Patient-specific biventricular computational models associated with a normal subject and a patient diagnosed with pulmonary arterial hypertension (PAH) were developed to investigate the effects of this disease on ventricular mechanics. These models were developed using geometry reconstructed from magnetic resonance (MR) images, and constitutive descriptors of passive and active mechanics. Model parameter values associated with ventricular mechanical properties and myofiber architecture were obtained by fitting the models with the corresponding measured pressure-volume loops and the circumferential strain calculated from the MR images using a hyperelastic warping method. Our results shows that the peak right ventricle (RV) pressure was substantially higher in the PAH patient when compared to the normal (65 mmHg vs. 20 mmHg). Circumferential strain (E cc) and ejection fraction (EF) were comparatively lower in both the left ventricle (LV) and RV of the PAH patient (LV EF: 39% vs. 66% and RV EF: 18% vs. 64%; LV E cc :-2.1% vs-9.4% and RV E cc-6.8% vs.-13.2%). On the other hand, passive stiffness, contractility and myofiber stress were all found to be substantially increased in the PAH patient in both the RV and the left ventri-cle (LV). Septum in the PAH patient was also found to possess a smaller curvature than the LV free wall. Simulations using the PAH model with varying RV preload and afterload revealed an approximately linear relationship between the septum curvature and the transseptal pressure gradient at early-diastole and end-systole, respectively. These findings suggest that PAH can induce LV remodeling and measurements of sep-tum curvature may be useful in quantifying the transseptal pressure gradient in PAH patients.