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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Nelson et al. (1978) studied this question.
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