CLINICALLY STABLE ANGINA-PECTORIS IS NOT NECESSARILY ASSOCIATED WITH HISTOLOGICALLY STABLE ATHEROSCLEROTIC PLAQUES

Objective-To investigate the extent of plaque inflammation in culprit lesions of patients with chronic stable angina. Design-Retrospective s tudy. Setting-Amsterdam reference centre. Subjects-89 consecutive pati ents who underwent directional coronary atherectomy, 58 of whom met th e following inclusion criteria: chronic stable angina (Canadian Cardio vascular Society classification 1-3 (group 1, n = 28)); unstable angin a (Braunwald class II (group 2, n = 18)); unstable angina (Braunwald c lass III (group 3, n = 12)). Interventions-Directional atherectomy in patients with angina pectoris. Main outcome measures-Tissue areas of c ulprit lesions occupied by inflammatory cells and smooth muscle cells related to clinically defined ischaemic syndrome. Results-Areas (% of total surface area (mean (SEM)) rich in smooth muscle cells were large r in patients with chronic stable angina (group 1, 51.2 (20.9)) than i n those with unstable angina (group 2, 42.1 (20.5); group 3, 29.5 (19. 4)) (1 v 2 and 2 v 3, NS; 1 v 3, P < 0.004). Macrophage rich areas wer e significantly smaller in patients with stable angina (group 1, 21.8 (11.9)) than in those with unstable angina (group 2, 31.5 (14.6); grou p 3, 46.4 (16.7)) (1 v 2, P < 0.02; 2 v 3, P < 0.02; 1 v 3, P < 0.001) . Mean numbers of T cells per mm(2) were as follows: group 1, 17 (9.4) ; group 2, 25 (15.9); group 3, 41 (30.6) (1 v 2, P 0.04; 2 v 3, P 0.07 ; 1 v 3, P < 0.001). Areas with HLA-DR positive cells showed the same pattern as macrophages and T cells and were smaller in stable (29.9 (1 2.4)) than in unstable angina (group 2, 40.4 (17.6); group 3, 52.4 (12 .0)) (1 v 2, P < 0.02; 2 v 3, P < 0.05; 1 v 3, P < 0.001). Conclusion- The inverse relation between the extent of inflammatory activity in pl aque tissues of culprit lesions and the clinical stability of the isch aemic syndrome supports the concept that reduction of inflammation fav ours plaque stabilisation. At the same time, the considerable overlap between groups indicates that patients with clinically stable angina d o not all have histologically stable plaques.