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Developments in heart failure
management and clinical practice
in the UK
Jamil Mayet
Department of Cardiology
St Mary’s Hospital
Problems in heart failure
management
• Accurate diagnosis
• Optimising drug therapy
• Identification of patients who will benefit
from revascularisation
Heart failure therapy - rule of halves
Treatment no CCF
CCF inadequate
therapy
CCF appropriate
therapy
Cardiac failure - diagnosis
Electrocardiogram
If ECG normal very unlikely to be systolic dysfunction
Echocardiography
• Confirms / refutes diagnosis of systolic
dysfunction
• Can exclude significant valvular disease
• Can suggest ischaemic aetiology if regional
wall motion abnormality
• Can assess diastolic dysfunction
Easy access to investigations
• GP education
– Every patient with possible cardiac failure should
be considered for echocardiography
• Open and rapid access to echocardiography
• Clear user-friendly reports
– “Mild MR; this is not clinically significant”
– “In the absence of clinical contra-indications…”
Optimising drug therapy
• ACE inhibitors
– High doses used in clinical trials
– If cough AII antagonists
– If contra-indications hydralazine/nitrates
• Beta blockers
• Spironolactone
ACE inhibitor doses used in large
controlled trials
•
•
•
•
CONSENSUS
V-HeFT II
SOLVD
SAVE
*twice daily
Enalapril
Enalapril
Enalapril
Captopril
20mg*
10mg*
10mg*
50mg**
**three times a day
• ATLAS study showed significant decrease in
mortality+hospital admissions in high dose
versus low dose lisinopril
Treatment – AII antagonists
• ELITE STUDY
• 722 patients 65 years with:
– CCF (NYHA class II-IV)
– LVEF  40%
• Captopril vs. losartan
• FU 1 year
• Mortality:
– 4.8% losartan
– 8.7% captopril (p=0.035)
• ELITE II
Evaluation of Losartan in the Elderly. Lancet 1997;349:747-52
Treatment – beta blockers
Beta-blockers for CCF
CIBIS-II: cardiac insufficiency bisoprolol study (II)
• >2500 patients
– EF  35% ; NYHA III-IV; 50% IHD
– ~ all on ACE I & diuretics; 50% on digoxin
• Bisoprolol vs. placebo
– Starting dose 1.25mg, gradually  to 10mg od over 4/52
• Study ended prematurely after 1.3 years:
– Annual mortality:
• 8.8% bisoprolol; 13.2% placebo; Hazards Ratio 0.66
• Risk reduction greatest in patients with IHD
Lancet 1999 Jan 02; 353:9-13
Treatment – beta blockers
Patients were largely in NYHA class II-III
Benefits are additive to those conferred by ACEI
Treatment – beta blockers
Treatment – spironolactone
• 1663 patients with:
–
–
–
–
Stable CCF NYHA III-IV
LVEF 35%
On ACE I and diuretics
Some also on digoxin
• Spironolactone (25-50mg od) vs. placebo
• Primary endpoint: death from any cause
• Study stopped prematurely:
– 30%  mortality in spironolactone group
• Significant improvement in functional class
Randomized Aldactone Evaluation Study. NEJM 1999;341:709-717
Diagnosing ischaemic heart
disease
• 75% of white males in SOLVD were related
to ischaemic heart disease
• 50% of patients in Framingham had an
ischaemic aetiology to their heart failure
• Identification of patients who will benefit
from revascularisation
Hibernating myocardium
• Chronic LV dysfunction does not
necessarily imply dead myocardium
• “Hibernating myocardium” termed by
Rahimtoola in 1989
• LV systolic function improved following
coronary revascularisation
Rahimtoola. Am Heart J 1989;117:211-21
Hibernating myocardium
Prediction of functional recovery
following revascularisation
Technique
Sensitivity
Specificity
Number of
Patients
Number of
Studies
Tc 99m MIBI
Scanning
83%
69%
207
10
Dobutamine
Stress Echo
84%
81%
448
16
Th 201 Stress
Redistribution
86%
47%
209
7
18F
88%
73%
327
12
90%
54%
145
8
PET
Th 201 Rest
Redistribution
Wijns et al. N Engl J Med 1998;339:173-81
Implications of viable
myocardium
•
•
•
•
•
87 patients with ischaemic CHF, LVEF<0.35
Low dose stress echo
40+/-17 months follow up
37 patients received revascularisation
22 cardiac related deaths
Senior et al. J Am Coll Cardiol 1999;33:1848-54
Implications of viable myocardium
MV - revascularised
MV – med Px
No MV – med Px
No MV - revascularised
Senior et al. J Am Coll Cardiol 1999;33:1848-54
Cardiac failure – services
available at St Mary’s
• Open access ECG / CXR / echocardiography
• Routine outpatients for specialist opinion and
invasive investigation
• Emergency assessment in A+E
• Specialist cardiac failure follow up clinic
• Specialist heart failure nurse
Specialist referral
• Confirm diagnosis
• Invasive assessment to diagnose underlying
ischaemic aetiology
• Addition of beta-blockers and/or
spironolactone
• Management of difficult / deteriorating
cases
Heart failure specialist nurse
• Monitoring weight and blood tests
• Educating patient and family
– Daily weighing
– Self management of diuretics
– Regular exercise
• Promoting long term compliance
• Implementing treatment protocols
Diastolic heart failure
• Up to a third of patients have clinical heart
failure with normal LV systolic function
• Underlying pathophysiology relates to
diastolic dysfunction
• Commonest underlying pathologies
– Normal ageing
– Hypertension
– Myocardial ischaemia
Mechanisms of diastolic
dysfunction
• Impaired ventricular relaxation
– Energy dependent process
– Susceptible to myocardial ischaemia
• Decreased myocardial compliance
– Altered compliance mediated by collagen
– Fibrosis related to activation of RAAS
Doppler patterns of diastolic
dysfunction
• Impaired relaxation
– Reduced E/A ratio
– Increased EDT
– Increased IVRT
• Restriction
–
–
–
–
LA pressure increases due to myocardial stiffness
High peak E wave velocity
Short EDT
Very short IVRT
Treatment of diastolic heart
failure
• Treat underlying cause eg ischaemia
• Impaired relaxation
– Theoretically rate-limiting agents effective
•
•
•
•
Beta-blockers, verapamil
Reduce HR and prolong diastole
Reduce myocardial oxygen demand
Lower BP and reduce LVH
Treatment of diastolic heart
failure
• Restriction
– Drugs which reduce fibrosis and lower LA
pressure theoretically should be effective
• ACEI
• AII blockers
• Diuretics
– If LA pressure lowered too much cardiac output
significantly worsened
• Can cause significant morbidity