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J Am Coll Cardiol, 2000; 35:176-182
© 2000 by the American College of Cardiology Foundation
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CLINICAL STUDIES

A comparison of the acute hemodynamic effects of inhaled nitric oxide and aerosolized iloprost in primary pulmonary hypertension

Marius M. Hoeper, MD*, Horst Olschewski, MD{dagger}, Hossein A. Ghofrani, MD{dagger}, Heinrike Wilkens, MD{ddagger}, Joerg Winkler, MD§, Mathias M. Borst, MD||, Jost Niedermeyer, MD*, Helmut Fabel, MD*, Werner Seeger, MD{dagger} the German PPH Study Group

* Departments of Pulmonary Medicine, Hannover Medical School, Hannover, Germany
{dagger} Department of Internal Medicine, Justus Liebig University, Giessen, Germany
{ddagger} Department of Pulmonary Medicine, University of the Saarland, Homburg, Germany
§ Department of Internal Medicine, University of Leipzig, Heidelberg, Germany
|| Department of Internal Medicine, University of Heidelberg, Heidelberg, Germany

Manuscript received April 22, 1999; revised manuscript received July 23, 1999, accepted September 13, 1999.

Reprint requests and correspondence: Dr. Marius M. Hoeper, Department of Pulmonary Medicine, Hannover Medical School, 30623 Hannover, Germany
KMHoeper{at}AOL.com

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 µg 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·s·cm–5 vs. –183 ± 305 dyne·s·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.

Abbreviations and Acronyms
  CO = cardiac output
  NO = nitric oxide
  NYHA = New York Heart Association
  PCWP = pulmonary capillary wedge pressure
  PGI2 = prostacyclin
  PPH = primary pulmonary hypertension




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