Key result
Aerosolized iloprost reduces pulmonary artery pressure ~4 mmHg more than inhaled nitric oxide in PPH.
Why the study?
Inhalation of the stable prostacyclin analogue iloprost was recently described as a novel therapeutic strategy for PPH and may offer an alternative to continuous intravenous prostacyclin or inhaled NO, motivating a comparison of the acute hemodynamic effects of inhaled NO and aerosolized iloprost.
Does aerosolized iloprost produce greater acute improvements in pulmonary hemodynamics compared to inhaled nitric oxide in patients with primary pulmonary hypertension?
Does aerosolized iloprost produce greater acute improvements in pulmonary hemodynamics compared to inhaled nitric oxide in patients with primary pulmonary hypertension?
During acute hemodynamic testing in primary pulmonary hypertension, aerosolized iloprost is a more potent pulmonary vasodilator than inhaled nitric oxide at the tested doses.
Answers are grounded in this paper and cite their sources.
Aerosolized iloprost may provide greater acute pulmonary vasodilation than inhaled NO in PPH; leaves open optimal agent selection and long-term outcomes.
Objective We sought to compare the acute hemodynamic effects of inhaled nitric oxide (NO) and aerosolized iloprost in primary pulmonary hypertension (PPH). Background Inhalation of the stable prostacyclin analogue iloprost has recently been described as a novel therapeutic strategy for PPH and may offer an alternative to continuous intravenous infusion of prostacyclin or inhalation of NO. Methods During right heart catheterization, 35 patients with PPH sequentially inhaled 40 ppm of NO and 14 to 17 microg of iloprost, and the effects on hemodynamics and blood gases were monitored. Results Both NO and iloprost caused significant increases in cardiac output, mixed-venous oxygen saturation and stroke volume as well as significant decreases in pulmonary artery pressure and pulmonary vascular resistance, whereas only inhaled iloprost significantly increased the arterial PO2 (p = 0.01). Compared with inhaled NO, aerosolized iloprost was more effective in reducing pulmonary artery pressure (-8.3 +/- 7.5 mm Hg vs. -4.3 +/- 8.8 mm Hg; p = 0.0001) and the pulmonary vascular resistance (-447 +/- 340 dynes x s x cm(-5) vs. -183 +/- 305 dyne x s x cm(-5); p < 0.0001). Furthermore, aerosolized iloprost caused a significantly greater increase of the cardiac output compared with NO (+0.7 +/- 0.6 liter/min vs. +0.3 +/- 0.4 liter/min; p = 0.0002) and had a more pronounced effect on the mixed-venous oxygen saturation (p = 0.003). Conclusions During acute drug testing, aerosolized iloprost was more potent than inhaled NO as a pulmonary vasodilator in PPH at the doses used in this study.
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Hoeper et al. (2000) studied Primary pulmonary hypertension (PPH) (n=35). Aerosolized iloprost vs. Inhaled nitric oxide (40 ppm) was evaluated on Acute change in pulmonary artery pressure and pulmonary vascular resistance (p=0.0001). Aerosolized iloprost reduced pulmonary artery pressure and vascular resistance more effectively than inhaled nitric oxide in PPH.
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