[Risk factors of arteriosclerosis. Differential profile--various mechanisms?]

Up to the present more than 250 factors have been discussed as being risk factors for arteriosclerosis. Yet only a very few pathogenetic mechanisms have actually been proven to be causative in maintaining or complicating the disease. Experimental research in atherosclerosis reflects on a history of approximately 80 years, starting with the remarkable discovery by Windaus in 1912, who for the first time described that in atherosclerotic material 30 times more cholesterol is found as compared to healthy material. Today, due to an enormous quantity of experimental, biochemical, cellular and molecular biological data it is clear that the cholesterol of an atherosclerotic plaque is not being built at the location of deposit but rather derives from circulating plasmalipoproteins, especially from the LDL and IDL particles. Predisposition requires exceeding a threshold concentration of approximately 100 mg/dl cholesterol in plasma and its biological modification. In atherogenesis essentially five cell types are involved: the endothelium, the thrombocytes, the monocyte/macrophage system, the smooth muscle cells of the intima, and the T-lymphocytes. As a consequence of a rather complicated interaction of lipoproteins with these cells changes of the endothelium are initiated which eventually lead to lipid deposition. From early clusters, the so-called fatty streaks, and under unfavorable circumstances and unlimited growth atherosclerotic plaques may develop with the inherent danger of rupture and thrombotic occlusion. The vulnerability respectively the resistance of the arterial wall towards hypercholesterolemia is influenced by other so-called primary risk factors such as hypertension, cigarette smoking, diabetes mellitus, and hyperfibrinogenemia.(ABSTRACT TRUNCATED AT 250 WORDS)