Key result
Pulmonary arterial hypertension was associated with substantially higher peak right ventricular pressure (65 vs 20 mmHg) and reduced ejection fraction in both ventricles compared to a normal subject.
Why the study?
How does pulmonary arterial hypertension alter biventricular mechanics compared to a normal subject?
How does pulmonary arterial hypertension alter biventricular mechanics compared to a normal subject?
Patient-specific computational modeling demonstrates that PAH induces significant biventricular mechanical alterations, including LV remodeling, and suggests septum curvature may be useful for quantifying transseptal pressure gradients.
Patient-specific PAH models suggest biventricular involvement; leaves open septum curvature for quantifying transseptal gradients in larger studies.
Patient-specific biventricular computational models associated with a normal subject and a pulmonary arterial hypertension (PAH) patient were developed to investigate the disease effects on ventricular mechanics. These models were developed using geometry reconstructed from magnetic resonance (MR) images, and constitutive descriptors of passive and active mechanics in cardiac tissues. Model parameter values associated with ventricular mechanical properties and myofiber architecture were obtained by fitting the models with measured pressure-volume loops and circumferential strain calculated from MR images using a hyperelastic warping method. Results show that the peak right ventricle (RV) pressure was substantially higher in the PAH patient (65 mmHg versus 20 mmHg), who also has a significantly reduced ejection fraction (EF) in both ventricles (left ventricle (LV): 39% versus 66% and RV: 18% versus 64%). Peak systolic circumferential strain was comparatively lower in both the left ventricle (LV) and RV free wall (RVFW) of the PAH patient (LV: -6.8% versus -13.2% and RVFW: -2.1% versus -9.4%). Passive stiffness, contractility, and myofiber stress in the PAH patient were all found to be substantially increased in both ventricles, whereas septum wall in the PAH patient possessed a smaller curvature than that in the LV free wall. Simulations using the PAH model revealed an approximately linear relationship between the septum curvature and the transseptal pressure gradient at both early-diastole and end-systole. These findings suggest that PAH can induce LV remodeling, and septum curvature measurements may be useful in quantifying transseptal pressure gradient in PAH patients.
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Xi et al. (2016) studied Pulmonary Arterial Hypertension (n=2). Pulmonary arterial hypertension vs. Normal subject was evaluated on Ventricular mechanics (peak RV pressure, ejection fraction, circumferential strain). Pulmonary arterial hypertension was associated with substantially higher peak right ventricular pressure (65 vs 20 mmHg) and reduced ejection fraction in both ventricles compared to a normal subject.
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