DOI: 10.36347/sjams.2018.v06i09.009

Pages: 3269-3275

Acute Myocardial Infarction (AMI) is one of the most common causes of mortality in human beings. To the multifactorial risk factors of AMI, a small lipoprotein, Lp(a) has been included as an independent risk factor for premature atherosclerosis and AMI because of the prothrombotic and proatherogenic properties of the Lp(a). With the above view, this study aimed to find the association between Lp(a) and AMI, the diagnostic efficacy of Lp(a) in the confirmation of AMI and if the intensity of Lp(a) increase is related to the development of Atherosclerosis, the prime causative factor of the former disease. The biochemical determination of Lp(a) along with serum analysis of CPK-MB, Lipid profile, Blood Urea and sugar were undertaken altogether in 80 subjects of whom 40 were apparently normal subjects. 40 AMI patients without history of smoking, wherein AMI is proved by coronary angiography and who came 4-6 weeks after the attack for review to Cardiology OP has been selected for study population. There is no appreciable change in the level of any of the parameters with respect to sex. There is a highly significant increase in Serum Lp(a) level, Serum TGL, Total Cholesterol and LDL-C levels in AMI patients when compared to the controls. There is a positive correlation of Lp(a) with lipid fractions – TC, LDL-C, TGL. By analysing the sensitivity, specificity, positive predictive value and negative predictive value for various cut off values, 28 mg% was selected as the most approximate cut off level of Lp(a). Above 28 mg%, Lp(a) can speed up atherosclerosis resulting in AMI. Increase in Lp(a) is associated with AMI and the increase is due to inheritance of higher Lp(a) levels which should have existed even before the occurrence of the disease.