Biomechanical and Hemodynamic Measures of Right Ventricular Diastolic Function: Translating Tissue Biomechanics to Clinical Relevance
Vanderpool, Rebecca R.
Bachman, Timothy N.
Simon, Marc A.
AffiliationUniv Arizona, Dept Med
MetadataShow full item record
CitationBiomechanical and Hemodynamic Measures of Right Ventricular Diastolic Function: Translating Tissue Biomechanics to Clinical Relevance 2017, 6 (9):e006084 Journal of the American Heart Association
Rights© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License.
Collection InformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at firstname.lastname@example.org.
AbstractBackground 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 (E-1 and E-2, respectively). Hemodynamic analysis revealed significantly increased end-diastolic elastance (E-ed) in PAB (control: 55.1 mm Hg/mL [interquartile range: 44.785.4 mm Hg/mL]; PAB: 146.6 mm Hg/mL [interquartile range: 105.8155.0 mm Hg/mL]; P=0.010). Longitudinal E1 was increased in PAB (control: 7.2 kPa [interquartile range: 6.718.1 kPa]; PAB: 34.2 kPa [interquartile range: 18.144.6 kPa]; P=0.018), whereas there were no significant changes in longitudinal E-2 or circumferential E-1 and E-2. Last, wall stress was calculated from hemodynamic data by modeling the right ventricle as a sphere: (stress = Pressure x radius/2 x 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 E-1. 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.
NoteOpen Access Journal; Creative Commons Attribution Non-Commercial License
VersionFinal published version
SponsorsAmerican Heart Association [10BGIA3790022]; Pittsburgh Foundation [M2010-0052]; National Institutes of Health [P01 HL103455]