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Hemodynamic and gas exchange effects of inhaled iloprost in patients with COPD and pulmonary hypertension

Authors Wang L, Jin YZ, Zhao QH, Jiang R, Wu WH, Gong SG, He J, Liu J, Jing ZC

Received 14 May 2017

Accepted for publication 1 August 2017

Published 22 November 2017 Volume 2017:12 Pages 3353—3360

DOI https://doi.org/10.2147/COPD.S141798

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Charles Downs

Peer reviewer comments 2

Editor who approved publication: Dr Richard Russell


Lan Wang,1,* Yuan-Zhe Jin,2,* Qin-Hua Zhao,1 Rong Jiang,1 Wen-hui Wu,1 Su-Gang Gong,1 Jing He,1 Jin-Ming Liu,1 Zhi-Cheng Jing1,3

1Department of Pulmonary Circulation, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China; 2Department of Cardiology, The Fourth Affiliated Hospital of China Medical University, Liaoning, China; 3Thrombosis and Vascular Medicine Center, State Key Laboratory of Cardiovascular Disease, FuWai Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China

*These authors contributed equally to this work

Abstract: Studies have shown that vasodilators such as iloprost can be useful for treating pulmonary hypertension (PH). However, in patients with COPD, vasodilators may inhibit hypoxic pulmonary vasoconstriction and impair gas exchange. The efficacy and safety of iloprost inhalation was assessed in 67 patients with PH associated with COPD (COPD-PH), diagnosed by right heart catheterization. Of these, 37 patients had severe PH (mean pulmonary arterial pressure [mPAP] >35 mmHg or mPAP 25–35 mmHg with low cardiac index [<2.0 L·min-1·m-2]). All patients received a single 20 µg dose of iloprost via a nebulizer (4.4 µg delivered at the mouthpiece). No serious adverse events were reported. Hemodynamic and gas exchange parameters (arterial blood gas and shunt fraction [Qs/Qt]) were measured or calculated at baseline and 10 min after iloprost inhalation. mPAP decreased by 2.1 mmHg (95% CI, -3.3 to -1.0), pulmonary vascular resistance (PVR) decreased by 62.4 dyn·s·cm-5 (95% CI, -92.9 to -31.8), and cardiac output increased by 0.4 L·min-1 (95% CI, 0.2–0.5). There was a more significant decline in PVR in patients with severe COPD-PH than in those with nonsevere COPD-PH. Hypoxemia and intrapulmonary shunt were more extreme in patients with severe COPD-PH. However, there were no significant differences in arterial blood gas and Qs/Qt between patients with nonsevere and severe forms of COPD-PH. In conclusion, iloprost improved pulmonary hemodynamics without detrimental effects on arterial oxygenation in patients with COPD-PH, even in those with severe PH. These findings suggest that the short-term use of iloprost in patients with COPD-PH is effective and well tolerated.

Keywords:
iloprost, pulmonary hypertension, COPD pulmonary gas exchange
 
 

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