Download including sampling procedure if any

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA, BANGALORE
ANNEXURE II
PROFORMA FOR REGISTRATION OF SUBJECTS FOR DISSERTATION
1.
Name
of
the
Candidate
and Dr. ANISHA
Address (in block letters)
POST GRADUATE STUDENT,
DEPARTMENT OF PHYSIOLOGY,
J.J.M. MEDICAL COLLEGE,
DAVANGERE-577004.
2.
Name of the Institution
J.J.M. MEDICAL COLLEGE,
DAVANGERE-577004,
KARNATAKA.
3.
Course of Study & Subject
M.D. PHYSIOLOGY
4.
Date of Admission to Course
15-05-2012
5.
Title of the topic
“STUDY OF HEART RATE VARIABILITY
AND ECG CHANGES IN SMOKERS,
ALCOHOLICS AND NORMAL”
6.
Brief resume of the intended work:
6.1 Need for the study:
The autonomic nervous system plays an important role not only in
physiological situations, but also in various pathological settings. Autonomic imbalance
associating increased sympathetic activity and reduced vagal tone has been strongly
implicated in the pathophysiology of arrhythmogenesis and sudden cardiac death.
Among the different available noninvasive techniques for assessing the
autonomic status, heart rate variability has emerged as a simple, noninvasive method to
evaluate the sympathovagal balance at the sinoatrial level.1
The Electrocardiogram is a graphic recording of electric potentials generated
by the heart. It is a simple and non-invasive, inexpensive, and highly versatile test helps
in assessing the cardiovascular status.2
Alcohol consumption causes ECG changes which include cardiac conduction
abnormalities, prolongation of the QT interval, prolongation of ventricular
repolarisation and sympathetic stimulation.3
Cigarette smoking is a well established risk factor for ischemic stroke, and
myocardial infarction.4 Cigarette smoking increased the risk of acute cardiac events and
increased sympathetic activity. Impaired autonomic nervous activity is recognized as a
considerable symptom of cardiac dysfunction and is strongly associated with increased
risk overall mortality.5
Therefore this study is undertaken to detect the ECG changes and heart rate
variability in smokers and alcoholics and thereby assessing the cardiovascular status.
6.2 Review of literature :
In a community based study showed, smoking is the risk factor for the
development of major abnormal Q/QS wave patterns, T wave abnormalities and
development of ST segment depression.6
Eight percent smoker showed changes of P Pulmonale on their ECG. This
might be due to development of corpulmonale subsequently producing right atrial
hypertrophy as a result of chronic smoking.7
Longitudinal results indicated that R, S and T wave amplitude decreased at
greater rates in smokers than in nonsmokers. It is also associated with prolonged QTc
(correct QT interval) in healthy smokers.8
Moderate dose of alcohol intake is associated with an increase in maximum
and the minimum P-wave duration which have been reported to represent an increased
risk for atrial fibrillation in patients with no underlying disease.9
Ryan and Howes10 in their study showed alcohol consumption is associated
with reduced vagal activity, may be mainly due to a positive association between
alcohol intake and heart rate in the age group of 33–68yrs.
Lorsheyd A et al11 showed that prolongation of the PR interval and QRS
complex after acute ingestion of alcohol.
It showed that, in subject with moderately elevated to high serum osmalilty, p
wave and QTc intervals were prolonged compared with sober subjects. P wave, PR,
QRS and QTc intervals were longer when the subjects had high blood ethanol levels.
Ethanol at high to very high blood concentration caused several changes in ECG that
might be associated with increased risk of arrhythmias.12
A study was conducted by Trejbal K, Mitro, showed that patients with acute
alcohol intoxication presented with pathological ECG changes, most frequent and
prognostically significant in chronic alcoholics in patients with ischemic heart disease.
