The reduction in clinical events observed in the angiographic lipid-lowering trials appears to be best explained bycolon; (1) the relationship of the lipid and foam cell content of the plaque to its likelihood of fissuring; and (2) the effects of lipid-lowering therapy on these 'high risk' features of plaque morphology. The composite of data presented here supports the hypothesis that lipid-lowering therapy selectively lipid-depletes (regresses) the relatively small but dangerous subgroup of vulnerable lesions that contain a large 'soft' lipid core and dense clusters of intimal macrophages. By doing so, these lesions are effectively stabilized and clinical event rate is accordingly decreased.
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