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Fibrinogen and smooth muscle cell detection in atherosclerotic plaques fromstable and unstable angina -- an immunohistochemical study.

Teresa Wagner, Ewa Walczak, Marek Dabrowski, Marios Loukas, Adam Witkowski, Witold Ruzyłło

Med Sci Monit 2002; 8(4): BR144-148

ID: 420878

BACKGROUND: This study presents a systematic analysis of atherothromboticlesions taken by percutaneous atherectomy and post mortem examination from coronary arteries, in orderto identify: a) the topographic occurrence of fibrinogen and smooth muscle cells (SMCs), b) their independentexpression in stable and unstable plaques, and c) their co-expression, which can provide a better understandingof the involvement of fibrinogen and SMCs in the development and progression of atherosclerotic plaques.MATERIAL/METHODS: 120 specimens from atherosclerotic lesions were collected, using directional coronaryatherectomy; 40 additional specimens were collected from postmortem examinations. All specimens werestained by immunohistochemical methods with monoclonal and polyclonal antibodies (DAKO) for fibrinogenand SMCs. RESULTS: Fibrinogen appeared to be a component of all stable and unstable coronary atheroscleroticplaques, with a significant predominance in unstable angina. No significant difference was observed betweenSMC-stained areas in stable and unstable angina; however, a significant difference exists in co-expressionof SMCs and fibrinogen between unstable and stable angina. Interestingly, the total number of SMCs atthe first stages of formation of unstable plaques is less than in stable plaques. However, in a numberof advanced coronary atherosclerotic plaques associated with unstable angina, we observed an increasinglyprogressive inflammatory cell activity, in which SMC areas were significantly increased. CONCLUSIONS:This distribution of fibrinogen and SMCs suggests the possibility of a link between SMC migration andproliferation, intensifying the increased fibrinogen concentration in atherosclerotic plaques.

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