Genetic risk factors for myocardial infarction

Myocardial infarction (MI) is a complex phenotype caused by interaction of a number of genetic and environmental factors. A genetic susceptibility to MI was observed in a familial aggregation and studies in twins. Advances in molecular genetics have led to identification of a number of potential genetic risk factors for MI, such as variants of genes involved in vascular homeostasis, thrombosis, and lipid metabolism. Functional variants of angiotensin-1-converting enzyme (ACE), beta-fibrinogen, plasminogen activator inhibitor-1, methylenetetrahydrofolate reductase, glycoprotein IIIa, and many apolipoprotein genes are considered excellent candidate risk factors for MI. Interaction of the susceptibility genes with modifier genes, environmental factors, and conventional risk factors results in the final phenotype of MI. Understanding the complex interaction between these factors is expected to provide significant insights into the pathogenesis of MI and lead to development of genetic-based risk stratification, prevention, and treatment.