Myocardial infarction (MI) is a complex phenotype caused by interactio
n of a number of genetic and environmental factors. A genetic suscepti
bility to MI was observed in a familial aggregation and studies in twi
ns. Advances in molecular genetics have led to identification of a num
ber of potential genetic risk factors for MI, such as variants of gene
s involved in vascular homeostasis, thrombosis, and lipid metabolism.
Functional variants of angiotensin-1-converting enzyme (ACE), beta-fib
rinogen, plasminogen activator inhibitor-1, methylenetetrahydrofolate
reductase, glycoprotein IIIa, and many apolipoprotein genes are consid
ered excellent candidate risk factors for MI. Interaction of the susce
ptibility genes with modifier genes, environmental factors, and conven
tional risk factors results in the final phenotype of MI. Understandin
g the complex interaction between these factors is expected to provide
significant insights into the pathogenesis of MI and lead to developm
ent of genetic-based risk stratification, prevention, and treatment.