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Strategies to achieve coronary arterial plaque stabilization Rabbani R; Topol EJCardiovasc Res 1999[Feb]; 41 (2): 402-17Acute coronary syndromes result from fissure, erosion or rupture of a vulnerable atherosclerotic plaque. The characteristics of a vulnerable plaque include a large lipid pool, an abundance of inflammatory cells and mediators, a reduced smooth muscle cell and collagen content and a thin overlying fibrous cap. Potential therapeutic strategies at achieving plaque stabilization have targeted these features. Lipid lowering agents, beta-adrenergic blockers, angiotensin converting enzyme inhibitors and antioxidants have been shown to reduce the incidence of acute coronary syndromes, presumably through plaque stabilization. Matrix metalloproteinase inhibitors as well as macrolide antibiotics and gene therapy approaches show promise in achieving plaque stabilization. The evidence supporting plaque stabilization by these agents and the mechanisms by which these agents stabilize plaques are discussed in detail in this review.|Adrenergic beta-Antagonists/therapeutic use[MESH]|Angiotensin-Converting Enzyme Inhibitors/therapeutic use[MESH]|Animals[MESH]|Anti-Bacterial Agents/therapeutic use[MESH]|Antioxidants/*therapeutic use[MESH]|Coronary Artery Disease/*therapy[MESH]|Female[MESH]|Genetic Therapy[MESH]|Humans[MESH]|Hypolipidemic Agents/*therapeutic use[MESH]|Macrolides[MESH]|Male[MESH]|Metalloendopeptidases/therapeutic use[MESH]|Myocardial Infarction/*prevention & control[MESH] |
