HISTOLOGICAL PATTERNS OF ATHEROSCLEROTIC PLAQUES IN UNSTABLE ANGINA PATIENTS VARY ACCORDING TO CLINICAL PRESENTATION

Background-Unstable angina is a heterogeneous clinical syndrome. The d iverse 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 pat ients with stable angina pectoris and patients with diverse clinical p resentations of unstable angina. Methods-48 patients who underwent cor onary atherectomy for management of ischaemic heart disease: 23 had st able angina and 25 had unstable angina. Of the latter, 11 patients wer e classified as Braunwald's IIB and 14 as Braunwald's IIIB unstable an gina. 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 s mooth muscle cells and macrophages within atherosclerotic plaque fragm ents. Results-Fresh thrombus was more frequently found in patients wit h Braunwald's IIIB unstable angina (64%) than in patients with stable angina (22%) or IIB unstable angina (27%) (p < 0.0006). A pattern of s mooth muscle cell proliferation (''accelerated progression pattern'') was observed which was also associated with coronary thrombus. This pa ttern was present in 30% of patients with stable angina, 64% of patien ts with IIIB unstable angina, and in all patients (100%) with IIB unst able angina, Atherosclerotic plaques with thrombus, cholesterol clefts , and macrophages were more common in patients with unstable angina th an in stable angina patients. Conclusion-The presence of a specific sm ooth muscle cell proliferation (accelerated progression) pattern in pa tients with unstable angina, particularly in those with Braunwald's II B unstable angina, suggests that episodic plaque disruption and subseq uent healing may be an important mechanism underlying angina symptoms in these patients.