• Carmine Dario Vizza, Irene M Lang, Roberto Badagliacca, Raymond L Benza, Stephan Rosenkranz, R James White, Yochai Adir, Arne K Andreassen, Vijay Balasubramanian, Sonja Bartolome, Isabel Blanco, Robert C Bourge, Jørn Carlsen, CamachoRafael Enrique CondeRECCritical Medicine and Intensive Care, Pulmonology, Vascular Pulmonary Center, Pulmonology Foundation of Colombia, University Clinic Colombia, Bogota, Colombia., Michele D'Alto, Harrison W Farber, Robert P Frantz, H James Ford, Stefano Ghio, Mardi Gomberg-Maitland, Marc Humbert, Robert Naeije, Stylianos E Orfanos, Ronald J Oudiz, Sergio V Perrone, Oksana A Shlobin, Marc A Simon, Olivier Sitbon, Fernando Torres, Luc VachieryJeanJPulmonary Vascular Diseases and Heart Failure Clinic, Department of Cardiology, Cliniques Universitaires de Bruxelles-Hôpital Erasme, Brussels, Belgium., Kuo-Yang Wang, Magdi H Yacoub, Yan Liu, Gil Golden, and Hiromi Matsubara.
• Dipartimento di Scienze Cliniche Internistiche Anestesiologiche e Cardiovascolari, Università di Roma La Sapienza, Rome, Italy.
• Am. J. Respir. Crit. Care Med. 2022 Apr 1; 205 (7): 751760751-760.

AbstractDespite numerous therapeutic advances in pulmonary arterial hypertension, patients continue to suffer high morbidity and mortality, particularly considering a median age of 50 years. This article explores whether early, robust reduction of right ventricular afterload would facilitate substantial improvement in right ventricular function and thus whether afterload reduction should be a treatment goal for pulmonary arterial hypertension. The earliest clinical studies of prostanoid treatment in pulmonary arterial hypertension demonstrated an important link between lowering mean pulmonary arterial pressure (or pulmonary vascular resistance) and improved survival. Subsequent studies of oral monotherapy or sequential combination therapy demonstrated smaller reductions in mean pulmonary arterial pressure and pulmonary vascular resistance. More recently, retrospective reports of initial aggressive prostanoid treatment or initial combination oral and parenteral therapy have shown marked afterload reduction along with significant improvements in right ventricular function. Some data suggest that reaching threshold levels for pressure or resistance (components of right ventricular afterload) may be key to interrupting the self-perpetuating injury of pulmonary vascular disease in pulmonary arterial hypertension and could translate into improved long-term clinical outcomes. Based on these clues, the authors postulate that improved clinical outcomes might be achieved by targeting significant afterload reduction with initial oral combination therapy and early parenteral prostanoids.

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