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 less than 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 less than 0.01) in association with a reflex increase in heart rate (11 beats per minute, P less than 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.
Packer et al. (1982) studied this question.