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 stenosis depends on plaque deposition and degree of vessel remodeling, features poorly assessed by coronary angiography. This postmortem study tested the hypothesis that the size of coronary atheroma and the type of remodeling distinguish culprit lesion responsible for fatal AMI from equi-stenotic nonculprit lesion in the same coronary tree. The main coronary branches from 36 consecutive patients with fatal AMI were studied. The culprit lesion (Group 1) and an equi-stenotic nonculprit segment (Group 2) obtained in measurements of another coronary branch from the same patient were compared. Morphometry and plaque composition was assessed in both groups. Compared to Group 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 1 than Group 2: 21/30 (70%) vs. 8/26 (31%). Plaque area correlated positively with lipid core and macrophages and negatively with fibrosis and smooth muscle cells. Atherosclerotic plaques that cause fatal thrombosis are more frequently positively remodeled and tend to be larger than nonculprit plaques with the same degree of cross-sectional stenosis. We tested whether arterial remodeling and plaque size vary between segments containing a fatal thrombosed plaque versus an equi-stenotic nonculprit plaque. 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 limitations of angiography in identifying plaques and provide new insights into the role of remodeling in plaque instability.
Bezerra
H G
HG
Heart Institute (InCor) of University of São Paulo Medical School, Av Dr Eneas Carvalho de Aguiar, 44, São Paulo, SP CEP 05403/000, Brazil. hiram@osite.com.br
Higuchi
M L
ML
Gutierrez
P S
PS
Palomino
S A
SA
Silvestre
J M
JM
Libby
P
P
Ramires
J A
JA
D015703:Antigens, CD / Q000276:immunology; D015214:Antigens, Differentiation, Myelomonocytic / Q000276:immunology; D003251:Constriction, Pathologic; D003324:Coronary Artery Disease / Q000150:complications / Q000473:pathology*; D003328:Coronary Thrombosis / Q000209:etiology* / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology*; D005260:Female; D005355:Fibrosis; D006801:Humans; D007150:Immunohistochemistry; D008055:Lipids / Q000097:blood; D008264:Macrophages / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000473:pathology; D012189:Retrospective Studies; D000097382:CD68 Molecule
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D008055:Lipids; C067980:CD68 antigen, human; D000097382:CD68 Molecule