Ulcerated atheromatous plaque of the left main coronary artery in a patient with a recent extensive anterior myocardial infarction.

with a history of arterial hypertension and dyslipidaemia, was admitted to our department for a scheduled coronary angiographic examination. Two months before entry, the patient had been admitted to another hospital for an extensive anterior myocardial infarction, treated with intravenous thrombolysis. The coronary angiogram recorded one week after the acute infarction depicted an ulcerated atheromatous plaque in the left main coronary artery, along with subtotal occlusion of the left anterior descending artery in its proximal part, and non-significant stenoses in the (dominant) circumflex, one before the origin of the first obtuse marginal branch and another in its peripheral part. The right coronary artery was a small vessel without stenoses, while left ventriculography showed akinesis of the anterior wall of the left ventricle, with an apical aneurysm and severely impaired contractility (ejection fraction ~30%). A cardiac surgical evaluation, requested by the treating cardiologist, recommended conservative treatment, given that the residual lumen and the flow in the left main coronary artery were very satisfactory. During the postinfarction period the patient reported exertional dyspnoea and moderate fatigue, without, however, typical anginal discomfort. The echocardiographic examination revealed akinesis and thinning in the region supplied by the left anterior descending artery, while a dobutamine stress echo test showed no viability in that region, nor any evidence of ischaemia in the other myocardial territories, during infusion of maximal dobutamine dose. A coronary angiographic examination was then performed for re-evaluation of the atheromatous plaque in the left main coronary artery and again showed a crater-like formation in the middle part of the vessel, communicating with the lumen via a thin stem (Figures 1, 2). The dimensions and morphology of the structure did not differ from the previous angiogram, while its external boundary, on cine-angiography, was seen to be a continuation of the adventitia of the left anterior descending artery, a finding strongly suggestive of an ulcerated atheromatous plaque. The left anterior descending artery, in contrast to the initial study, was patent, with a stenosis of approximately 85%, while the findings in the remaining vessels were unchanged. From a comparative study of the two successive angiograms we speculated that rupture of the atheromatous plaque in the main coronary artery had contributed to the complete embolic occlusion of a critically stenotic left anterior descending artery, which on the second angiogram, as stated above, was patent although stenotic.