T he transition of coronary lesions from the stable to unstable state is the pathophysiologic mechanism underlying myocardial infarction and unstable angina pectoris. Angiographic, angioscopic and postmortem pathologic studies suggest that this transition is mainly due to atherosclerotic plaque fissuring and associated thrombus formation.'.2 The present study examines the tiistopathologic characteristics of the "culprit lesion" obtained during directional coronary atherectomy of patients with acute coronary syndromes. Directional atherectomy provides a unique opportunity for studying the composition of unstable lesions in living symptomatic patients. Case histories of consecutive patients referred to the University of Michigan Medical Center for directional coronary atherectomy after May I, 1989 were analyzed. All patients selected for inclusion in this study had angina, objective evidence of myocardial ischemia and cineangiograms showing 21 lesion with >50% diameter stenosis of an epicardial coronary artery. The unstable group comprised patients who had experienced ischemic pain at rest accompanied by transient ST-T changes on the electrocardiogram, or acute myocardial infarction during the 2-week period preceding directional atherectomy. The stable group comprised patients who had not had ischemic pain at rest, progressive angina, recent-onset angina or acute myocardial infarction during the 3-month period preceding directional atherectornv. Directional atherectorny was petformed as described previously.3 The atherectomy device (Devices for Vascular Intervention Inc., Redwood City, California) consists of a cylindrical metal housing, with a window opening an eccentric balloon on the opposite side of the window, and a cylindrical, rotating, cutting blade inside the housing. The device was advanced to the coronary stenosis over a 0.014-inch guide wire through a special II or 9.5Fr guiding catheter (Devices for Vascular Intervention Inc.). Each lesion was crossed with the device (5 to 7Fr), and a series of cuttings were made under @oroscopic guidance; then, the atherectomy device was removed, and the tissue specimens were collected. Histopathologic analysis of the atherectomy specimen was performed as previously descrihed.4 Briefly, immediately after removal from the atherectomy device, From the Cleveland Clinic Foundation, Desk F25, One Clinic Center.
