Platelets and foam cells in the evolution of atherosclerosis. Histological and immunohistological studies of human lesions.

Sixty-seven coronary, aortic and other lesions (39 subjects) ranging from minor to advanced disease were studied histologically and by immunohistology for antigens of platelets, beta-lipoprotein (LpB) and fibrinogen. Collections of lipid-filled foam cells were found in nearly every lesion mainly in the thickened intima, sometimes associated with macrophages. Foam cells were also present elsewhere including, in advanced lesions, necrotic zones filled with cholesterol needles. Then they too were necrotic. Platelets were observed in many lesions as small free clusters and/or phagocytosed in foam cells and sometimes also in macrophages. Cellular and extracellular reactions for platelet derivatives and for LpB were very frequent. Reactions for fibrinogen were only extracellular. Foam cell cytoplasm reacted for platelet derivatives and for LpB whilst macrophages, endothelium and certain other cells sometimes reacted for platelet derivatives but rarely for LpB. The studies indicate that: Foam cells originate from macrophages mainly in the intima and many migrate elsewhere. Their formation and their uptake of LpB requires cellular acquisition of a platelet factor or factors. Acquisition of platelet factor(s) is by phagocytosis of intact platelets and/or uptake of extracellular soluble derivatives from disrupted platelets. These processes begin early, are likely to be continuous and are significant for the evolution of atherosclerosis including the necrotic foci of advanced lesions.