Ultrastructural findings on platelet depositions in initial atherogenesis.

Morphological methods, especially scanning electron microscopy, were used in mini-pigs to prove that locally and systemically acting angiopathic stimuli caused an initial adhesion of platelets with altered shape to apparently intact arterial endothelium in a highly reproducible manner. These angiopathy models imitate the risk factors for human arteriosclerosis. Transmission electron microscopic studies, on the other hand, showed very early changes in endothelial and media cells subjected to suitable stimuli. The effective stimuli for angiopathy were local contact of the arteries with ice or epinephrine, the inhalation of cigarette smoke or carbon monoxide, a high-cholesterol diet, renovascular hypertension, and insulin-dependent diabetes. On acting over a longer period these stimuli caused intimal thickening, formation of microparietal thrombi consisting of platelets and fibrin on the endothelium. Within half a year the stimuli led to the formation of lipid-containing plaques of the intima. Several of these stimuli led to increased platelet aggregation. According to these findings we see the decisive mechanism for the pathogenesis of all stenosing, obliterative arteriopathies in a disturbed interaction between vessel wall and arterially circulating blood. Adherence of platelets to the arterial endothelium appears to play a key role in the initial phase of atherogenesis. This concept is supported and augmented by a multitude of partly very recent findings cited in the literature.