Abstract
Overview of the concept ofoxidative modification ofLDL There can be no doubt now that there is a continuum of increasing risk for complications ofatherosclerosis when plasma levels exceed 160-180 mg/dl. Many types of experimental and clinical evidence substantiate the cholesterol hypothesis. Many primary and secondary prevention trials, including the recent angiographic trials(CLAS andFATS) document that reduction of plasma is as powerful as has been predicted in slowing the progression and clinical expression ofcoronary atherosclerosis. However, the cellular and molecular mechanisms linking hypercholesterolemia to atherogenesis and its sequelae remain unclear. Iflowering ofLDL is efficacious in ameliorating the atherogenic process, why then should one bother to understand the mechanisms? Simply because loweringLDL will not be a total solution. Although it may be true that ifcholesterol levels were reduced to < 150 mg/dl there would be little if any coronary artery disease (CAD),' it is not likely that this will occur any time soon. At any given level ofLDL there is great variability in the clinical expression of the disease. Patients with heterozy
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