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(Circulation. 1999;99:60-64.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Department of Medicine, Division of Cardiology, The Albert Einstein College of Medicine, Bronx, NY.
Correspondence to Thierry H. Lejemtel, MD, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461.
BackgroundIn patients with severe congestive heart failure (CHF), short-term administration of dobutamine exerts sustained clinical benefits that are partially mediated by a training-like effect on skeletal muscle. Recently, physical training has been shown to enhance endothelial function in the skeletal muscle vasculature by improving endothelial function. Whether the dobutamine-induced training effect is also associated with an improvement in endothelial function in the skeletal muscle vasculature is currently unknown.
Methods and ResultsFlow-mediated vasodilation in response to
peak reactive hyperemia was evaluated in the forearms of 9
patients with severe CHF who were treated with dobutamine
for 72 hours. Resting and peak hyperemic brachial artery blood
flow and diameter (BABF [mL/min] and BAD [mm], respectively) were
measured by 2-dimensional and Doppler ultrasonography at baseline,
at 3 and 72 hours during dobutamine infusion, and at 2 and
4 weeks after discontinuation of dobutamine therapy. In
addition, the brachial artery response to sublingual (SL)
administration of nitroglycerin (NTG) was evaluated at
baseline and at 2 and 4 weeks after discontinuation of
dobutamine therapy. Ten patients with severe CHF who did
not receive dobutamine served as control subjects. Resting
BABF was significantly increased at 3 and 72 hours (391.2±31.8 and
366.8±31.0 mL/min, respectively, compared with 289.8±18.6 mL/min at
baseline; P<0.05). Peak hyperemic BABF was not
altered by dobutamine infusion compared with baseline
values. The increase in BAD during peak hyperemic response was
greater after infusion of dobutamine for 72 hours
(15.2±2.7% versus 9.1±1.8%, P<0.05) and remained
significantly greater for
2 weeks after discontinuation of
dobutamine (12.3±2.2% versus 9.1±1.8%,
P<0.05). In contrast to the peak hyperemic
response, the increase in BAD (%) induced by SL NTG was unchanged by
administration of dobutamine for 72 hours. Two and 4 weeks
after discontinuation of dobutamine, NTG-induced increases
in BAD were similar to the BAD noted at baseline.
ConclusionsIn patients with severe CHF, short-term
administration of dobutamine for 72 hours selectively
improves vascular endothelial function for
2 weeks.
Key Words: heart failure nitroglycerin vasodilation
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