TY - JOUR
T1 - Influence of right ventricular pressure and volume overload on right and left ventricular diastolic function
AU - Right Heart Research Group
AU - Jani, Vivek
AU - Konecny, Filip
AU - Shelby, Aaron
AU - Kulkarni, Aparna
AU - Hammel, James
AU - Schuster, Andreas
AU - Lof, John
AU - Zhan, Junzhen
AU - Barnes, Benjamin
AU - Fernandes, Joao Filipe
AU - Danford, David
AU - Kutty, Shelby
N1 - Funding Information:
Supported by a grant from the Children’s Hospital and Medical Center Foundation , Omaha, Nebraska. F. Konecny receives support from the American Heart Association . V. Jani receives support from the National Institutes of Health (T32 Grant GM73009 ). Transonic Scisense , Inc, provided instrumentation and technical support.
Funding Information:
Supported by a grant from the Children's Hospital and Medical Center Foundation, Omaha, Nebraska. F. Konecny receives support from the American Heart Association. V. Jani receives support from the National Institutes of Health (T32 Grant GM73009). Transonic Scisense, Inc, provided instrumentation and technical support.
Publisher Copyright:
© 2021 The American Association for Thoracic Surgery
PY - 2022/4
Y1 - 2022/4
N2 - Background: Ventricular interdependence may account for altered ventricular mechanics in congenital heart disease. The present study aimed to identify differences in load-dependent right ventricular (RV)–left ventricular (LV) interactions in porcine models of pulmonary stenosis (PS) and pulmonary insufficiency (PI) by invasive admittance-derived hemodynamics in conjunction with noninvasive cardiovascular magnetic resonance (CMR). Methods: Seventeen pigs were used in the study (7 with PS, 7 with PI, and 3 controls). Progressive PS was created by tightening a Teflon tape around the pulmonary artery, and PI was created by excising 2 leaflets of the pulmonary valve. Admittance catheterization data were obtained for the RV and LV at 10 to 12 weeks after model creation, with the animal ventilated under temporary diaphragm paralysis. CMR was performed in all animals immediately prior to pressure–volume catheterization. Results: In the PS group, RV contractility was increased, manifested by increased end-systolic elastance (mean difference, 1.29 mm Hg/mL; 95% confidence interval [CI], 0.57-2.00 mm Hg/mL). However, in the PI group, no significant changes were observed in RV systolic function despite significant changes in RV diastolic function. In the PS group, LV end-systolic volume was significantly lower compared with controls (mean difference, 25.1 mL; 95% CI, -40.5 to -90.7 mL), whereas in the PI group, the LV showed diastolic dysfunction, demonstrated by an elevated isovolumic relaxation constant and ventricular stiffness (mean difference, 0.03 mL−1; 95% CI, -0.02 to 0.09 mL−1). Conclusions: The LV exhibits systolic dysfunction and noncompliance with PI. PS is associated with preserved LV systolic function and evidence of some LV diastolic dysfunction. Interventricular interactions influence LV filling and likely account for differential effects of RV pressure and volume overload on LV function.
AB - Background: Ventricular interdependence may account for altered ventricular mechanics in congenital heart disease. The present study aimed to identify differences in load-dependent right ventricular (RV)–left ventricular (LV) interactions in porcine models of pulmonary stenosis (PS) and pulmonary insufficiency (PI) by invasive admittance-derived hemodynamics in conjunction with noninvasive cardiovascular magnetic resonance (CMR). Methods: Seventeen pigs were used in the study (7 with PS, 7 with PI, and 3 controls). Progressive PS was created by tightening a Teflon tape around the pulmonary artery, and PI was created by excising 2 leaflets of the pulmonary valve. Admittance catheterization data were obtained for the RV and LV at 10 to 12 weeks after model creation, with the animal ventilated under temporary diaphragm paralysis. CMR was performed in all animals immediately prior to pressure–volume catheterization. Results: In the PS group, RV contractility was increased, manifested by increased end-systolic elastance (mean difference, 1.29 mm Hg/mL; 95% confidence interval [CI], 0.57-2.00 mm Hg/mL). However, in the PI group, no significant changes were observed in RV systolic function despite significant changes in RV diastolic function. In the PS group, LV end-systolic volume was significantly lower compared with controls (mean difference, 25.1 mL; 95% CI, -40.5 to -90.7 mL), whereas in the PI group, the LV showed diastolic dysfunction, demonstrated by an elevated isovolumic relaxation constant and ventricular stiffness (mean difference, 0.03 mL−1; 95% CI, -0.02 to 0.09 mL−1). Conclusions: The LV exhibits systolic dysfunction and noncompliance with PI. PS is associated with preserved LV systolic function and evidence of some LV diastolic dysfunction. Interventricular interactions influence LV filling and likely account for differential effects of RV pressure and volume overload on LV function.
KW - congenital heart disease
KW - pressure–volume loop
KW - pulmonary regurgitation
KW - pulmonary stenosis
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U2 - 10.1016/j.jtcvs.2021.07.040
DO - 10.1016/j.jtcvs.2021.07.040
M3 - Article
C2 - 34446290
AN - SCOPUS:85113353597
SN - 0022-5223
VL - 163
SP - e299-e308
JO - Journal of Thoracic and Cardiovascular Surgery
JF - Journal of Thoracic and Cardiovascular Surgery
IS - 4
ER -