Aortic degenerative changes and thrombus formation: An unusual cause of massive myocardial infarction with normal coronary arteries

More than 90% of acute transmural myocardial infarctions are associated with thrombosis of atherosclerotic coronary arterial stenoses [1,2]. However, as reported by Cheitlin et al [3], there are less common causes of myocardial infarction that occur without coronary atherosclerosis or thrombosis. These include vasospasm, coronary arteritis, trauma, luminal compromise due to accumulation of material in the arterial wall secondary to inborn errors of metabolism, anomalous origin of the coronary arteries, hematologic disorders causing in situ thrombosis, myocardial oxygen demand-supply imbalance, and coronary artery emboli. Sources of coronary emboli include infective or non-bacterial thrombotic endocarditis originating on native or prosthetic valves, atria1 or ventricular mural thrombi, tumors such as cardiac myxomas or papillary fibroelastoma of the aortic valve, and dislodgement of thrombi or atherosclerotic plaques during coronary artery bypass surgery or cardiac catheterization. We report a previously unrecognized cause of coronary artery obstruction. Elastin fragmentation and cystic medial necrosis considered by some as part of the normal aging process [4] led to mild aortic root dilatation and stress-induced fracture of a fibrous atherosclerotic plaque with exposure of a thrombogenic surface and subsequent aortic mural thrombus formation. This thrombus then occluded the left main coronary artery ostium, with subsequent partial fragmentation and embolization into the coronary circulation. The process caused massive transmural myocardial infarction, cardiogenic shock, and death in a 49-yearold black woman who had normal coronary arteries documented angiographically.