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Comparative Study of Lipid Profile in Chronic Smokers with and without Acute Myocardial Infarction


Affiliations
1 Dept. of Biochemistry, D. Y. Patil Medical College, Khollapur, Maharashtra, India
2 Dept. of Community Medicine S.N. Medical College, Bagalkot, Karnataka, India
3 Dept. of Biochemistry, S.N. Medical College, Bagalkot, Karnataka, India
4 Dept. of Biochemistry, SIMS Shimoga , Karnataka, India
5 Dept. of Biochemistry, M.R. Medical College, Gulbarga, Karnataka, India
     

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Background

Smoking is one of the major risk factors in the genesis of coronary atherosclerosis and development of coronary heart disease. Smoking may alter normal plasma lipoprotein levels.

Objective

The present study was undertaken to compare the lipid profile between chronic smokers (Group A) and chronic smokers with myocardial infarction (Group B).

Material and Methods

Fifty apparently healthy chronic smokers and 50 smokers with myocardial infarction were selected for the study. Fasting venous blood sample was collected in controls, in AMI patients sample was collected before any intervention, and total cholesterol (TC), triglycerides (TG), 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. Statistical analysis was done by Z test.

Results

The lipid profile was compared between Group A and Group B. There was a significant rise in TC, TG, LDL-C, VLDL-C and significant decrease in HDL-C in Group B as compared to Group A.

Conclusion

Cigarette smoking modulates the IHD risk through geneenvironment interaction and smoking increases the risk of atherosis. Further studies are required to ascertain the gene environment interaction .


Keywords

Chronic Smokers, Myocardial Infarction, Lipid Profile
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  • Ning L, Xudong J, Oliver Chen CY et al. Almond consumption reduces oxidative DNA damage and lipid peroxidation in male smokers. J. Nutr. 2007 137; 2717- 2722.
  • Pasupathi P, Sarvanan G, Farook J et al. Oxidative stress biomarkers and antioxidant status in cigarette smokers compared to non-smokers. J. Pharm.sci. & Res. 2009; 1(2): 55- 62.
  • Khaled AAS. Effect of exercise on cardiovascular dysfunction induced by cigarette smoking.Journal of stress physiology and biochemistry. 2008;4/2; 14-29.
  • Akbari M A, Bhatti M S, Shakoor M. Lipid profile in smoking. JAMC 2000;12 (3) : 19-21.
  • Buccolo G. and David H. Quantitative determination of serum triglycerides by the use of enzymes. Clinical Chemistry 1973;19:476-482.
  • Werner M, Gabrielson D G, Eastman J. Ultramicro Determination of Serum Triglycerides by Bioluminescent Assay. Clinical Chemistry 1981;27(2):268- 271.
  • Allen J K, Hensley W J, Nicholls A V et al. An Enzymic and Centrifugal Method for Estimating High-Density Lipoprotein Cholesterol. Clinical Chemistry 1979; 25(2):325- 327.
  • Lopes-Virella M F, Pamela S, Ellls S et al. Cholesterol Determination in High- Density Lipoproteins Seperated by Three Different Methods. Clinical Chemistry 1977;23(5):882- 884.
  • Miller N E, Forde O H, Thelle D S et al. High density lipoprotein and coronary heart disease - a prospective case-control study. Lancet 1977;1:965-968.
  • Friedwald W T, Levy R I, Fredrickson D S. Estimation of the Concentration of Low-Density Lipoprotein Cholesterol in Plasma Without Use of the Preparative Ultracentrifuge. Clinical Chemistry 1972;18:499-502
  • John A, Rajat SB. The pathophysiology of cigarette smoking and cardiovascular disease. JACC 2004 May 19; 43/10: 1731- 1737.
  • Cole J W, Brown D W,Giles W H et al. Ischaemic stroke risk, smoking, and the genetics of inflammation in a biracial population: The stroke prevention in young women study. Thrombosis Journal 2008;6(11):1-8.
  • Xing LW, rainwater DL, Vandeberg JF et al. Genetic contributions to plasma total antioxidant activity. Arterioscler Thromb Vasc Biol 2001; 21: 1190-1195

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  • Comparative Study of Lipid Profile in Chronic Smokers with and without Acute Myocardial Infarction

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Authors

Pampareddy B. Kollur
Dept. of Biochemistry, D. Y. Patil Medical College, Khollapur, Maharashtra, India
R. Manjula
Dept. of Community Medicine S.N. Medical College, Bagalkot, Karnataka, India
Sangappa V. Kashinakunti
Dept. of Biochemistry, S.N. Medical College, Bagalkot, Karnataka, India
Gurupadappa S. Kallaganada
Dept. of Biochemistry, SIMS Shimoga , Karnataka, India
Jagadish B. Ingin
Dept. of Biochemistry, M.R. Medical College, Gulbarga, Karnataka, India

Abstract


Background

Smoking is one of the major risk factors in the genesis of coronary atherosclerosis and development of coronary heart disease. Smoking may alter normal plasma lipoprotein levels.

Objective

The present study was undertaken to compare the lipid profile between chronic smokers (Group A) and chronic smokers with myocardial infarction (Group B).

Material and Methods

Fifty apparently healthy chronic smokers and 50 smokers with myocardial infarction were selected for the study. Fasting venous blood sample was collected in controls, in AMI patients sample was collected before any intervention, and total cholesterol (TC), triglycerides (TG), 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. Statistical analysis was done by Z test.

Results

The lipid profile was compared between Group A and Group B. There was a significant rise in TC, TG, LDL-C, VLDL-C and significant decrease in HDL-C in Group B as compared to Group A.

Conclusion

Cigarette smoking modulates the IHD risk through geneenvironment interaction and smoking increases the risk of atherosis. Further studies are required to ascertain the gene environment interaction .


Keywords


Chronic Smokers, Myocardial Infarction, Lipid Profile

References