Abstract
Increasing pathological insights have highlighted the role of plaque instability in the pathogenesis of acute ischemic syndromes. These studies have identified a specific plaque phenotype, characterized by large burden, expansive arterial wall remodeling, and greater composition of lipid, inflammatory, and necrotic material, as the disease most likely to rupture and provoke acute ischemia. Accordingly, considerable efforts have been made to develop more effective strategies to identify patients more likely to harbor such lesions and to passivate this disease from both a prophylactic and a therapeutic perspective. The approaches to management of plaque stabilization are reviewed.
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