Genomics of Myocardial Infarction

Publisher Summary Coronary artery disease (CAD) and myocardial infarction (MI) are leading causes of death in the world. Although a number of risk factors contribute to the development of cardiovascular disease, a family history of CAD remains one of the most powerful independent predictors of risk. This suggests a significant genetic component to the disease. Several linkage studies suggest that the genes responsible for plaque rupture and thrombosis may differ from the genes responsible for atherosclerotic disease progression, which may account for the discrepancy. The catastrophic consequences of CAD are related to acute MI due to the rupture of vulnerable plaques and subsequent occlusive thrombosis. The molecular events that lead to plaque rupture and acute MI are influenced by a host of intricately related genetic factors involved in a variety of cellular processes such as inflammatory cascade, extracellular matrix regulation, apoptosis, and lipid metabolism. Advances in molecular biology provide an array of tools to elucidate the genetic factors underlying these diverse mechanisms. The recent discovery of a strong association of a region of chromosome 9p21 with MI has been replicated in four separate genome-wide association studies spanning multinational cohorts including thousands of cases and controls.