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Hydralazine-Induced Tachycardia and Sodium Retention in Heart FailureHemodynamic and Symptomatic Correction by Prazosin Therapy
Lawrence J. Laslett, MD;
Anthony N. DeMaria, MD;
Ezra A. Amsterdam, MD;
Dean T. Mason, MD
Arch Intern Med. 1978;138(5):819-820.
Abstract
Severe tachycardia, ventricular ectopy, and sodium retention manifested by hemodynamic deterioration developed with hydralazine hydrochloride therapy in chronic coronary heart disease with congestive failure refractory to digitalis, diuretics, and nitrates. Coronary care unit admission with Swan-Ganz catheterization corrected hemodynamics by sodium nitroprusside treatment after hydralazine withdrawal. Satisfactory cardiac performance with oral long-acting nitrates were unsuccessful. However, the new oral vasodilator, prazosin hydrochloride, achieved considerable hemodynamic benefit by greatly reducing elevated left ventricular filling pressure and increasing severely depressed cardiac index to normal, accompanied by striking symptomatic improvement. Furthermore, long-term enhancement of cardiac dynamics and salutary functional status was maintained by ambulatory oral prazosin therapy for several months. This experience demonstrates the favorable alternative of prazosin nitroprusside-like actions over hydralazine-nitrate therapy in heart failure therapy and emphasizes prazosin's utility when untoward side effects to hydralazine develop.
(Arch Intern Med 138:819-820, 1978)
Author Affiliations
From the Section of Cardiovascular Medicine, University of California at Davis, School of Medicine and Sacramento Medical Center, Davis and Sacramento, Calif.
Footnotes
Accepted for publication Jan 9, 1978.
Reprint requests to Section of Cardiovascular Medicine, University of California, School of Medicine, Davis, CA 95616 (Dr Laslett).
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