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ENGLISH ABSTRACT
JOURNAL ARTICLE
[Pulmonary arterial hypertension treated with prostacyclin or calcium blockers].
BACKGROUND: Until recently, medical treatment of pulmonary arterial hypertension in Norway has included diuretics, anticoagulation and calcium channel blockers. We describe our experience with prostacyclin (epoprostenol) in the treatment of this disease.
MATERIALS AND METHODS: After diagnostic procedures, 11 patients with pulmonary arterial hypertension in functional class III or IV were treated with oral calcium channel blockade or intravenous epoprostenol. Choice of medical agent was based on right heart catheterisation with acute vasodilator testing. Functional capacity and haemodynamics were assessed at referral and after three months of therapy.
RESULTS: Acute vasodilator testing revealed a much greater improvement in haemodynamics in the two patients subsequently treated with nifedipine than in the nine patients found to be candidates for epoprostenol. In the latter group, a significant median reduction in pulmonary arterial pressure of 23% and pulmonary vascular resistance of 59% together with a significant increase in cardiac index of 90% and mixed venous oxygen saturation of 17% was found after three months of treatment. All 10 survivors significantly improved their functional class to I or II and peak exercise oxygen consumption by 60%.
INTERPRETATION: Epoprostenol is a valuable agent in severe pulmonary arterial hypertension for non-responders to acute vasodilator testing. The treatment is complex and demands considerable patient involvement.
MATERIALS AND METHODS: After diagnostic procedures, 11 patients with pulmonary arterial hypertension in functional class III or IV were treated with oral calcium channel blockade or intravenous epoprostenol. Choice of medical agent was based on right heart catheterisation with acute vasodilator testing. Functional capacity and haemodynamics were assessed at referral and after three months of therapy.
RESULTS: Acute vasodilator testing revealed a much greater improvement in haemodynamics in the two patients subsequently treated with nifedipine than in the nine patients found to be candidates for epoprostenol. In the latter group, a significant median reduction in pulmonary arterial pressure of 23% and pulmonary vascular resistance of 59% together with a significant increase in cardiac index of 90% and mixed venous oxygen saturation of 17% was found after three months of treatment. All 10 survivors significantly improved their functional class to I or II and peak exercise oxygen consumption by 60%.
INTERPRETATION: Epoprostenol is a valuable agent in severe pulmonary arterial hypertension for non-responders to acute vasodilator testing. The treatment is complex and demands considerable patient involvement.
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