Transient neonatal tricuspid regurgitation: possible relation with premature closure of the ductus arteriosus.
Normal fetal circulation requires patency of the ductus arteriosus. Prenatal ductal closure causes profound circulatory changes, such as massive tricuspid regurgitation. After delivery, the clinical picture of these severely distressed cyanotic newborns usually improves rapidly as the circulation is no longer dependent on ductal patency after onset of respiration. This case report deals with a newborn infant with severe tricuspid regurgitation and a large atrial right to left shunt who was treated with prostaglandin E1 infusion at 12 hours of age and in whom cardiac angiography revealed no evidence of either patent or functionally closed ductus arteriosus and no anatomic cardiac abnormalities at 30 hours of age. On the basis of physiologic and morphologic observations in this infant, the possible role of premature ductal narrowing or closure in the pathogenesis of transient neonatal tricuspid regurgitation is discussed. It is recommended that documentation of ductal presence or absence should become part of the diagnostic evaluation of newborns with transient tricuspid regurgitation.
D000328:Adult; D000527:Alprostadil; D004373:Ductus Arteriosus / Q000002:abnormalities* / Q000187:drug effects; D005260:Female; D006344:Heart Septal Defects, Atrial / Q000150:complications; D006801:Humans; D007231:Infant, Newborn; D011458:Prostaglandins E / Q000627:therapeutic use; D014262:Tricuspid Valve Insufficiency / Q000209:etiology*
D011458:Prostaglandins E; D000527:Alprostadil