Myocardial changes in immature infants requiring prolonged ventilation.
Open Access
- 1 February 1977
- journal article
- research article
- Published by BMJ in Archives of Disease in Childhood
- Vol. 52 (2) , 138-147
- https://doi.org/10.1136/adc.52.2.138
Abstract
Fourteen infants who had required prolonged ventilation with high concentrations of oxygen for 14 days or more, were studied at necropsy. 11 infants of immature gestation at birth had gross cardiac hypertrophy, defined as a heart weight greater than 2 SD above the mean for their age. No congenital malformation of valves or septum was found, and in the 7 youngest infants with hypertrophy, the ductus arteriosus was anatomically patent. 3 of these 7 infants had an accompanying nurmur. All 11 infants had severe bronchopulmonary dysplasia. The cardiac hypertrophy affected both ventricles and septum in an irregular fashion and was associated with areas of necrosis, progressing to coarse fibroelastotic scars. The intramural vessels showed marked intimal thickening but the main coronary vessels were normal. The 2 youngest infants with cardiac hypertrophy showed the presence of intravascular and endocardial platelet thrombi. In the 3 infants without cardiac hypertrophy less severe zones of necrosis and scarring were present, and only occasional bundles of hypertrophied muscle fibres were seen. In an attempt to understand these hitherto undescribed lesions, a group of 50 fresh stillbirths and 50 first-week neonatal deaths of comparable gestational age were studied. In 19 of these infants foci of myocardial fibre necrosis were present. It is suggested that the lesions in the older infants represent a more advanced and continuing stage of that seen in the younger infants, and that the foci of necrosis are the result of continuing hypoxia and related problems to a failing coronary circulation. The possibility of myocardial damage represents a serious hazard to the successful therapy of the immature asphyxiated infants.This publication has 25 references indexed in Scilit:
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