Effect of cigarette smoking on myocardial workload in young adults DR. SUNIL KUMAR JENA Senior Resident VIMSAR

Background Cigarette smoking is an established risk factor of coronary artery disease. Different researchers reported that cigarette smoking affects myocardial workload. Very few studies evaluate the effect of very low intensity of smoking on heart. Thus I proposed this study to evaluate the effect of very low intensity of smoking on myocardial workload in young adults.

AIM & OBJECTIVE 1 To assess smoking status of young adults 2 To observe the effect of cigarette smoking on HR, SBP and RPP 3 To quantify the association between cigarette smoking and risk of heart disease

Material and Method Study Place – Department of Physiology ,VIMSAR Study Period – Jan 2016 – Dec 2016 Type of study – Comparative Subjects – 108 (MBBS Students) 1.Case 60 (smoker) 2.Control 48 (nonsmoker)

Material and method Case (n=60) - Apparently healthy male medical students, current smokers, minimum 1 year H/O smoking Control (n=48) - Apparently healthy male medical students, never smoke any cigarette or consume any nicotine product Exclusion criteria – Occasional smokers, Cardiovascular disease, Endocrinal disorder, Renal disease, Neural disease, F/H of DM Information sheet Name- Age- Are you a smoker ? – yes/no Duration of smoking- No of cigarettes smoke per day H/O any systemic disease F/H of disease -

Material and method PY = No of Cigarettes smoke per day × No of years of smoking / 20 (Bernaards CM et al. Addiction 2001;96:1653-61.) Measurement of HR – Carotid pulsation Avg HR= BP – Sphygmomanometry HR and BP was recorded after 10 min of rest RPP = HR × SBP×10-2 (White WB. Am J Hypertens 1999;12:S50-5) HR1+HR2+HR3 --------------------- 3

Statistical analysis SPSS 16 Unpaired T test P< 0.05 Odd’s Ratio

result Variables Minimum Maximum Mean±SD Duration of smoking in year 1 13 3.6±2.94 No of cigarettes smoke per day 2 12 3.8±2.1 Pack Year 0.1 3.3 0.679±0.670

RESULT Variables Case (n=60) (Mean±SD) Control (n=48) p HR 84±9.1 75±8.7 <0.0001 SBP 133±10.5 117±7.5

result Variable Case (n=60) (Mean±SD) Control (n=48) p RPP 113.9±1.94 88.6±1.19 < 0.0001

Result Variables Risk of Heart Disease (RPP>100) No Risk of Heart Disease (RPP≤100) Odd’s Ratio p Case (n=60) 44 16 19.25 < 0.0001 Control (n=48) 6 42

DISCUSSION To avoid gender and age variation of different hemodynamic variables subjects were selected from single gender i.e. male and within a narrow range of age group i.e. between 19 to 24 years. Increase in HR, SBP and RPP in smoker than nonsmoker may be due to sympathovagal imbalance.

Decrease Cardiac vagal tone DISCUSSION Neuropeptide Y Decrease Cardiac vagal tone Nicotine Impaired baroreceptor sensitivity Increase sympathetic discharge

DISCUSSION HR, SBP and RPP are valuable markers of MVO2. There is linear relationship between these markers and MVO2. Increase in MVO2 signifies increase in myocardial workload. This study suggested that in smokers MVO2 is high, hence very low intensity smoking increases myocardial workload.

LIMITATIONS Mismatch of BMI of the subjects. Did not exclude the sleep habit and stress level of students. HR was calculated by carotid pulsation, not by ECG.

CONCLUSION Summarizing this study it is concluded that very low intensity of cigarette smoking also increases myocardial workload, hence risk of heart disease.

MESSAGE TO SOCIETY Prevention is better than cure. Therefore young adults should be counseled and motivated to avoid cigarette smoking for fit and healthy life.

ACKNOWLEDGEMENT I am very much thankful to Dr. Palas Kumar Majhisamanta, intern VIMSAR for substantial contribution towards this study. Also thankful to subjects, without whom accomplishment of this study was not possible.

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