1994 Volume 40 Issue 1 Pages 61-70
Stenosis of an infarct-related coronary artery, which was successfully recanalized after thrombotic therapy, is frequently not as severe as expected in patients with acute myocardial infarction (AMI) without preceding angina pectoris (AP). To clarify the mechanism of the sudden onset type of AMI, we conducted a morphological study of 40 autopsied patients (35men/5 women with a mean age of 68 years), who died within one week after the first episode of AMI. Among these 40 patients, the coronary lesions in 21 cases (group A) that dies of AMI without preceding AP were histopathologically compared with those of 19 AMI cases (group B) that did have preceding chronic stable AP. There was no significant difference in the clinical profiles between the two groups, including age, gender distribution, coronary risk factors, or location of infarct-related coronary arteries. In group A compared with group B, the grade of luminal narrowing at the coronary lesion was significantly lower (A : 81% vs B : 93%), the incidence of plaque rupture was higher (A : 86% vs B : 53%), and the mean percent area of lipid deposition was much higher (A : 79% vs B : 58%) (p<0.01). The characteristic morphological feature of coronary lesion in group A was an eccentric lipid-rich plaque with rupture showing mild stenosis and presence of occlusive thrombosis superimposed on the location of intramural hemorrhage. Local thinning of the fibrous cap with abundant macrophages and foam cell invasion, rich cholesterol deposition causing a large necrotic core within the intima, and a reduction of muco-polysaccharides in the extracellular matrix of the intima were also frequently observed. The risk of rupture is much higher in developing lipid-rich plaque than in organized collagen-rich plaque and despite a small size compatible with low grade angiographic narrowing, this type of coronary lesion can be responsible for sudden onset type of acute myocardial infarction.
