Title of article :
Comparative study of lipid profile in non-smokers, chronic smokers, and chronic smokers with acute myocardial infarction in men
Author/Authors :
Kollur، Pampareddy B نويسنده Assistant Professor, Department of Biochemistry, D. Y. , , Biradar، Satish B نويسنده Assistant Professor, Department of General medicine, S. , , Kashinakunti، Sangappa V نويسنده Associate Professor, Department of Biochemistry, S. , , Kallaganada، Gurupadappa S نويسنده Professor and HOD, Department of Biochemistry, Shimoga Institute Medical Sciences Shimoga , , Manjula R، Manjula R نويسنده Assistant Professor, Department of Community Medicine S. , , Ingin، Jagadish B نويسنده Professor and HOD, Department of Biochemistry ,
Abstract :
Abstract:
Introduction: Smoking is a major risk factor in the genesis of coronary atherosclerosis and development of
coronary heart disease. Smoking may alter normal plasma lipoprotein levels. The present study was undertaken to
compare the lipid profile between non- smokers (Group A) and chronic smokers (Group B) and also between
chronic smokers (Group B) and chronic smokers with acute myocardial infarction (AMI) (Group C).
Methods: Thirty six apparently healthy non- smokers, 36 apparently healthy chronic smokers and 36 chronic
smokers with AMI were selected for the study. Fasting venous blood samples were collected; triglycerides (TG),
total cholesterol (TC) and high density lipoprotein cholesterol (HDL-C) were measured. Low-density lipoprotein
cholesterol (LDL-C) and very low-density lipoprotein cholesterol (VLDL-C) were calculated by Friedwald’s
formula.
Results: The lipid profile was compared between Group A and Group B and also between Group B and Group C.
There was a significant rise in TG, TC, LDL-C, VLDL-C and significant decrease in HDL-C in Group B compared
to Group A. There was a significant rise in TG, TC, LDL-C, VLDL-C and significant decrease in HDL-C in Group
C compared to Group B.
Conclusion: Smoking increases the risk of atherosis and smoking modulates the ischemic heart disease risk through
gene-environment interaction. Further studies are required to ascertain the gene environment interaction.