Thirteen consecutive patients with primary and secondary pulmonary hypertension who had normal left ventricular function were treated with hydralazine in an effort to reduce pulmonary vascular resistance and clinical symptoms. Despite marked decreases in systemic vascular resistance (40 per cent; P<0.001), hydralazine produced only moderate decreases in pulmonary arteriolar resistance (21 per cent), without improving stroke volume or pulmonary-artery pressure. Instead, mean arterial pressure fell markedly (17.5 mm Hg, P<0.01) in association with a reflex increase in heart rate (11 beats per minute, P<0.01). Four patients became symptomatically hypotensive within 24 hours of the initiation of treatment; two of these four required pressors for circulatory support, and one died. Progressive renal insufficiency developed in one patient, and a symptomatic decrease in systemic arterial oxygen saturation occurred in another; both changes were reversed upon discontinuation of the drug. In conclusion, hydralazine fails to produce consistent hemodynamic and clinical benefits in patients with primary and secondary pulmonary hypertension, and it frequently causes serious adverse reactions. (N Engl J Med. 1982; 306:1326–31.) ALTHOUGH vasodilator drugs have proved useful in the treatment of patients with systemic hypertension and severe left ventricular failure, early experience with these agents in patients with pulmonary hypertension associated with normal left ventricular function has not been encouraging. Many of these drugs were effective only when administered intravenously or directly into the pulmonary artery.1 2 3 4 5 The fraction of responsive patients was small,3 4 5 6 7 8 and adverse effects were frequent.4 5 6,8 9 10 11 12 Although long-term hemodynamic and symptomatic benefit from phentolamine, diazoxide, or isoproterenol in patients with pulmonary hypertension has occasionally been reported,4,13 14 15 16 no pharmacologic approach has proved satisfactory in the treatment of most patients with.
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