ECG picture showed that there is significant extension in intervals with possible
manifestation of latent conduction disturbance. Apart from heart rate disturbances it
often shows non-specific repolarisation.13
The mean R-R interval, the standard deviation of R-R interval, and the root
mean square of successive R-R interval differences significantly decreased within the
first 5-minute period compared with baseline, and then the standard deviation of R-R
interval increased within the 20- to 30-minute period. The LF/HF ratio significantly
decreased within the first 5 minutes after smoking and then remained unchanged
throughout the study period. Similarly, low-frequency and high-frequency power
increased within the first 5 minutes compared with baseline. Acute cigarette smoking
alters HRV parameters, particularly within the first 5 to 10 min after smoking.14
While LF and LF/HF ratio were significantly higher, standard deviation of all
NN intervals (SDNN), standard deviation of the 5-minute mean RR intervals (SDANN),
root mean square of successive differences (RMSSD), and high-frequency (HF) values
were significantly lower in heavy smokers.15
Baseline SDNN and RMSSD values were found to be lower in smokers than
in non smokers. Baseline LF/HF ratio was also found to be higher in smokers than in
non smokers. The other HRV parameters including R-R interval, LF, and HF were not
significantly different. During CR, expected increase in RR, SDNN, and RMSSD did
not occur in smokers, while it did occur in non smokers. In addition, the duration of
smoking was found to be inversely correlated with RMSSD and HF and positively
correlated with LF/HF ratio.16
Smoking impairs sympathovagal balance and decreases the heart rate
variability in healthy subjects. And even a one cigarette smoking leads to overt
sympathetic excitation.5
With respect to time-domain analysis, one drink of ethanol or red wine did not
alter RMSSD, STD (in ms), or STD (in min ) from their respective baseline values but
compared with the response to one glass of water, STD (in ms), RMSSD, and pNN50 all
decreased significantly. Two glasses of either alcoholic drink caused significant
suppression of all time domain parameters except STD. RMSSD, for example,
decreased by 28% after ethanol and by 33% after wine.17
Wine intake was associated with increased HRV in both time and frequency
domains independently of other clinical covariates (for example, in SDNNI was 3.89
among wine drinkers v 3.59 among wine non-drinkers in the multivariate model;
(p =0.014). In contrast, consumption of beer and spirits and the total amount of alcohol
consumed did not relate significantly to any of the HRV parameters.18
This study showed that in healthy young subjects the ingestion of 60 g of
ethanol increases heart rate and reduces HRV. These findings suggest that alcohol
acutely promotes vagal withdrawal and increases sympathetic activity that persists for at
least 10 h after ingestion.19
6.3. Objectives of the study:
1. To study the heart rate variability changes in smokers, alcoholics and normal.
2. To study the ECG changes in smokers, alcoholics and normal.
3. To compare the same with that in normal subjects.
7.
Materials and methods:
7.1 Source of data:
The present study will be done in a period of 2 years in the Dept of
Physiology, JJM Medical College, Davangere.
In this study a total of 50 smokers, 50 alcoholics and 50 non-smokers and
non-alcoholics of age matched controls from general population of Davangere satisfying
the inclusion criteria will be included.
Inclusion criteria:
 Smokers of age group 20-50 years are selected as per World Health Organization
(WHO) 10th revision of International Statistical Classification of Diseases and
related health problems (ICD-10) criteria of harmful use.20
 Alcoholic men of age group 20-50 years, confirming to DSM-IV Criteria of
substance use of American Psychiatric Association are randomly selected from
the general population.21

Non-smokers and non-alcoholics of age matched subjects as control group.
 Males are included.
Exclusion criteria:
 Subjects below 20 years and above 50 years.
 Both smokers and alcoholics.
 Medical H/O any diseases known to affect the autonomic cardiac function such
as cardiovascular, neurological or endocrine diseases.
 Renal, Hepatic and thyroid disease.
 Obese, Diabetics and hypertensive’s.
 Patients on medications.
 Females.
7.2 Method of collection of data (including sampling procedure if any):
50 smokers and 50 alcoholics and 50 non-smokers and non-alcoholics of age
matched controls, satisfying inclusion criteria will be included in the study. The subjects
will be randomly selected from general population of Davangere.
The detailed history, examination will be taken. Procedure of this study will
be explained in detail to the subjects after taking valid consent from the subjects.
Height and weight of the subjects will be recorded and BMI calculated as
Weight (kg)/height2 (m) Quetelet’s index.
Following tests will be performed 2-3 hours after light breakfast in sequence
after familiarising the subjects with the testing procedures.
1. Resting BP using sphygmomanometer.
2. 12 lead ECG obtained at the supine position at rest.
3. Resting heart rate and Heart rate variability in supine position will be measured
using Niviqure computerised ECG system.
The data collected is analysed and the results obtained will be compared
between study and control groups.
Statistical analysis :
Results will be subjected for appropriate statistical analysis.
One way ANOVA will be used for multiple group comparisons and Student’s
unpaired t-test will be used to compare different parameters between study and control
groups.
7.3. Does the study require any investigations or interventions to be conducted on
patients or other humans or animals? If so, please
describe briefly
- Yes
Non invasive investigations –height, weight, heart rate, blood pressure, ECG, and heart
rate variability.
7.4 Has ethical clearance been obtained from your institution in case of 7.3?
-Yes
8.
List of References:
1. Sztajzel J. Heart rate variability: a non-invasive electrocardiographic method to
measure the autonomic nervous system. Swiss Med wkly 2004; 134: 514-22.
2. Goldberger AL. Electrocardiography. In: Braunwald E, Fauci AS, Kasper DL,
Hauser SL, Longo DL, Jameson JL, Editors. Harrison’s Principles of Internal
Medicine.
Chapter
210.
16th
ed.
Newyork:
Mc
Graw
Hill
Co
2004: vol 1, pp. 1311-1319.
3. Rossinen J, Sinisalo J, Partanen J, Nieminen MS, Viitasalo M. Effects of acute
alcohol infusion on duration and dispersion of QT interval in male patients with
coronary artery disease and in healthy controls. Clin Cardiol 1999; 22:591-594.
