PREMATURE CONSTRICTION OF THE DUCTUS ARTERIOSUS

Acute fetal occlusion of the ductus arteriosus in lambs results in a rise in pulmonary arterial pressure, right ventricular dilatation, reversible tricuspid regurgitation, decreased right ventricular output, increased left ventricular output and a fall in combined output (1).

Indomethacin causes constriction of the ductus and similar changes in pregnant ewes (2). There is also evidence that in utero exposure of the fetus to prostoglandin synthetase inhibitors may be one of the causes of persistent pulmonary hypertension of the newborn secondary to ductal constriction (3).

Intrauterine constriction of the ductus may cause persistent pulmonary hypertension or persistent fetal circulation in the newborn infant, permanent or transient tricuspid insufficiency and neonatal myocardial ischemia.

Transient ductal constriction in the human fetus with and without tricuspid regurgitation has been demonstrated by doppler echocardiography in fetuses in which the mother has been on indomethacin therapy (4,5).

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