Circulation, Vol 88, 55-61, Copyright © 1993 by American Heart Association
SD Katz, M Schwarz, J Yuen and TH LeJemtel
BACKGROUND. The vasodilatory response to intra-arterial administration of
acetylcholine is reduced in patients with congestive heart failure compared
with that of normal subjects. The reduced response to acetylcholine may be
related to decreased endothelial release of nitric oxide, interaction with
peripheral alpha-adrenergic transmission, or production of
cyclooxygenase-dependent vasoconstricting substances. The extent to which
each of these mechanisms contributes to the reduced vasodilatory response
to acetylcholine in patients with congestive heart failure is not known.
METHODS AND RESULTS. Thirty-one patients with congestive heart failure (New
York Heart Association functional class II-III) and five age-matched normal
subjects were studied. Regional vascular responses in the forearm to
infusions of acetylcholine, an endothelium-dependent vasodilator (10(-7) to
10(-5) mol/L) and nitroglycerin, an endothelium-independent vasodilator
(10(- 6) mol/L) in the brachial artery were determined with venous
occlusion plethysmography before and after regional alpha-adrenergic
blockade with intra-arterial phentolamine (25 micrograms/min) and systemic
cyclooxygenase with oral indomethacin (50 mg). Administration of
phentolamine significantly increased resting baseline forearm blood flow in
11 patients with congestive heart failure (2.9 +/- 0.4 to 5.4 +/- 0.8
mL.min-1.100 mL-1) and normal subjects (4.6 +/- 0.3 to 11.3 +/- 2.1
mL.min-1.100 mL-1). Before administration of phentolamine, intra- arterial
infusions of acetylcholine 10(-7), 10(-6), and 10(-5) mol/L increased
forearm blood flow to 4.0 +/- 1.0, 6.0 +/- 1.7, and 16.1 +/- 4.0
mL.min-1.100 mL-1, respectively, in patients with congestive heart failure
and to 14.7 +/- 6.2, 20.2 +/- 4.7, and 38.7 +/- 7.9 mL.min- 1.100 mL-1,
respectively, in normal subjects. After administration of phentolamine, the
vasodilatory responses to intra-arterial infusions of acetylcholine and
nitroglycerin did not change in either patients or normal subjects.
Administration of indomethacin did not alter resting forearm blood flow in
15 patients with congestive heart failure (2.7 +/- 0.4 to 2.7 +/- 0.4
mL.min-1.100 mL-1) or normal subjects (4.6 +/- 0.3 to 5.4 +/- 0.8
mL.min-1.100 mL-1). Administration of indomethacin significantly increased
the vasodilatory response to infusion of acetylcholine by an average of 39%
in patients with congestive heart failure but did not change the
vasodilatory response to acetylcholine in normal subjects. In patients with
congestive heart failure, baseline forearm blood flow and the vasodilatory
responses to intra-arterial infusions of acetylcholine and nitroglycerin
were significantly less than those of normal subjects both before and after
administration of phentolamine and indomethacin. CONCLUSIONS. The reduced
vasodilatory response to intra-arterial infusion of acetylcholine in
patients with congestive heart failure probably results from several
coexistent abnormalities in peripheral vascular function, including
abnormal production of cyclooxygenase-dependent vasoconstricting factor,
impaired endothelial release of nitric oxide, and decreased vascular smooth
muscle responsiveness to cyclic GMP-mediated vasodilation.
ARTICLES
Impaired acetylcholine-mediated vasodilation in patients with congestive heart failure. Role of endothelium-derived vasodilating and vasoconstricting factors
Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461.
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