Key result
Histologic study of a newborn with congenital tricuspid insufficiency revealed myxomatous degeneration with increased glycosaminoglycans and decreased mature collagen in the affected valves.
Case Report (n=1)
This case expands the etiology of congenital tricuspid insufficiency in newborns to include failure of the tricuspid valve leaflets to develop normally, presenting as myxomatous degeneration.
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Myxomatous degeneration may underlie congenital tricuspid insufficiency in newborns; extends the etiologic spectrum but remains hypothesis-generating.
A case of congenital tricuspid insufficiency in the newborn secondary to myxomatous degeneration of the tricuspid valve is described. There were myxomatous changes of the pulmonary and aortic valves. The mitral valve was normal. Histologic study showed an increased amount of glycosaminoglycans and a decreased amount of mature collagen of the tricuspid, aortic, and pulmonary valves. The etiology of congenital tricuspid insufficiency of the newborn can be expanded to include failure of the tricuspid valve leaflets to develop normally, a condition that is histologically similar to myxomatous degeneration in the adult.
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Moodie et al. (1985) conducted a case report in Congenital tricuspid insufficiency (n=1). Histologic study of a newborn with congenital tricuspid insufficiency revealed myxomatous degeneration with increased glycosaminoglycans and decreased mature collagen in the affected valves.
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