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J Am Coll Cardiol, 2000; 36:845-851 © 2000 by the American College of Cardiology Foundation |
a Division of Circulatory Physiology, Columbia Presbyterian Medical Center, New York, New YorkUSA
b Division of Cardiology, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York, USA
Manuscript received August 13, 1999; revised manuscript received March 7, 2000, accepted April 14, 2000.
Reprint requests and correspondence: Dr. Stuart D. Katz, Columbia Presbyterian Medical Center, Division of Circulatory Physiology, Room MHB5-435, 177 Fort Washington Avenue, New York, New York 10032
sdk8{at}columbia.edu
OBJECTIVES
To determine the acute effects of type 5 phosphodiesterase inhibition with sildenafil on flow-mediated vasodilation in the brachial artery of patients with chronic heart failure.
BACKGROUND
Impaired endothelium-dependent, flow-mediated vasodilation in patients with heart failure is partly attributable to hyporesponsiveness of cyclic guanosine monophosphate (cGMP) mediated vasorelaxation effector mechanisms in vascular smooth muscle. The effect of inhibition of cGMP degradation with sildenafil, a specific type 5 cGMP phosphodiesterase inhibitor, on flow-mediated dilation in heart failure is unknown.
METHODS
Flow-mediated vasodilation after release of 1, 3 and 5 min of transient arterial occlusion was measured in the brachial artery with high resolution two-dimensional ultrasound imaging in 48 patients with chronic heart failure before and 1 h after randomized, double-blind assignment to a single oral dose of sildenafil 12.5, 25 or 50 mg or matching placebo.
RESULTS
In response to oral administration of a single dose of study drug, the change in flow-mediated vasodilation after release of 1, 3 and 5 min of arterial occlusion was significantly greater in patients receiving sildenafil 25 mg (3.3 ± 1.9, 3.8 ± 1.8 and 4.0 ± 1.8%, respectively, p < 0.05) and patients receiving sildenafil 50 mg (3.7 ± 1.3, 4.1 ± 1.1, 3.9 ± 1.3%, respectively, p < 0.05) than that of patients receiving placebo (0.7 ± 1.1, 0.2 ± 1.2, 0.6 ± 0.8%, respectively).
CONCLUSIONS
Acute type 5 phosphodiesterase inhibition with sildenafil 25 and 50 mg increases endothelium-dependent, flow-mediated vasodilation in patients with chronic heart failure when compared with placebo.
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