Pulmonary arterial hypertension (PAH) is a fatal, rapidly progressive disease with a 5-year survival rate of 37% if untreated. PAH is characterized by an increase in pulmonary arterial pressure, leading to right ventricular (RV) hypertrophy and eventually RV failure and death. Although RV function mainly determines the clinical outcome of patients with PAH, currently no effective drug exists for the RV. Another important fact in PAH is sex paradox: although PAH occurs ~4 times more frequently in females than in males, females with PAH have better RV function and survival than the males with PAH.

RV failure in PAH is characterized by reduced RV contractility, dilatation and fibrosis. The function decline is associated with structural and mechanical changes. Altered mechanical properties has been reported with PAH development, and acute change of biomechanics can improve RV performance in animal study. RV biomechanics have been shown to be associated with the degree of PAH severity. However, the biology and the associated sex differences of RV biomechanics in PAH are understudied.

The study of mechanobiology has been extensively investigated in the pulmonary vasculature in PAH. Similarly, mechanobiological mechanisms in cardiac remodelling, particularly in the left ventricle, have been widely studied. However, despite the critical role of the RV in PAH progression and outcomes, RV mechanobiology in the condition of PAH remains poorly understood and represents a significant knowledge gap.

This project aims to investigate the mechanobiology mechanism in the right heart and the role of mechanics on right heart failure in PAH.