Atheromas that cause fatal thrombosis are usually large and frequently accompanied by vessel enlargement

Several lines of clinical evidence show that AMI frequently occurs at sites with mild to moderate degree of coronary stenosis. The degree of luminal s tenosis depends on plaque deposition and degree of vessel remodeling, featu res poorly assessed by coronary angiography. This postmortem study tested t he hypothesis that the size of coronary atheroma and the type of remodeling distinguish culprit lesion responsible for fatal AMI from equi-stenotic no nculprit lesion in the same coronary tree. The main coronary branches from 36 consecutive patients with fatal AMI were studied. The culprit lesion (Gr oup 1) and an equi-stenotic nonculprit segment (Group 2) obtained in measur ements of another coronary branch from the same patient were compared. Morp hometry and plaque composition was assessed in both groups. Compared to Gro up 2, Group 1 had larger areas of plaque 9.6 vs. 4.7 mm(2), vessel 12.7 vs. 7.4 mm(2) and lumen 1.7 vs. 1.2 mm(2); (P < .01). Positive remodeling was more frequent in Group I than Group 2: 21/30 (70%) vs. 8/26 (31%). Plaque a rea correlated positively with lipid core and macrophages and negatively wi th fibrosis and smooth muscle cells. Atherosclerotic plaques that cause fat al thrombosis are more frequently positively remodeled and tend to be large r than nonculprit plaques with the same degree of cross-sectional stenosis. We tested whether arterial remodeling and plaque size vary between segment s containing a fatal thrombosed plaque versus an equi-stenotic nonculprit p laque. Culprit vessel segments had higher cross-sectional areas of intimal plaque and of vessel wall than equi-stenotic nonculprit plaques. The cross- sectional area of the vessel correlated positively with both the lipid core area and CD68(+) macrophage content, and negatively with fibrosis area and smooth muscle cell content. These results add elements explaining limitati ons of angiography in identifying plaques and provide new insights into the role of remodeling in plaque instability. (C) 2001 Elsevier Science Inc. A ll rights reserved.