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J Am Coll Cardiol, 1997; 30:694-702
© 1997 by the American College of Cardiology Foundation
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Pathology of unstable plaque: correlation with the clinical severity of acute coronary syndromes

C Depre, W Wijns, AM Robert, JP Renkin, and X Havaux

Laboratory of Cardiovascular Pathology, University of Louvain Medical School, Brussels, Belgium.

OBJECTIVES: The aim of this study was to relate the various clinical presentations of acute coronary syndromes to the underlying plaque morphology as assessed from histopathologic analysis of plaque fragments obtained by directional coronary atherectomy (DCA). BACKGROUND: Autopsy studies have shown that unstable angina and infarction are related to plaque instability and involve events such as fissure or rupture of the fibrous cap, thrombosis and inflammation. The clinical severity and prognosis of acute coronary syndromes can be estimated by the Braunwald classification of unstable angina. Whether plaque morphology can be related to the Braunwald classification has not been evaluated. METHODS: Plaque fragments were obtained by DCA in 75 patients: 38 with unstable angina, 19 with stable angina and 18 with no symptoms after infarction. The presence of fibrous tissue, thrombus, high cellularity, inflammatory cells, atheroma, neovessels and "stellar-shaped" smooth muscle cells was evaluated in 7-micron thick sections by appropriate staining. The patients were classified according to clinical presentation without knowledge of the results of pathologic examination, and a plaque instability score was assigned. The risk of further cardiac events was classified as low, medium or high. RESULTS: Increasing severity of the score of unstable angina was associated with increasing prevalence of thrombus, high cellularity, atheroma and neovessels. Plaque from patients with unstable angina considered to be at low risk of further events appeared very similar to that of patients with stable angina, whereas the specific morphologic characteristics of plaque instability were more frequently observed as the clinical score and the risk of further events increased. After thrombolyzed infarction, plaque morphology depends on the delay between the acute event and DCA. Within 1 week after infarction, plaque still showed the morphologic characteristics of instability, whereas late DCA provided samples with morphologic features similar to those observed in patients with stable angina. CONCLUSIONS: The morphologic features of plaque fragments vary at different stages of acute coronary disease. The specific features of plaque instability correlate with the clinical scoring system of the Braunwald classification.


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