The development of coronary artery disease, and specifically myocardial infarction, involves hyperplasia of arterial smooth muscle, the development of fatty streaks, atheroma formation, plaque rupture, and ultimately thrombus formation and vessel occlusion.¹ These changes are in part genetically determined, as demonstrated by the fact that the risk of myocardial infarction in persons who have a first-degree relative with myocardial infarction is seven times the risk in persons who do not.²,³ This finding is often used to argue that coronary artery disease has a genetic basis, but the extent to which a shared environment contributes to the risk must also . . .