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Abstract

A decrease of prostacyclin plays an important role in the pathogenesis of pulmonary arterial hypertension (PAH). Prostacyclin replacement therapy using prostacyclin and prostacyclin analogues has been developed for treatment of PAH. Prostacyclin has not only potent vasodilatory effects but also antiproliferative and pro-apoptotic effects on pulmonary artery smooth muscle cells, which lead to the potential for reverse remodeling of pulmonary arteries. Prostacyclin analogues, iloprost and treprostinil, improve exercise capacity, symptoms, and hemodynamics. Prostacyclin, epoprostenol, improves exercise capacity, symptoms, and hemodynamics and is the only treatment shown to reduce long-term mortality in patients with idiopathic PAH. Furthermore, high-dose intravenous epoprostenol therapy has a potential for remarkable improvement of hemodynamics and exercise capacity. Intravenous delivery of epoprostenol requires a central catheter, which sometimes causes catheter-related troubles. Catheter-related infection is the most serious complication and causes aggravation of PAH. Use of a closed-hub system could prevent bacterial invasion from the catheter hub in patients treated with intravenous epoprostenol. Prostacyclin is a key factor in pathogenesis and treatment of PAH.

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Akagi, S. (2017). Prostacyclin. In: Fukumoto, Y. (eds) Diagnosis and Treatment of Pulmonary Hypertension. Springer, Singapore. https://doi.org/10.1007/978-981-287-840-3_10

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  • DOI: https://doi.org/10.1007/978-981-287-840-3_10

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