An emerging concept, which is relevant to the issue of triggering of acute coronary disease, is that of plaque stabilization (11,12). An atherosclerotic lesion, which is more resistant to rupture, will be less likely to do so when exposed to a trigger that can induce plaque disruption. Angiographic studies of aggressive lipid-lowering therapy identified a disproportionately dramatic reduction in cardiac events compared to tiny changes in the arteriographic appearance of the coronary arteries. Large clinical studies demonstrating the success of both primary (180) and secondary (181) coronary event prevention strategies, using b-hydroxy-b-methylglutaryl (HMG) CoA reductase inhibitors (statins), have supported the concept that these drugs have their beneficial effects on coronary events by altering the composition and milieu of the plaque rather than by reducing plaque bulk and coronary stenosis severity. There are a variety of mechanisms by which the most prominent effect of statins, lipid lowering, may improve plaque stability. These include increases in collagen content, decreases in macropahges, and decreases in the expression of metalloproteinases and proinflammatory substances (11,12). Dietary factors (182) and other drugs, such as fibrates, which do not lower low-density lipoprotein (LDL) but have statin-like effects on cardiac event rates (183), can affect the function of receptors that limit the activation of vascular inflammatory responses (11,12). These represent changes that favor plaque stability and, thus, reduced susceptability to triggering of acute coronary disease.
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