Differential effects of milrinone and dobutamine on right ventricular preload, afterload and systolic performance in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

To compare the effects of intravenous dobutamine and milrinone on right ventricular (RV) systolic function, 14 patients with severe congestive heart failure underwent simultaneous radionuclide-hemodynamic study. Patients were randomized to receive intravenous milrinone (50 micrograms/kg bolus then 0.5 microgram/kg/min) or dobutamine (2.5 to 15 micrograms/kg/min) to achieve equal increases in cardiac output. Both drugs significantly improved cardiac performance, with identical 24% increases in mean cardiac index (p less than 0.05 vs baseline; difference not significant for milrinone vs dobutamine) and no change in heart rate. Neither drug substantially altered RV preload, as reflected by mean right atrial pressure and RV end-diastolic volume. Both drugs caused similar increases in RV ejection fraction (mean +/- standard deviation; dobutamine: 0.32 +/- 0.09 to 0.40 +/- 0.11; p less than 0.05; milrinone: 0.35 +/- 0.19 to 0.43 +/- 0.21; p less than 0.05) resulting from reductions in RV end-systolic volume. RV afterload reduction contributed substantially to drug effect on RV systolic performance in patients treated with milrinone but not those treated with dobutamine. With doses effecting equal increases in cardiac index and RV systolic performance, pulmonary artery end-systolic pressure was significantly reduced by milrinone (40 +/- 12 to 33 +/- 12 mm Hg; p less than 0.05), but not by dobutamine. Thus, in patients with congestive heart failure milrinone's effect on RV systolic function is explainable, at least in part, by RV afterload reduction, whereas RV inotropic augmentation contributed more strongly to dobutamine's effect.

Hemodynamic correlates of left ventricular versus right ventricular radionuclide volumetric responses to vasodilator therapy in congestive heart failure secondary to ischemic or dilated cardiomyopathy.

Previous studies have failed to demonstrate the clinical relevance of radionuclide functional measurements during treatment of congestive heart failure (CHF). In the present study, data derived before and during nitroprusside infusion were analyzed in 16 patients with CHF to compare correlations of changes in left (LV) and right ventricular (RV) radionuclide measurements with simultaneous changes in 8 hemodynamic variables. Nitroprusside infusion decreased systemic artery pressure, pulmonary arterial wedge pressure, pulmonary artery pressure, right atrial pressure, and pulmonary and systemic vascular resistance, and increased cardiac output. Nitroprusside decreased LV and RV end-diastolic and end-systolic volumes and increased LV and RV ejection fraction and stroke volume. Changes in RV volumes exceeded changes in LV volumes. LV radionuclide measurements did not correlate significantly with any hemodynamic measurement except for a weak correlation between changes in LV end-systolic volume and right atrial pressure (r = 0.51). In contrast, the combination of changes in RV end-systolic volume and stroke volume predicted changes in pulmonary artery peak systolic (r = 0.90) and mean (r = 0.89) pressures. Changes in pulmonary arterial wedge pressure correlated with changes in RV end-diastolic (r = 0.78) and end-systolic (r = 0.71) volumes. In conclusion, LV radionuclide measurements are of limited value in predicting hemodynamic responses to vasodilator therapy in CHF, whereas RV volumes are strongly influenced by load changes. Their responses to nitroprusside correlate well with changes in pulmonary artery and pulmonary arterial wedge pressures.

Contribution of reduced mitral regurgitant volume to vasodilator effect in severe left ventricular failure secondary to coronary artery disease or idiopathic dilated cardiomyopathy.

Although vasodilators improve cardiac output in severe left ventricular (LV) failure, the degree to which reduction in mitral regurgitation (MR) contributes to this response is unknown. In the present study, nitroprusside-induced changes in forward cardiac output were compared with simultaneous radionuclide LV output in 14 patients with severe LV systolic dysfunction in the absence of known primary valvular disease. Regurgitant output was estimated as LV output minus forward output and regurgitant fraction was calculated as regurgitant output/LV output. At rest, LV ejection fraction averaged 0.16 +/- 0.04 (mean +/- standard deviation). Patients were classified into 2 groups based on regurgitant fraction at rest. Group I (n = 5) had little or no detectable valvular regurgitation, with regurgitant fraction less than 0.10; group II (n = 9) had evidence of MR with regurgitant fraction greater than 0.30. Nitroprusside increased forward cardiac output in all patients in both groups, but this effect was significantly greater in group II (64 +/- 34%) than in group I (31 +/- 17%) (p less than 0.01). Nitroprusside decreased regurgitant fraction in all group II patients, with mean regurgitant fraction decreasing from 0.44 +/- 0.12 to 0.26 +/- 0.15 (p less than 0.005). Thus, a large percentage of patients with severe LV systolic dysfunction have clinically relevant MR, defined as a regurgitant fraction greater than 0.30. Nitroprusside has a greater effect on forward cardiac output in patients with LV failure and MR than in patients with comparable ventricular dysfunction in the absence of detectable MR.(ABSTRACT TRUNCATED AT 250 WORDS)

Relative contribution of inotropic and vasodilator effects to amrinone-induced hemodynamic improvement in congestive heart failure.

The relative contribution of inotropic and vasodilator effect to amrinone-induced hemodynamic improvement in congestive heart failure (CHF) is unknown. In 9 patients with CHF, the effects of amrinone and nitroprusside on hemodynamic and radionuclide measurements were compared to determine whether reduced afterload accounts for the amrinone-induced decrease in left ventricular end-systolic volume. In each patient, the end-systolic pressure-volume relation was derived using nitroprusside. After terminating nitroprusside treatment, intravenous amrinone (3 mg/kg) caused end-systolic volume to decrease from 148 +/- 32 ml/m2 (mean +/- standard deviation) to 133 +/- 32 ml/m2 (p less than 0.05), causing an increase in cardiac index from 1.9 +/- 0.8 to 2.7 +/- 0.8 liters/min/m2 (p less than 0.001). Arterial end-systolic pressure decreased in all patients during amrinone administration, from 96 +/- 22 to 84 +/- 19 mm Hg (p less than 0.005), as did systemic vascular resistance. Nitroprusside doses needed to match the decrease in LV end-systolic volume induced by amrinone caused significantly greater decreases in arterial end-systolic pressure than did amrinone (p less than 0.01). The amrinone-induced decrease in end-systolic volume exceeded that predicted for a pure vasodilator based on arterial end-systolic pressure and the nitroprusside-derived pressure-volume relation in 6 patients. In 3 patients, the decrease in end-systolic volume did not exceed that expected for a pure vasodilator. In conclusion, after amrinone treatment, afterload reduction occurs in all patients with severe CHF and is the sole effect in some.(ABSTRACT TRUNCATED AT 250 WORDS)