. Heart 2005;91 Suppl 5:v1-52.
5. Williams B, Poulter NR, Brown MJ, Davis M, McInnes GT, Potter JF et al. British Hypertension Society guidelines for hypertension
management 2004 (BHS-IV): summary. BMJ 2004;328:634-40.
6. Lindstrom J,.Tuomilehto J. The diabetes risk score: a practical tool to predict type 2 diabetes risk. Diabetes Care 2003;26:725-31.
7. Prodigy Guidance. Cardiovascular risk assessment. http://www.cks.library.nhs.uk/Cardiovascular_risk/. 2007.
8. Prodigy Guidance. Physical activity. http://www.cks.library.nhs.uk/cardiovascular_risk/view_whole_guidance.
2007.
9. Prodigy Guidance. Smoking Cessation. http://www.cks.library.nhs.uk/smoking_cessation/in_depth. 2007.
10. National Institute for Clinical Excellence. Smoking Cessation: Brief interventions and referral for smoking cessation in primary care and
other settings. Public health intervention guidance. 2006. http://guidance.nice.org.uk/PHI1/
11. National Institute for Clinical Excellence. TA039 Smoking cessation - bupropion and nicotine replacement therapy: Guidance. 2002.
http://www.nice.org.uk/TA039
12. British Nutrition Foundation. Healthy Eating for Cardiovascular disease. 2007.
13. Prodigy Guidance. 5 Choices. http://www.cks.library.nhs.uk/Cardiovascular_risk/ 2006.
14. Prodigy Guidance. Lipid Management. http://www.cks.library.nhs.uk/lipids_management/view_whole_guidance. 2007.
15. Department of Health. Improving working lives. 2000.
http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_4010416
16. Nursing & Midwifery Council. The NMC code of professional conduct: standards for conduct, performance and ethics. 2004.
http://www.nmc-uk.org/aDisplayDocument.aspx?DocumentID=338
17. Storey L. The 'Crackerjack' model of nursing and its relationship to accountability. ISSN 1471-5953. Nurse Education in Practice
2007;2:133-41.
18. Working in Partnership Program. http://www.wipp.nhs.uk/178.php. 2007.
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Further copies of this document can be downloaded at:
www.screening.nhs.uk/vascular
Additional copies are available by contacting prolog on 0870 1555455
ref Vascular 03/2008