Effects of intravenous sildenafil on hemodynamics and cardiac sympathetic activity in chronic human heart failure

Erectile dysfunction is common in patients with chronic heart failure and sildenafil is an effective treatment option in this population. Sildenafil has been reported to increase sympathetic outflow in normal volunteers. To date, experience with sildenafil in patients with congestive heart failure is limited and the impact of phosphodiesterase-5 inhibition on sympathetic activity in this population has not been evaluated.

Methods and results
10 patients with heart failure (ejection fraction 23 ± 3%) were studied. Generalized and cardiac sympathetic activity responses to an intravenous infusion of sildenafil were measured by the norepinephrine spillover method. In response to sildenafil, there was a significant reduction in mean pulmonary artery (− 26 ± 5%, P < 0.01) and mean arterial pressures (− 8 ± 1%, P < 0.01). These hemodynamic responses were accompanied by a 22 ± 5% reduction in cardiac norepinephrine spillover (P < 0.02) but no change in total body norepinephrine spillover.

The acute administration of sildenafil is associated with a modest reduction in systemic arterial blood pressure and a more substantial reduction in pulmonary arterial pressure. These hemodynamic changes are observed in the absence of systemic sympathetic activation and are associated with a reduction in cardiac norepinephrine spillover in patients with chronic heart failure. These observations are relevant given the high prevalence of erectile dysfunction in this patient population.

Keywords: Autonomic nervous system; Heart failure; Sildenafil

Abdul Al-Hesayena, John S. Florasa and John D. Parker,
Division of Cardiology, Department of Medicine, Mount Sinai Hospital and University Health Network, University of Toronto, Ontario, Canada M5G 1X5

Corresponding author. Mount Sinai and University Health Network Hospitals, University of Toronto, 600 University Avenue, Suite 1609, Toronto, Ontario, Canada M5G 1X5. Tel.: +1 416 586 4794; fax: +1 416 586 8413.

European Journal of Heart Failure
Volume 8, Issue 8 , December 2006, Pages 864-868


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