This study was proposed to study the effects of cigarette smoking and myocardial Infarction on platelet size. A total of 298 adults (18 years above) patients with clinically suspected acute coronary syndrome who attended in cardiac emergency and admitted in coronary care unit in the department of Cardiology, King George’s Medical University, India were enrolled in this study. Among them 248 patients had ECG changes (ST-elevation, ST- depression, T-inversion, appearance of Q-wave) with or without elevated troponin I and treated with anti-plate- let drugs. They were considered as cases (group I). The rest 50 Patients had normal ECG findings, normal cardiac troponin I and did not receive anti-platelet therapy. They were considered as controls (group II). Clinical history, medical reports, findings and information were documented in a pre-designed data sheet with informed and written consent. Blood samples for mean platelet volume (MPV) were obtained in the catheterization laboratory before coronary angiography and determined by auto- mated analyzer. The mean age of controls was 40.9±17.9 and that in cases was 59.2±11.9. Among them 72.2% were smokers in cases groups while 60% were nonsmokers in control group. The mean platelet in case group was 301.01±177.1 and in control group 304.7±132.5. While the mean MPV in case group was 8.5.0±1.2 fl and in control group 7.8±0.4 fl (p 0.05). It was observed that at all these groups higher mean was observed in smoker in cases groups than other groups i.e. 307.6±192.72. In MPV; statistically significant difference was observed between smoking status (smoker or nonsmoker for both groups cases and controls) (p value < 0.05). It was observed that at all these groups higher mean was observed in smoker in cases groups than other groups i.e. 8.58±1.41. These results suggest that smoking may increase platelet consumption in atherosclerotic vessels and that subsequently megakaryocytes are activated to produce larger platelets, which are more active. Thus, an increase in MPV due to smoking may also contribute to the acceleration of atherosclerosis and should be considered as a risk factor for atherosclerotic disease
