Genetics of coronary artery disease

Abstract

Coronary artery disease (CAD) and its major complication myocardial infarction (MI) are the leading causes of death worldwide, which often occurs with the accumulation of atherosclerotic plaques in the walls of the coronary arteries. The heritability of CAD has been estimated between 40% and 60%, indicating genetic factor holds an equal or more important contribution to risk of CAD with the other traditional risk factors (i.e., lipid abnormalities, smoking, hypertension, diabetes, and obesity) [1]. In the genetics studies of CAD, the primary goal is to identify causative variants, genes or genetic loci that contribute to the risk of CAD. Given the fact that many risk factors are also strongly are modulated by genetic factors, Mendelian Randomization studies have been designed to estimate causative effects of risk factors on CAD, singlenucleotide polymorphisms (SNPs) servers as instruments [2]. Due to the clinical heterogeneity of CAD, the genetic architecture of CAD is not fully elucidated yet.