Pulmonary arterial hypertension causes an increase in the mechanical loading imposed on the right ventricle that results in progressive changes to its mechanics and function. Here, we quantify the mechanical changes associated with PAH by assimiliating clinical data consisting of reconstructed 3D geometry, pressure and volume waveforms as well as regional strains measured in PAH patients (n = 12) and controls (n = 6) within a computational modeling framework of the ventricles. Modeling parameters reflecting regional passive stiness and load-independent contractility as indexed by the tissue active tension were optimized so that simulation results matched the measurements The optimized parameters were compared with clinical metrics to and usable indicators associated with the underlying mechanical changes. Peak contractility of the RV free wall γRWFW,max was found to be strongly correlated, and had an inverse relationship with the RV and left ventricle end-diastolic volume ratio (i.e., RVEDV/LVEDV) (γRWFW,max=-0.13(RVEDV/LVEDV)+0.44, R2=0.77). Correlation with RV ejection fraction (R2=0.5) and end-diastolic volume index (R2=0.4) were comparatively weaker. Patients with RVEDV/LVEDV≤1.5 had 18% higher γRWFW,max (P = 0.09) than that of the control whereas those with RVEDV/LVEDV > 1.5 had 25% lower γRWFW,max (P<0.05). On average, RVFW passive stiffness increased progressively with the degree of remodeling as indexed by RVEDV/LVEDV and RVFW myofiber stress was increased by 49% only in patients with RVEDV/LVEDV ≥ 1.5 (P = 0.14). These results provide the mechanical basis of using RVEDV/LVEDV as a clinical index for delineating disease severity and estimating RVFW contractility in PAH patients.