1978/08/01 by Barry Greenberg, B M Massie, Bruce H. Brundage +3 · 1 citation
Medicine · #Anesthesia #Blood pressure #Cardiac output #Cardiac, Anesthesia and Surgical Outcomes #Cardiology #Ejection fraction #Heart failure #Hemodynamic Monitoring and Therapy #Hemodynamics #Hydralazine #Internal medicine #Medicine #Mitral regurgitation #Nitric oxide #Renal function and acid-base balance #Sodium nitroprusside #Stroke volume #Vascular resistance
paper · pdf · doi:10.1161/01.cir.58.2.273
openalex publication_date 1978/08/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/06/11
The severity of mitral regurgitation is, in part, determined by aortic impedance to left ventricular outflow. Sodium nitroprusside acutely decreases regurgitant flow, but the importance of its dual vasodilating effects, the lowering of peripheral vascular resistance and increasing of venous capacitance, is unclear. We studied the hemodynamic response to intravenous hydralazine, which selectively acts on the arteriolar resistance bed, in 10 patients with severe mitral regurgitation. Hydralazine produced a 50% increase in forward stroke volume (22 +/- 2 to 33 +/- 3 ml/m2, P less than 0.001) and a 33% reduction in regurgitant stroke volume (40 +/- 6 to 27 +/- 6 ml/m2, P less than 0.001), with a resultant fall in pulmonary capillary wedge v wave and mean pressures. Unlike nitroprusside, it did not alter left ventricular end-diastolic volume or pressure. Oral hydralazine maintained this hemodynamic improvement for at least 48 hours and, in three patients, provided more sustained clinical improvement. We conclude that hydralazine, by virtue of its selective lowering of aortic impedance, reduces the amount of mitral regurgitation and thus may be a useful mode of interim or chronic therapy in selected patients.