Right ventricular (RV) function is a main determinant of outcome in pulmonary arterial hypertension (PAH) [1]. Increased neuro-humoral activation associated with decreased survival in PAH may worsen RV adaptation to increased afterload [2, 3]. There is rationale therefore for the use of β-blockers in PAH, especially given their beneficial effect on RV function in experimental PAH models [4, 5]. Small clinical studies in PAH using bisoprolol and carvedilol have demonstrated acceptable patient tolerance, however no change in exercise capacity was seen and, concerningly, resting cardiac output (CO) decreased despite unchanged or even mild improvement in RV ejection fraction (EF) [6, 7].