July 2021 Br J Cardiol 2021;28:105–8 doi:10.5837/bjc.2021.032
Sarah Cullivan, Anandan Natarajan, Niamh Boyle, Ciara McCormack, Sean Gaine, Brian McCullagh
Abstract
Introduction
Pulmonary arterial hypertension (PAH) is a devastating disease characterised by irreversible pulmonary vascular proliferation and remodelling, resulting ultimately in right heart failure. Current therapy targets the nitric oxide, endothelin and prostacyclin pathways to promote pulmonary vasodilatation and reduce right ventricular afterload.1,2 Selexipag is an oral selective prostacyclin-receptor agonist that is used in the treatment of PAH. In the GRIPHON (Prostacyclin [PGI2] Receptor Agonist In Pulmonary Arterial Hypertension) trial the optimum dose of selexipag for maximum therapeutic benefit frequently differed between individ
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