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Heart 1998;80:19-22; doi:10.1136/hrt.80.1.19
Copyright © 1998 BMJ Publishing Group Ltd & British Cardiovascular Society

Heart 1998;80:19-22 ( July )

Histological patterns of atherosclerotic plaques in unstable angina patients vary according to clinical presentation

J M Mann,a J C Kaski,a W I Pereira,b S Arie,b J A Ramires,b F Pileggib

a Department of Cardiological Sciences, St George's Hospital Medical School, Cranmer Terrace, London SW13 0RE, UK, b INCOR, Sao Paulo, Brazil

Correspondence to: Dr Kaski

Accepted for publication 18 February 1998

Background---Unstable angina is a heterogeneous clinical syndrome. The diverse clinical presentations of unstable angina may reflect different pathogenic mechanisms within the plaque.
Objective---To investigate the cellular constituents of culprit coronary atheromatous plaques in patients with stable angina pectoris and patients with diverse clinical presentations of unstable angina.
Methods---48 patients who underwent coronary atherectomy for management of ischaemic heart disease: 23 had stable angina and 25 had unstable angina. Of the latter, 11 patients were classified as Braunwald's IIB and 14 as Braunwald's IIIB unstable angina. The presence of thrombus, cholesterol clefts, and smooth muscle cell proliferation was assessed in atherectomy samples using standard histological techniques. Monoclonal antibodies were used to identify smooth muscle cells and macrophages within atherosclerotic plaque fragments.
Results---Fresh thrombus was more frequently found in patients with Braunwald's IIIB unstable angina (64%) than in patients with stable angina (22%) or IIB unstable angina (27%) (p < 0.0006). A pattern of smooth muscle cell proliferation ("accelerated progression pattern") was observed which was also associated with coronary thrombus. This pattern was present in 30% of patients with stable angina, 64% of patients with IIIB unstable angina, and in all patients (100%) with IIB unstable angina. Atherosclerotic plaques with thrombus, cholesterol clefts, and macrophages were more common in patients with unstable angina than in stable angina patients.
Conclusion---The presence of a specific smooth muscle cell proliferation (accelerated progression) pattern in patients with unstable angina, particularly in those with Braunwald's IIB unstable angina, suggests that episodic plaque disruption and subsequent healing may be an important mechanism underlying angina symptoms in these patients.

Keywords: angina pectoris;  atherosclerosis;  unstable angina;  accelerated progression pattern

© 1998 by Heart
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