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Mast cell infiltration in acute coronary syndromes: implications for plaque rupture.

Abstract：

OBJECTIVES:To define the role of mast cells in plaque destabilization. BACKGROUND:Inflammation is an essential feature of human coronary plaques. Macrophages and T lymphocytes are considered to contribute to destabilization of the plaques. The role of mast cells in this setting is less well studied. We therefore counted the mast cells in coronary atherectomy specimens from patients with chronic stable angina, unstable angina and severe unstable angina. METHODS:Patients studied had chronic stable angina (group 1, n=11), "stabilized" unstable angina (group 2; Braunwald's class I and II, n=11) and "refractory" unstable angina (group 3; Braunwald's class III, n=7). Samples of culprit lesions (n=29) were obtained by directional atherectomy, snap-frozen and analyzed immunohistochemically. The numbers of mast cells and T lymphocytes per square millimeter squared were counted and the areas containing macrophages and smooth muscle cells were measured by computed planimetry. RESULTS:We found that the numbers of mast cells and T lymphocytes increased from group 1 through groups 2 to 3. Specimens from group 3 also contained the largest numbers of tumor necrosis factor alpha (TNF-alpha)-positive mast cells and of matrix metalloproteinase (MMP)-9 (92 kD gelatinase)-positive macrophages. CONCLUSIONS:Unstable coronary syndromes are associated with increased numbers of mast cells in culprit lesions. Activated mast cells secrete neutral proteases capable of degrading the extracellular matrix and TNF-alpha, capable of stimulating macrophages to synthesize MMP-9. Our observations suggest that mast cells, in addition to macrophages, contribute to matrix degradation and, hence, to progression of coronary syndromes.

journal_name

J Am Coll Cardiol

journal_title

Journal of the American College of Cardiology

authors

Kaartinen M,van der Wal AC,van der Loos CM,Piek JJ,Koch KT,Becker AE,Kovanen PT

doi

10.1016/s0735-1097(98)00283-6

subject

Has Abstract

pub_date

1998-09-01 00:00:00

pages

606-12

issue

3

eissn

0735-1097

issn

1558-3597

pii

S0735-1097(98)00283-6

journal_volume

32

pub_type

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