Is coronary artery disease initiated perinatally?
Fetal origins of coronary disease were proposed recently on the basis of evidence that intrauterine growth retardation predisposed to precocious coronary disease. Recent ultrastructural studies suggest a pathogenesis supporting perinatal origins of coronary atherosclerosis. Half of infants show coronary intimal lesions with foam cells. Intimal proliferative lesions, precursive to lipid insudation of coronary arteries, have been reported in fetuses and newborns. Acute hypertension increases and promotes the progression of preexisting modified smooth muscle cell plaques in perinatal animals by developing prominent fibroplasia and collagenization. Such perinatal surges in blood pressure may be involved in the perinatal initiation of atherogenesis. Modification of naturally occurring lesions may depend on perinatal circumstances superimposed on the transition between fetal and adult patterns of circulation. Unusual perinatal stresses involving anoxia or catecholamine release in the mother, fetus, or newborn may predispose to the development of precocious coronary atherosclerosis later in life.
Leistikow
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EA
Biology Department, University of North Carolina at Wilmington, USA.
D000328:Adult; D000818:Animals; D001724:Birth Weight; D003327:Coronary Disease / Q000196:embryology* / Q000453:epidemiology / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology; D004198:Disease Susceptibility; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D005260:Female; D005316:Fetal Distress / Q000150:complications; D005317:Fetal Growth Retardation / Q000150:complications; D005487:Foam Cells / Q000473:pathology; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000196:embryology; D007231:Infant, Newborn; D050356:Lipid Metabolism; D008297:Male; D009638:Norepinephrine / Q000502:physiology; D011817:Rabbits; D012737:Sex Factors
D009638:Norepinephrine