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Is coronary artery disease initiated perinatally?
1Biology Department, University of North Carolina at Wilmington, USA.
Insights
Coronary artery disease may begin in infancy. Early life stresses and high blood pressure during the perinatal period can initiate the development of coronary atherosclerosis, leading to early-onset heart disease.
Area of Science:
- Cardiovascular Science
- Developmental Biology
- Pathology
Background:
- The fetal origins of coronary disease hypothesis suggests intrauterine growth retardation leads to early coronary disease.
- Recent ultrastructural studies indicate a pathogenesis supporting perinatal origins of coronary atherosclerosis.
- Intimal lesions and foam cells are observed in infants, with precursive lesions found in fetuses and newborns.
Purpose of the Study:
- To explore the perinatal origins of coronary atherosclerosis.
- To investigate the role of perinatal factors in the initiation of atherogenesis.
- To understand how perinatal circumstances influence the development of coronary lesions.
Main Methods:
- Review of ultrastructural studies on infant and perinatal coronary arteries.
- Analysis of animal models demonstrating the effects of hypertension on perinatal lesions.
- Examination of the impact of perinatal stresses on cardiovascular development.
Main Results:
- Half of infants exhibit coronary intimal lesions with foam cells.
- Intimal proliferative lesions, precursors to lipid insudation, are present in fetuses and newborns.
- Acute hypertension in perinatal animals promotes fibroplasia and collagenization of existing plaques.
Conclusions:
- Perinatal factors, including hypertension and stress (anoxia, catecholamine release), may initiate atherogenesis.
- Circumstances during the perinatal period, superimposed on circulatory transition, can modify naturally occurring lesions.
- These perinatal events may predispose individuals to precocious coronary atherosclerosis later in life.
Abstract:
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.