Abstract
RECENTLY, we reported 14 term newborn infants affected by severe perinatal stress who subsequently manifested cyanosis, congestive heart failure and transient murmurs of tricuspid insufficiency.1 The clinical picture, including the ST-segment and T-wave changes on the electrocardiogram, and the constant history of perinatal asphyxia, suggested to us that the hypoxic stress that these infants encountered led to a generalized myocardial dysfunction syndrome similar to that described by Burnard and James,2 and Rowe and Hoffman.3 Furthermore, post-mortem examination of the two patients in our series who died showed extensive patchy necrosis of the anterior papillary muscle of the tricuspid valve. The . . .
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