Reducing the pressure in pulmonary arterial hypertension: sotatercept, haemodynamics and the right ventricle

Pulmonary arterial hypertension (PAH) is a severe progressive disease characterised by obliterative vascular remodelling and increased resistance in small and medium sized pulmonary arteries. Contributing factors to PAH pathogenesis include genetic mutations including those in bone morphogenetic protein receptor type 2 (BMPR2), perivascular inflammation, systemic immune dysregulation, and imbalanced pulmonary vascular cell proliferation versus apoptosis [1]. We reflect on the crucial role for a reverse remodelling approach supported by the echo and haemodynamic data from this post hoc analysis of STELLAR.