Concepts in acute coronary syndromes.

Landmark pathological studies have deepened our understanding of the mechanisms behind acute coronary syndromes over the last decade. Thrombosis plays a key role and is a unifying feature in the pathogenesis. Platelet-rich thrombus superimposed over the disrupted atherosclerotic plaque or eroded plaque endothelium, with or without fibrin-thrombus extension, is evident in postmortem necropsy, angiographic and angioscopic studies. However features which contribute to the risk of acute events lie in the atherosclerotic plaque itself. Plaque content and not plaque size is the important factor. A vulnerable plaque may be invisible on clinical stress testing and even coronary angiography; but it is prone to rupture if it has only a thin cap and a proportionally larger lipid core. There is a cellular preponderance of activated macrophages and T-lymphocytes; and high activity of matrix metalloproteinases in vulnerable plaques. Smooth muscle cell proliferation and collagen synthesis are downregulated. These features may serve as possible targets for detecting plaques at risk or for reversing the risk of vulnerable plaques.