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Epoprostenol sodium for treatment of pulmonary arterial hypertension

Authors Saito Y, Nakamura K, Akagi S, Sarashina T, Ejiri K, Miura A, Ogawa A, Matsubara H, Ito H

Received 5 January 2015

Accepted for publication 18 March 2015

Published 14 May 2015 Volume 2015:11 Pages 265—270

DOI https://doi.org/10.2147/VHRM.S50368

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 4

Editor who approved publication: Dr Daniel Duprez


Yukihiro Saito,1 Kazufumi Nakamura,1 Satoshi Akagi,1 Toshihiro Sarashina,1 Kentaro Ejiri,1 Aya Miura,1 Aiko Ogawa,2 Hiromi Matsubara,2 Hiroshi Ito1

1Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan; 2Division of Cardiology, National Hospital Organization Okayama Medical Center, Okayama, Japan

Abstract: The release of endogenous prostacyclin (PGI2) is depressed in patients with pulmonary arterial hypertension (PAH). PGI2 replacement therapy by epoprostenol infusion is one of the best treatments available for PAH. Here, we provide an overview of the current clinical data for epoprostenol. Epoprostenol treatment improves symptoms, exercise capacity, and hemodynamics, and is the only treatment that has been shown to reduce mortality in patients with idiopathic PAH (IPAH) in randomized clinical trials. We have reported that high-dose epoprostenol therapy (>40 ng/kg/min) also results in marked hemodynamic improvement in some patients with IPAH. High-dose epoprostenol has a pro-apoptotic effect on PAH-PASMCs via the IP receptor and upregulation of Fas ligand (FasL) in vitro. However, long-term intravenous administration of epoprostenol is sometimes associated with catheter-related infections and leads to considerable inconvenience for the patient. In the future, the development of new routes of administration or the development of powerful PGI2 analogs, IP-receptor agonists, and gene and cell-based therapy enhancing PGI2 production with new routes of administration is required.

Keywords: pulmonary arterial hypertension, prostacyclin, apoptosis

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