Geert Kleinnibbelink

RV Strain-Area Loop following Selexipag 8 181 risk stratification and follow-up of patients with PAH. Moreover, this may facilitate early identification of responders and non-responders upon pharmacological treatment and support the clinician to switch, add-on or increase dosage of a drug. However, this remain speculative and should be investigated in larger, well-powered studies. Limitations . Some limitations warrant consideration. First, this exploratory study is limited by its restricted sample size of n=8 and may therefore be underpowered. Second, we did not perform right heart catheterisation preventing us to show invasive cardiopulmonary haemodynamic data and relate to echocardiographic RV function. Third, we did only include patients with a treatment of Selexipag. This prevents us to extrapolate our findings in PAH patients using other pharmacological treatment. CONCLUSION In conclusion, this exploratory analysis showed that 17-weeks of Selexipag does not alter RV function in all patients with PAH. However, when stratified to clinical responders vs. non-responders, we found opposite changes in peak longitudinal strain and uncoupling of the RV strain-area loop. Specifically, this means that responders to 17-week Selexipag treatment also demonstrate improvement in RV systolic and diastolic function, while such improvements are absent (or even deteriorated) for RV function in PAH patients that do not demonstrate clinical improvement. This suggests that improvement in RV function may translate to a clinical benefit upon 17-week Selexipag treatment in patients with PAH.