SUMMARYIn order to evaluate the circulatory action of vasodilator therapy in patients with significant mitral regurgitation, sodium nitroprusside was infused intravenously in 14 patients who had mitral regurgitation due to a variety of causes. In 13 of these patients, valvular insufficiency had been present for several years. The mean arterial pressure fall from 88 ± 1.2 to 71 ± 2.1 mm Hg was accompanied by a significant decrease in pulmonary artery pressure (from 27.4 ± 2.7 to 19.1 ± 2.4 mm Hg), pulmonary artery wedge v wave (from 31.7 ± 3.3 to 17.0 ± 1.9 mm Hg), and left ventricular end-diastolic pressure (from 16.7 ± 1.6 to 9.3 1.2 mm Hg). In 10 patients significant decreases in angiographic end-diastolic volumes (from 196 10 to 177 ± 10 ml) and end-systolic volumes (from 90 ± 10 to 77 ± 9 ml) were accompanied by slight decreases in the total stroke volume and slight increases in the ejection fraction. The improved forward stroke volume index (from 27 3.0 to 33 ± 2.1 ml) was due to a very significant reduction in the regurgitant fraction (from 57 ± 6 to 42 6%). Nitroprusside, therefore, has beneficial hemodynamic effects in patients with chronic mitral regurgitation. Circulation, Volume 50, November 1974 valvular disease.3 In order to quantitate the changes which occur and to relate them to the severity of disease in a larger group of patients with chronic mitral regurgita.tion of moderate degree, we studied 14 patients at the time of diagnostic cardiac catheterization during control periods and during infusion of nitroprusside in doses large enough to profoundly influence the circulatory state of the patient.
Methods Patients StudiedFourteen patients with significant mitral insufficiency were studied at the time of diagnostic cardiac catheterization. The nature of the study and all risks were explained to each patient and informed consent was obtained. There were eight females and six males, ranging in age from 31 to 68 years, with a mean of 54 years. The etiology of the mitral regurgitation was rheumatic in eight, idiopathic ruptured chordae tendineae in two, papillary muscle dysfunction related to coronary artery disease in two, prolapse of the posterior leaflet of the mitral valve in one, and bacterial endocarditis with perforation of the anterior leaflet of the mitral valve in one. In all patients, except one with bacterial endocarditis, the valvular insufficiency was chronic, being of greater than three years' duration. Clinically, all patients were class III, New York Heart Association functional classification, and had clinical evidence of cardiomegaly. All were taking digitalis and diuretics at the time of the study. The clinical diagnosis of mitral insufficiency was confirmed in all patients by a left ventriculogram performed by the retrograde arterial approach. In 10 patients, a second left ventriculogram was performed during nitroprusside infusion for evaluation of changes in ventricular volumes. Nine
Twenty-one patients, 11 with normal pulomonary artery pressures and 10 with pulmonary hypertension, had haemodynamic measurements performed before and during dopamine infusion while undergoing cardiac catheterization, in order to evaluate the circulatory effects of dopamine in pulmonary hypertension. In both groups on average, heart rate, pulmonary artery mean pressure, aortic mean pressure, and cardiac index increased significantly, while systemic vascular resistance fell significantly during dopamine administration. In neither group did the average pulmonary vascular resistance or right ventricular end-diastolic pressure change significantly. We conclude that dopamine is a safe and potentially useful drug for the treatment of reduced cardiac output, even in patients with pulmonary hypertension.
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