A 60-year-old man has had angina on exertion for the past 6 years. A coronary angiogram performed 2 years ago showed 75% stenosis of the left circumflex coronary artery and 50% stenosis of the right coronary artery. For the past 3 weeks, the frequency and severity of his anginal attacks have increased, and pain sometimes occurs even when he is lying in bed. On physical examination, his blood pressure is 110/80 mm Hg, and pulse is 85/min with irregular beats. An ECG shows ST-segment elevation. Laboratory studies show serum glucose, 188 mg/dL; creatinine, 1.2 mg/dL; and troponin I, 1.5 ng/mL. Which of the following is most likely to explain these findings?

Marked coronary artery occlusion with this degree of stenosis prevents adequate perfusion of the heart when myocardial demand is increased during exertion. He has angina on exertion and recently developed unstable angina, which is manifested by increased frequency and severity of the attacks and angina at rest. The ST-segment elevation suggests a developing acute coronary syndrome with myocardial ischemia, but the lack of cardiac enzyme elevation suggests infarction has not yet occurred. In most patients, unstable angina is induced by disruption of an atherosclerotic plaque followed by a mural thrombus and possibly distal embolization, vasospasm, or both. An acute myocardial infarction (MI) can lead to focal fibrinous pericarditis, but it is unlikely to lead to extensive scarring that surrounds the heart. Fibrosis is a late finding from the healing of infarction. Hypertrophy of the heart is unlikely to progress significantly in this case because there is neither hypertension nor a valvular lesion. Mural thrombosis may develop on the endocardial surface overlying an infarction and may fill a ventricular aneurysm following an MI. An acute MI may be complicated by papillary muscle rupture with mitral valve insufficiency.