PURPOSE: Pulmonary hypertension is a common complication in COPD. Sildenafil and inhaled nitric oxide (iNO) have been demonstrated to cause pulmonary vasodilatation and reduce mean pulmonary arterial pressure (mPAP) COPD patients. We evaluated the acute hemodynamic effect of Sildenafil and iNO in COPD patients with and without pulmonary hypertension.
METHODS: 14 COPD patients, 6 without pulmonary hypertension (COPD non-PH) and 8 with pulmonary hypertension (COPD-PH) underwent right heart catheterisation with vasodilator testing using 20 ppm iNO and 50 mg of oral Sildenafil. mPAP was measured at baseline, after 5 minutes inhalation of 20 ppm NO and 1 hour after oral intake of Sildenafil.
RESULTS: Both patient groups showed a reduction in mPAP after iNO (16 ± 2 to 13 ± 4 mmHg p < 0.05, COPD non-PH and 33 ± 16 to 27 ± 14 mmHg, p = 0.09, COPD-PH). However, Sildenafil effectively reduced mPAP only in COPD non-PH (16 ± 2 to 13 ± 4 mmHg p = 0.06), and not in COPD-PH (33 ± 16 to 32 ± 18 mmHg, p = 0,68). In this group, 3 patients had no change in mPAP and in 2 patients the mPAP increased.
CONCLUSION: Both iNO and Sildenafil reduce mPAP in COPD patients with normal pulmonary artery pressure. However, in COPD patients with associated PH after iNO a reduction in mPAP is observed, but no acute effects are observed after Sildenafil.
CLINICAL IMPLICATIONS: These data suggest that some COPD patients may benefit from medication that acts on the pulmonary vascular bed.
DISCLOSURE: Heleen Rietema, None.