Biomechanical and hemodynamic measures of right ventricular diastolic function: Translating tissue biomechanics to clinical relevance

Background--Right ventricular (RV) diastolic function has been associated with outcomes for patients with pulmonary hypertension; however, the relationship between biomechanics and hemodynamics in the right ventricle has not been studied. Methods and Results--Rat models of RV pressure overload were obtained via pulmonary artery banding (PAB; control, n=7; PAB, n=5). At 3 weeks after banding, RV hemodynamics were measured using a conductance catheter. Biaxial mechanical properties of the RV free wall myocardium were obtained to extrapolate longitudinal and circumferential elastic modulus in low and high strain regions (E₁ and E₂, respectively). Hemodynamic analysis revealed significantly increased end-diastolic elastance (E_ed) in PAB (control: 55.1 mm Hg/mL [interquartile range: 44.7-85.4 mm Hg/mL]; PAB: 146.6 mm Hg/mL [interquartile range: 105.8-155.0 mm Hg/mL]; P=0.010). Longitudinal E₁ was increased in PAB (control: 7.2 kPa [interquartile range: 6.7-18.1 kPa]; PAB: 34.2 kPa [interquartile range: 18.1-44.6 kPa]; P=0.018), whereas there were no significant changes in longitudinal E₂ or circumferential E₁ and E₂. Last, wall stress was calculated from hemodynamic data by modeling the right ventricle as a sphere: (stress = Pressure×radius/ 2×thickness). Conclusions--RV pressure overload in PAB rats resulted in an increase in diastolic myocardial stiffness reflected both hemodynamically, by an increase in E_ed, and biomechanically, by an increase in longitudinal E₁. Modest increases in tissue biomechanical stiffness are associated with large increases in E_ed. Hemodynamic measurements of RV diastolic function can be used to predict biomechanical changes in the myocardium.