In 129 hearts with congenital malformations, endocardial fibrosis was associated with mechanical factors and hypoxia, with elastic tissue being a normal component of the fibrosis.
Observational (n=129)
Endocardial fibro-elastosis in congenital heart disease appears to be driven by mechanical stress and hypoxia, with elastic tissue proliferation being a normal component of the fibrotic response.
The site and degree of endocardial fibrosis has been estimated and recorded in 129 hearts with relatively uncomplicated congenital malformations. The great majority showed endocardial thickening. Mechanical factors, including increased pressure and abnormal currents of intracardiac blood, are of importance in the production of endocardial fibrosis, because the sites of fibrosis follow the same pattern in various examples of the same defect and occur where general increase in intracardiac pressure may be presumed to occur on where localized jets may impinge on cause vibration. The degree of fibrosis increases with age. Deficiency of oxygen in the coronary blood supply is also of importance, especially in cases of severe aortic stenosis or atresia and in hearts with a coronary artery arising from the pulmonary artery. A hypothesis is offered that the warty valvular vegetations occasionally seen with aortic stenoss represent the reaction of fetal valvular endocardium to mechanical factors combined with hypoxia. Elastic tissue stains show that proliferation of elastic fibers occurs in association with proliferation of the collagen in the thickened endocardium found in congenitally malformed hearts and in other types of heart disease. It is concluded that elastic tissue is a normal component of endocardial fibrosis.
Andersen et al. (Mon,) conducted a observational in Congenital malformations (n=129). Mechanical factors and hypoxia was evaluated on Site and degree of endocardial fibrosis. In 129 hearts with congenital malformations, endocardial fibrosis was associated with mechanical factors and hypoxia, with elastic tissue being a normal component of the fibrosis.