Identification of a characteristic morphology of a coronary stenosis likely to result inmyocardial infarction would facilitate the prospective evaluation of infarct prevention strategies and dentification of high-risk patients. We postulated that coronary lesions associated with recent myocardial nfarction or unstable angina would have an angiographic morphology suggesting disruption of an therosclerotic plaque and would appear morphologically different from lesions associated with chronic table angina. To test this hypothesis, quantitative coronary angiography (Brown-Dodge method) as performed in 15 patients 4 to 30 days after myocardial infarction, in 10 patients with the abrupt nset of unstable angina and single-vessel coronary disease, and in 15 patients with chronic stable ngina without prior myocardial infarction. Serial arterial diameters (20 to 40) within each lesion weredetermined and the degree of luminal irregularity was quantitated by calculation of an “ulceration” ndex. The majority of all lesions analyzed resulted in severe luminal stenosis (mean 78% area stenosis,all groups). Despite small differences in mean lesion severity among groups, overlap in the degree of uminal compromise prevented precise classification of lesions associated with myocardial infarction r unstable angina based on percent stenosis or minimum luminal cross-sectional area. The meanulceration index of lesions in patients with unstable angina and in the infarct-related vessel in those with cute myocardial infarction was 0.62 ± 0.05 (± SEM) and 0.61 ± 0.03, respectively. These were ignificantly different from the mean ulceration indexes of lesions in patients with stable angina (0.96 0.01, p<.05) or from indexes of lesions in the noninfarct-related vessel of patients with acute nfarction (0.90 ± 0.02, p<.05). None of 10 lesions associated with unstable angina and 14 of 15 nfarct-related lesions had an ulceration index less than 0.78. All lesions associated with stable angina nd each lesion in the noninfarct-related vessel in patients wth infarction had an ulceration index ofgreater than 0.83. The ulceration index did not vary significantly with the degree of luminal stenosis or rior treatment with thrombolytic agents. These data provide quantitative evidence that lesions associated ith myocardial infarction or the abrupt onset of unstable angina are of a similar characteristic ngiographic morphology that is suggestive of plaque disruption and not commonly seen in lesions ssociated with chronic stable angina. The ulceration index may provide a mechanism for the prospective dentification of high-risk coronary lesions Circulation.