4. Feigin VL, Rinkel GJE, Lawes CMM, Algra A, Bennett DA, Gijn JV et al. Risk
factors for subarachnoid hemorrhage: An updated systematic review of
epidemiological studies. Stroke 2005; 36: 2773–2780
5. Alyan O, Kacmaz F, Ozdemir O. Effects of cigarette smoking on heart rate
variability and plasma N-terminal pro-B-type natriuretic peptide in healthy
subjects: is there the relationship between both markers? Annals of Noninvasive
Electrocardiology 2008;13(2):137-44.
6. Moller CS, Byberg L, Sundstrom J, and Lind L. T wave abnormalities; high body
mass index, current smoking and high lipoprotein (a) levels predict the
development of major abnormal Q/QS patterns 20 years later. A populationbased study BMC Cardiovasc Disord 2006;6 :10-22.
7. Sharma SB, Dwivedi S, Parabhu K.M, Singh G, Kumar N & Lal M et al.
Coronary risk variable in young asymptomatic smokers. Indian J Med Res
2005;122: 205-210.
8. Singh K. Effect of smoking on QT interval, QT Dispersion and rate pressure
product. Indian Heart J 2004;56: 140-142.
9. Uyarel H, Ozdo¨l C, Karabulut A, Okmen E, Cam N. Acute alcohol intake and Pwave dispersion in healthy men – Original Investigation Anadolu Kardiyol Derg
2005;5:289-93.
10. Ryan JM and Howes LG. Relations between alcohol consumption, heart rate, and
heart rate variability in men. Heart 2002;88(6):641-642.
11. Lorsheyd A, De Lange DW, Hijmering ML, Cramer MJM, Van de Wiel A. PR
and QTC interval prolongation on the electrocardiogram after binge drinking in
healthy individuals. Neth J Med 2005;63(2):59-63.
12. Aasebo W, Erikssen J, Jonsbu J and Stavem K. ECG changes in patients with
acute
ethanol
intoxication
Scandinavian
cardiovascular
journal
2007;41( 2):79-84.
13. Trejbal K, Mitro P. ECG changes in alcoholic intoxication Vnitrni lekarstvi
2008; 54(4):330-331.
14. Karakaya O, Barutcu I, Kaya D, Esen AM, Saglam M, Melek M et al. Acute
effects
of
cigarette
smoking
on
Heart
Rate
Variability.
Angiology
2007;58(5): 620-624.
15. Cagira G, Cay S, Karakurt O. Influence of heavy cigarette smoking on heart rate
variability and heart rate turbulence parameters. Ann Noninvasive Electrocardiol
2009;14(4):327-32.
16. Barutcu I, Esen AM, Kaya D, Turkmen M, Karakaya O, Melek M et al. Cigarette
smoking and heart hate variability: dynamic influence of parasympathetic and
sympathetic maneuvers. Ann Noninvasive Electrocardiol 2005;10(3):324-9.
17. Spaak J, Tomlinson G, McGowan CL, Soleas GJ, Morris BL et al. Dose-related
effects of red wine and alcohol on heart rate variability; Am J Physiol Heart Circ
Physiol 2010; 298(6):2226-31.
18. Janszky, M Ericson, M Blom; Wine drinking is associated with increased heart
rate variability in women with coronary heart disease. Heart 2005; 91:314-318.
19. Bau PFD, Moraes RS, Claiton H.D. Acute ingestion of alcohol and cardiac
autonomic modulation in healthy volunteers. Alcohol 2011;45:123-29.
20. Diagnostic criteria for research. ICD-10 Classification of mental and behavioural
disorders WHO Geneva 1993: 75.
21. Jorome HJ. Substance related disorders In: Sadock BJ, Sadock VA, editors
Kaplan and Sadock’s Comprehensive Textbook of Psychiatry 7th ed.
Philadelphia: Lippincott Williams and Wilkins Company 1999, Vol2, pp. 928-32.
9.
Signature of the candidate
10. Remarks of the guide
This study helps to assess the cardiovascular function
and to detect the risk factors as early as possible and
hence to reduce morbidity and mortality among smokers
and alcoholics.
11. Name & Designation of
(in block letters)
11.1 Guide
Dr. S. CHANDRASEKHARAPPA
PROFESSOR,
DEPARTMENT OF PHYSIOLOGY,
J.J.M. MEDICAL COLLEGE,
DAVANGERE-577004.
11.2 Signature
11.3 Co-Guide (If any)
11.4 Signature
11.5 Head of Department
Dr. S. V. BRID M.D.
PROFESSOR AND HEAD,
DEPARTMENT OF PHYSIOLOGY,
J.J.M. MEDICAL COLLEGE,
DAVANGERE- 577004.
11.6 Signature
12. 12.1 Remarks of the
Chairman and Principal
12.2 Signature
M.Sc., Ph.D.