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Clinically Stable Angina Pectoris is Not Necessarily Associated with Histologically Stable Atherosclerotic Plaques

Overview

Overview

Journal Heart

Date 1996 Oct 1

PMID 8983676

Citations 7

Authors

Authors

A C van der Wal

A E Becker

K T Koch

J J Piek

P Teeling

C M van der Loos

G K David

Affiliations

Affiliations

Soon will be listed here.

Abstract

Objective: To investigate the extent of plaque inflammation in culprit lesions of patients with chronic stable angina.

Design: Retrospective study.

Setting: Amsterdam reference centre.

Subjects: 89 consecutive patients who underwent directional coronary atherectomy, 58 of whom met the following inclusion criteria: chronic stable angina (Canadian Cardiovascular Society classification 1-3 (group 1, n = 28)); unstable angina (Braunwald class II (group 2, n = 18)); unstable angina (Braunwald class III (group 3, n = 12)).

Interventions: Directional atherectomy in patients with angina pectoris.

Main Outcome Measures: Tissue areas of culprit 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 larger in patients with chronic stable angina (group 1, 51.2 (20.9)) than in 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 were 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); group 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 mm2 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 (12.4)) 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 plaque tissues of culprit lesions and the clinical stability of the ischaemic syndrome supports the concept that reduction of inflammation favours plaque stabilisation. At the same time, the considerable overlap between groups indicates that patients with clinically stable angina do not all have histologically stable plaques.

Citing Articles

Role of plaque inflammation in acute and recurrent coronary syndromes.

Meuwissen M, van der Wal A, Siebes M, Koch K, Chamuleau S, van der Loos C Neth Heart J. 2015; 12(3):106-109.

PMID: 25696307 PMC: 2497049.

Genetic inactivation of IL-1 signaling enhances atherosclerotic plaque instability and reduces outward vessel remodeling in advanced atherosclerosis in mice.

Alexander M, Moehle C, Johnson J, Yang Z, Lee J, Jackson C J Clin Invest. 2011; 122(1):70-9.

PMID: 22201681 PMC: 3248279. DOI: 10.1172/JCI43713.

Five-year follow-up of angiographic disease progression after medicine, angioplasty, or surgery.

Borges J, Lopes N, Soares P, Gois A, Stolf N, Oliveira S J Cardiothorac Surg. 2010; 5:91.

PMID: 20977758 PMC: 2987924. DOI: 10.1186/1749-8090-5-91.

Thrombus aspiration in a series of patients with stable or unstable angina pectoris and lesion-site thrombus formation.

Hermens J, van Houwelingen G, de Man F, Louwerenburg H, von Birgelen C Neth Heart J. 2010; 18(9):423-9.

PMID: 20862237 PMC: 2941128. DOI: 10.1007/BF03091809.

Colocalisation of intraplaque C reactive protein, complement, oxidised low density lipoprotein, and macrophages in stable and unstable angina and acute myocardial infarction.

Meuwissen M, van der Wal A, Niessen H, Koch K, de Winter R, van der Loos C J Clin Pathol. 2006; 59(2):196-201.

PMID: 16443738 PMC: 1860312. DOI: 10.1136/jcp.2005.027235.

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