Extract
Within recent years, right ventricular (RV) function has been recognised as a major determinant of outcome in pulmonary arterial hypertension (PAH) [1, 2]. Clinical [3] and in vitro experimental [4, 5] data suggest that prostacyclins, the treatment of choice for most severely ill PAH patients [6], might have a positive inotropic effect on RV function, and reduce pulmonary vascular resistance (PVR). Nevertheless, inotropic effects are difficult to demonstrate in vivo, as ventricular contractility adjusts to afterload to preserve ventricular-arterial coupling [7]. In fact, the ratio of ventricular end-systolic elastance (Ees), a measure of in vivo contractility, to pulmonary arterial elastance (Ea) or the “coupling ratio” (Ees/Ea), was restored by epoprostenol in a model of load-induced acute RV failure; however, this was explained by a reduction in afterload [8].
Abstract
Prostacyclin reduces right ventricular contractility, but improves ejection fraction and exercise capacity in PAH http://ow.ly/m5S830dpcZv
Footnotes
Support statement: The initial phase of this study (patients 1–15) was supported in part by United Therapeutics Corp., which did not participate in the design of the study, acquisition of data, analysis, interpretation of the results, or writing of the manuscript. The secondary phase of this study (patients 16–33) was supported in part by the U01 grant HL125208-01 from the National Heart Lung and Blood Institute (PVDOMICS) (F.P. Rischard, A.A. Desai, J.X.-J. Yuan and J.G.N. Garcia). Funding information for this article has been deposited with the Crossref Funder Registry.
Conflict of interest: Disclosures can be found alongside this article at erj.ersjournals.com
- Received February 24, 2017.
- Accepted May 29, 2017.
- Copyright ©ERS 2017