Postnatal endocardial fibroelastosis of the valve of the foramen ovale.
The valve of the foramen ovale of the heart changes at birth from a prenatal shunting device for the transseptal flow of systemic venous return to a postnatal active barrier to backflow of left atrial blood at higher pressure. To investigate the morphologic response to this functional change in the valve of the foramen ovale, we examined 200 hearts from embryos, fetuses and autopsy patients spanning over a millionfold range of heart weights (0.001 to 1,230 g). The relation of valve thickness to log heart weight was studied by a stepwise linear regression procedure that fitted the data to two linear regressions, one including observations made before birth and the other including observations made after birth. Analysis of variance tables demonstrated that the data are significantly better explained (p < 0.001) by two linear regressions that abruptly separate from one another at the time of birth than by a single linear regression. Histologic study showed that the prenatal valve consists of a thin myocardial layer with delicate endocardium. The postnatal thickening of the valve tissue occurs mainly by fibroelastotic thickening of the endocardium. The endocardial fibroelastosis of the valve develops after it closes and becomes a component of the left atrial wall. The observations support the concept that fibroelastosis is a nonspecific response of the lining of the cardiovascular system to increased mural tension.
D000293:Adolescent; D000375:Aging; D006332:Cardiomegaly / Q000473:pathology*; D002648:Child; D002675:Child, Preschool; D004547:Elastic Tissue / Q000473:pathology*; D004699:Endocardium; D005260:Female; D005333:Fetus / Q000473:pathology; D006321:Heart / Q000033:anatomy & histology; D006346:Heart Septum / Q000473:pathology; D006352:Heart Ventricles / Q000473:pathology*; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D009929:Organ Size; D011247:Pregnancy