TY - JOUR
T1 - Hemodynamic and gas exchange effects of sildenafil in patients with chronic obstructive pulmonary disease and pulmonary hypertension
AU - Blanco, Isabel
AU - Gimeno, Elena
AU - Munoz, Phillip A.
AU - Pizarro, Sandra
AU - Gistau, Concepción
AU - Rodriguez-Roisin, Robert
AU - Roca, Josep
AU - Barberá, Joan Albert
PY - 2010/2/1
Y1 - 2010/2/1
N2 - Rationale: Sildenafil, a phosphodiesterase-5 inhibitor, could be useful for treating pulmonary hypertension (PH) in chronic obstructive pulmonary disease (COPD). However, vasodilators may inhibit hypoxic pulmonary vasoconstriction and impair gas exchange in this condition. Objectives: To assess the acute hemodynamic and gas exchange effects of sildenafil in patients with COPD-associated PH. Methods: We conducted a randomized, dose comparison trial in 20 patients with COPD-associated PH. Eleven patients were assigned to 20 mg, and 9 patients to 40 mg, of sildenafil. Pulmonary hemodynamics and gas exchange, including ventilation-perfusion (V̇A/Q̇) relationships, were assessed at rest and during constant-work rate exercise, before and 1 hour after sildenafil administration. Measurements and Main Results: Both sildenafil doses reduced the mean pulmonary arterial pressure (PAP) at rest and during exercise, without differences between them. Overall, PAP decreased -6mmHg (95% confidenc einterval [95%CI], -7 to -4) at rest and -11mmHg (95% CI, -14 to 28) during exercise. After sildenafil, PaO2 decreased -6mmHg (95% CI, -8 to -4) at rest because of increased perfusion in units with low V̇A/Q̇ ratio, without differences between doses. No change in PaO2 (95% CI, -3 to 0.2 mm Hg) or V̇A/Q̇ relationships occurred during exercise after sildenafil. Changes induced by sildenafil in PaO2 and V̇A/Q̇ distributions at rest correlated with their respective values at baseline. Conclusions: In patients with COPD-associated PH, sildenafil improves pulmonary hemodynamics at rest and during exercise. This effect is accompanied by the inhibition of hypoxic vasoconstriction, which impairs arterial oxygenation at rest. The use of sildenafil in COPD should be done cautiously and under close monitoring of blood gases. Clinical trial registered with www.clinicaltrials.gov (NCT00491803).
AB - Rationale: Sildenafil, a phosphodiesterase-5 inhibitor, could be useful for treating pulmonary hypertension (PH) in chronic obstructive pulmonary disease (COPD). However, vasodilators may inhibit hypoxic pulmonary vasoconstriction and impair gas exchange in this condition. Objectives: To assess the acute hemodynamic and gas exchange effects of sildenafil in patients with COPD-associated PH. Methods: We conducted a randomized, dose comparison trial in 20 patients with COPD-associated PH. Eleven patients were assigned to 20 mg, and 9 patients to 40 mg, of sildenafil. Pulmonary hemodynamics and gas exchange, including ventilation-perfusion (V̇A/Q̇) relationships, were assessed at rest and during constant-work rate exercise, before and 1 hour after sildenafil administration. Measurements and Main Results: Both sildenafil doses reduced the mean pulmonary arterial pressure (PAP) at rest and during exercise, without differences between them. Overall, PAP decreased -6mmHg (95% confidenc einterval [95%CI], -7 to -4) at rest and -11mmHg (95% CI, -14 to 28) during exercise. After sildenafil, PaO2 decreased -6mmHg (95% CI, -8 to -4) at rest because of increased perfusion in units with low V̇A/Q̇ ratio, without differences between doses. No change in PaO2 (95% CI, -3 to 0.2 mm Hg) or V̇A/Q̇ relationships occurred during exercise after sildenafil. Changes induced by sildenafil in PaO2 and V̇A/Q̇ distributions at rest correlated with their respective values at baseline. Conclusions: In patients with COPD-associated PH, sildenafil improves pulmonary hemodynamics at rest and during exercise. This effect is accompanied by the inhibition of hypoxic vasoconstriction, which impairs arterial oxygenation at rest. The use of sildenafil in COPD should be done cautiously and under close monitoring of blood gases. Clinical trial registered with www.clinicaltrials.gov (NCT00491803).
KW - Arterial oxygen pressure
KW - Phosphodiesterase-5 inhibitors
KW - Pulmonary circulation
KW - Vasodilator agents
KW - Ventilation-perfusion relationships
UR - http://www.scopus.com/inward/record.url?scp=76749160426&partnerID=8YFLogxK
U2 - 10.1164/rccm.200907-0988OC
DO - 10.1164/rccm.200907-0988OC
M3 - Article
C2 - 19875684
AN - SCOPUS:76749160426
SN - 1073-449X
VL - 181
SP - 270
EP - 278
JO - American Journal of Respiratory and Critical Care Medicine
JF - American Journal of Respiratory and Critical Care Medicine
IS - 3
ER -