In addition to lifestyle and environmental factors, genes are important in the aetiology of CAD38. For early myocardial infarction, estimates of λs range from ~2 to ~7 (ref. 39). Genetic variation is thought likely to influence risk of CAD both directly and through effects on known CAD risk factors including hypertension, diabetes and hypercholesterolaemia. Genome-wide linkage studies have mapped several loci that may affect susceptibility to CAD/myocardial infarction40 although for only two of these has the likely gene been identified (ALOX5AP (arachidonate 5-lipoxygenase-activating protein) and LTA4H (leukotriene A4 hydrolase))41,42. Association studies have identified several plausible genetic variants affecting lipids, thrombosis, inflammation or vascular biology but for most the evidence is not yet conclusive40. We did not find evidence for strong association at any of these genes within our study (Table 2 and Supplementary Table 10).
