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.
Keywords:
Atherogenesis - perinatal stress - perinatal coronaries - intimal thickenings - atheroma
precursors
