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Phosphodiesterase type 5 inhibition does not reverse endothelial dysfunction in patients with coronary heart disease

S D Robinson1, C A Ludlam, N A Boon

  • 1Centre for Cardiovascular Sciences, University of Edinburgh, Edinburgh EH16 4SB, UK. simon.robinson@ed.ac.uk

Heart (British Cardiac Society)
|May 3, 2005
PubMed

Insights

Sildenafil citrate does not improve blood vessel or blood clotting function in patients with coronary heart disease. This phosphodiesterase type 5 inhibitor is unlikely to reverse generalized vascular dysfunction in these patients.

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology

Background:

  • Coronary heart disease (CHD) is associated with endothelial dysfunction.
  • Sildenafil citrate, a phosphodiesterase type 5 (PDE5) inhibitor, has shown vasodilatory effects.

Purpose of the Study:

  • To investigate the effect of sildenafil citrate on endothelial vasomotor and fibrinolytic function in patients with CHD.

Main Methods:

  • Randomized, double-blind, placebo-controlled, crossover study.
  • 16 male patients with CHD and 8 healthy men received intravenous sildenafil or placebo.
  • Forearm blood flow and tissue plasminogen activator release were measured in response to various infusions.

Main Results:

  • Sildenafil reduced mean arterial blood pressure in both patients and controls.
  • Sildenafil enhanced endothelium-independent vasodilation but did not affect endothelium-dependent responses.
  • Sildenafil did not alter the release of tissue plasminogen activator.

Conclusions:

  • Sildenafil does not improve peripheral endothelial vasomotor or fibrinolytic function in patients with CHD.
  • PDE5 inhibitors are unlikely to reverse generalized vascular dysfunction in CHD.
Abstract

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