Regional and global left ventricular function was assessed in 23 neonates with persistent pulmonary hypertension using computer assisted analysis of their left ventricular echocardiograms and compared with that in 50 healthy neonates. End diastolic left ventricular dimension was normal and end systolic dimension increased while percentage left ventricular shortening and peak velocity of circumferential fibre shortening decreased indicating impaired systolic performance. The peak rate of increase in left ventricular diameter in early diastole was significantly decreased and the durations of the rapid filling and isovolumic relaxation periods were prolonged suggesting resistance to left ventricular filling due to changes in diastolic myocardial properties. This abnormal left ventricular cavity function may have been due to a combination of increased diastolic wall thickness, reduced percentage systolic wall thickening, increased relative wall thickness, and pronounced reduction in peak rates of systolic wall thickening and diastolic wall thinning Seven neonates with persistent pulmonary hypertension died, and of the three examined at necropsy all had left ventricular hypertrophy and two extensive subendocardial haemorrhage and infarction affecting the right and left ventricular papillary muscles. Thus left ventricular dysfunction appears to be a common feature in neonates with this disorder and may be readily detected using computer analysis of left ventricular echocardiograms. Unfortunately, no single echo measurement was useful prognostically. Left ventricular dysfunction in persistent pulmonary hypertension probably results from a combination of hypoxaemia, acidaemia, and pulmonary hypertension, and although it may contribute to the high mortality in this syndrome, a correlation between the severity of left ventricular dysfunction and clinical outcome could not be shown.
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