Impact of short-term intermittent intravenous dobutamine therapy on endothelial function in patients with severe chronic heart failure

Intermittent intravenous dobutamine therapy is used to treat patients with decompensated end-stage chronic heart failure (CHF), in whom the vascular endothelium is usually impaired. Although it has been suggested that modification or reversal of endothelial dysfunction may be of significant therapeutic benefit, the impact of short-term intermittent intravenous dobutamine therapy on flow-mediated dilation (FMD) in patients with severe decompensated end-stage chronic CHF has not been assessed. We prospectively assessed the impact of intermittent intravenous low-dose dobutamine therapy on endothelium-dependent brachial artery FMD and endothelium-independent nitroglycerin (NTG)-mediated vasodilation using high resolution ultrasound scanning in 20 consecutive male patients with severe CHF and ischemic cardiomyopathy (New York Heart Association functional class IV), at baseline and after 4 months, and compared them to 20 age- and sex-matched control subjects. The cardiac index (CI), stroke index (SI), and systemic vascular resistance (SVR) were assessed non-invasively with a thoracic electrical bioimpedance device before and after intravenous dobutamine therapy. Intermittent intravenous dobutamine therapy resulted in significant improvement in post-intervention FMD compared with baseline (7.7% ± 2.4% vs 1.1% ± 2.6%; P = .001), a finding not evident in control subjects (1.3% ± 2.6% vs 1.2% ± 2.1%; P = .78). There was no significant effect of dobutamine treatment compared with control subjects on NTG-induced vasodilation (7.6% ± 5.5% vs 7.5% ± 8.8%, P = .979). Short-term dobutamine therapy also significantly improved SVR (1797 ± 926 dyne sec/cm 5 vs 2172 ± 1133 dyne sec/cm 5, P = .05), CI (2. 4± 0.6 L/min/m 2 vs 1.9 ± 0.6 L/min/m 2, P = .01), and SI (33.5 ± 11.7 mL/m 2 vs 27.2 ± 12.4 mL/m 2, P = .02). Short-term intermittent intravenous low-dose dobutamine therapy significantly improved vascular endothelial function, perhaps demonstrating an additional mechanism for improved SVR, CI, and SI in patients with severe CHF.