MAST-CELL INFILTRATION IN ACUTE CORONARY SYNDROMES - IMPLICATIONS FORPLAQUE RUPTURE

Objectives. To define the role of mast cells in plaque destabilization . Background. Inflammation is an essential feature of human coronary p laques. 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, unsta ble angina and severe unstable angina. Methods. Patients studied had c hronic stable angina (group 1, n = 11), ''stabilized'' unstable angina (group 2; Braunwald's class I and II, n = 11) and ''refractory'' unst able angina (group 3; Braunwald's class III, n = 7). Samples of culpri t lesions (n = 29) were obtained by directional atherectomy, snap-froz en 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 comput ed planimetry. Results. We found that the numbers of mast cells and T lymphocytes increased from group 1 through groups 2 to 3. Specimens fr om 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. Conclusion. Unstable coronary syndromes are associated with increased numbers of mast cell s in culprit lesions. Activated mast cells secrete neutral proteases c apable 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 deg radation and, hence, to progression of coronary syndromes. (J Am Coil Cardiol 1998;32:606-12) (C) 1998 by the American College of Cardiology .