Sildenafil improves the alveolar-capillary function in heart failure patients

Sildenafil is used for pulmonary hypertension treatment and its use is safe in chronic heart failure (HF) patients.

To analyze the effects of sildenafil on lung mechanics, gas diffusion, exhaled nitric oxide (eNO) at rest and during exercise in chronic HF. We did so to evaluate if sildenafil prevents exercise-induced pulmonary edema formation.

We studied 22 chronic HF males. We measured after a single dose of placebo, sildenafil (25 mg) and sildenafil (100 mg), lung diffusion (DLCO), molecular diffusion (DM), pulmonary capillary volume (VC), eNO, all at rest and during exercise, standard pulmonary function, and maximal cardiopulmonary exercise.

At rest sildenafil improved pulmonary mechanics and DLCO from 23.1+/-6.3 ml/mmHg/min to 23.9+/-6.4 (25 mg, p<0.05) and to 25.3+/-6.7 100 mg, p<0.02). Sildenafil (100 mg) prevents edema formation (highest DM/VC during exercise). At rest eNO was low and not affected by tested drugs. With light exercise eNO was higher with sildenafil 100 mg. Peak VO(2) increased with sildenafil from 1376+/-331 ml/min to 1471+/-375 (25 mg, p<0.01) and 1524+/-461 (100 mg, p<0.02). Peak VO(2) increase was related to DLCO improvement.

In chronic HF sildenafil increases exercise performance, improves lung mechanics and gas diffusion and prevents exercise-induced pulmonary edema formation probably by restoring NO pathways.