Childhood coronary sclerosis.
Childhood coronary sclerosis was studied histologically, histochemically immunohistochemically and biochemically on 60 autopsy cases aged from new-born to 20 years. Intimal thickening often started even in the newborn babies particularly at branching or bending points of the arteries, where fibrocellular proliferation with acid mucopolysaccharide accumulation was the main histological feature. Microthrombi were occasionally demonstrated even in infants, and fatty streaks appeared generally in the second decade. Microthrombi were usually smaller and fewer than fatty streaks. Beta-lipoprotein and fibrinogen infiltrations into intima were proven in some cases. Mural vascularization was occasionally observed especially in the areas beneath intimal thickening. Pressure effect of the blood stream and anatomically specific points in the arteries seemed to be important as initial factors of coronary sclerosis, where plasma constituents might pass in an easier manner into intimas by increased permeability. Secondarily mural capillaries might play some role in developing atheromas which would produce an eccentrically located luminal obstruction later in adulthood, by local circulatory disturbances within the arterial walls.
D000293:Adolescent; D000328:Adult; D000367:Age Factors; D001161:Arteriosclerosis / Q000473:pathology; D002648:Child; D002675:Child, Preschool; D003327:Coronary Disease / Q000378:metabolism / Q000473:pathology*; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology; D005260:Female; D006025:Glycosaminoglycans / Q000378:metabolism; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D050356:Lipid Metabolism; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D013927:Thrombosis / Q000473:pathology
D006025:Glycosaminoglycans; D008077:Lipoproteins, LDL