Key result
Inhaled epoprostenol and nitric oxide similarly reduce mPAP in PAH but offer no additive benefit.
Why the study?
Inhaled nitric oxide is used for acute vasoreactivity testing in PAH, but inhaled epoprostenol is less costly and their comparative acute hemodynamic effects and combination effects were unclear.
Does inhaled epoprostenol have comparable acute hemodynamic effects to inhaled nitric oxide in patients with PAH and HFpEF?
RCT (n=19)
cross-over
No
Does inhaled epoprostenol have comparable acute hemodynamic effects to inhaled nitric oxide in patients with PAH and HFpEF?
Effect estimate: r2 = 0.68 for mPAP correlation
p-value: p=<0.001
Inhaled epoprostenol is a viable alternative to inhaled nitric oxide for acute vasoreactivity testing in PAH, but both agents may worsen PAWP in HFpEF patients without providing hemodynamic benefit.
iPGI2 may offer a cost-effective alternative to iNO for PAH vasoreactivity testing; leaves open safety concerns in HFpEF and additive effects.
Inhaled nitric oxide (iNO) is used for acute vasoreactivity testing in pulmonary arterial hypertension (PAH) patients. Inhaled epoprostenol (iPGI2) has pulmonary selectivity and is less costly. We sought to compare acute hemodynamic effects of iNO (20 ppm) and iPGI2 (50 ng/kg/min) and determine whether their combination has additive effects. We conducted a prospective, single center, randomized, cross-over study in 12 patients with PAH and seven with heart failure with preserved ejection fraction (HFpEF). In PAH patients, iNO lowered mean pulmonary artery pressure (mPAP) by 9 ± 12% and pulmonary vascular resistance (PVR) by 14 ± 32% (mean ± SD). iPGI2 decreased mPAP by 10 ± 12% and PVR by 12 ± 36%. Responses to iNO and iPGI2 in mPAP and PVR were directly correlated (r(2) = 0.68, 0.70, respectively, P < 0.001). In HFpEF patients, mPAP dropped by 4 ± 7% with each agent, and PVR dropped by 33 ± 23% with iNO, and by 25 ± 29% with iPGI2 (P = NS). Pulmonary artery wedge pressure (PAWP) increased significantly with iPGI2 versus baseline (20 ± 3 vs. 17 ± 2 mmHg, P = 0.02) and trended toward an increase with iNO and the combination (20 ± 2, 19 ± 4 mmHg, respectively). There were no additive effects in either group. In PAH patients, the vasodilator effects of iNO and iPGI2 correlated at the doses used, making iPGI2 a possible alternative for testing acute vasoreactivity, but their combination lacks additive effect. Exposure of HFpEF patients to inhaled vasodilators worsens the PAWP without hemodynamic benefit.
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Preston et al. (2013) conducted an RCT in Pulmonary arterial hypertension (PAH) and heart failure with preserved ejection fraction (HFpEF) (n=19). Inhaled nitric oxide (iNO) and inhaled epoprostenol (iPGI2) vs. Cross-over comparison and combination was evaluated on Mean pulmonary artery pressure (mPAP) and pulmonary vascular resistance (PVR) (r2 = 0.68 for mPAP correlation, p=<0.001). Inhaled epoprostenol and inhaled nitric oxide produced correlated reductions in mean pulmonary artery pressure (r2=0.68, P<0.001) in PAH patients, with no additive effect when combined.
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