TY - JOUR
T1 - Right ventricular myocardial energetic model for evaluating right heart function in pulmonary arterial hypertension
AU - Scott, Jacqueline V.
AU - Tembulkar, Tanuf U.
AU - Lee, Meng-Lin
AU - Faliks, Bradley T.
AU - Koch, Kelly L.
AU - Vonk-Noordegraaf, Anton
AU - Cook, Keith E.
N1 - Funding Information: This project was funded in part by an NIH grant (National Institutes of Health, R01 HL089043, PI: Dr. Keith Cook, ARRA Administrative Supplement to Compliant Thoracic Artificial Lungs). Publisher Copyright: © 2022 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.
PY - 2022/5/1
Y1 - 2022/5/1
N2 - Background: Pulmonary arterial hypertension (PAH) increases right ventricular (RV) workload and decreases myocardial oxygen reserve, eventually leading to poor cardiac output. This study created and assessed a novel model of RV work output based on RV hemodynamics and oxygen supply, allowing new insight into causal mechanisms of RV dysfunction. Methods: The RV function model was built upon an earlier, left ventricular model and further adjusted for more accurate clinical use. The model assumes that RV total power output (1) is the sum of isovolumic and stroke power and (2) is linearly related to its right coronary artery oxygen supply. Thus, when right coronary artery flow is limited or isovolumic power is elevated, less energy is available for producing cardiac output. The original and adjusted models were validated via data from patients with idiopathic PAH (n = 14) and large animals (n = 6) that underwent acute pulmonary banding with or without hypoxia. Results: Both models demonstrated strong, significant correlations between RV oxygen consumption rate and RV total power output for PAH patients (original model, R 2 = 0.66; adjusted model, R 2 = 0.78) and sheep (original, R 2 = 0.85; adjusted, R 2 = 0.86). Furthermore, the models demonstrate a significant inverse relationship between required oxygen consumption and RV efficiency (stroke power/total power) (p < 0.001). Lastly, higher NYHA class was indicative of lower RV efficiency and higher oxygen consumption (p = 0.013). Conclusion: Right ventricular total power output can be accurately estimated directly from pulmonary hemodynamics and right coronary perfusion during PAH. This model highlights the increased vulnerability of PAH patients with compromised right coronary flow coupled with high afterload.
AB - Background: Pulmonary arterial hypertension (PAH) increases right ventricular (RV) workload and decreases myocardial oxygen reserve, eventually leading to poor cardiac output. This study created and assessed a novel model of RV work output based on RV hemodynamics and oxygen supply, allowing new insight into causal mechanisms of RV dysfunction. Methods: The RV function model was built upon an earlier, left ventricular model and further adjusted for more accurate clinical use. The model assumes that RV total power output (1) is the sum of isovolumic and stroke power and (2) is linearly related to its right coronary artery oxygen supply. Thus, when right coronary artery flow is limited or isovolumic power is elevated, less energy is available for producing cardiac output. The original and adjusted models were validated via data from patients with idiopathic PAH (n = 14) and large animals (n = 6) that underwent acute pulmonary banding with or without hypoxia. Results: Both models demonstrated strong, significant correlations between RV oxygen consumption rate and RV total power output for PAH patients (original model, R 2 = 0.66; adjusted model, R 2 = 0.78) and sheep (original, R 2 = 0.85; adjusted, R 2 = 0.86). Furthermore, the models demonstrate a significant inverse relationship between required oxygen consumption and RV efficiency (stroke power/total power) (p < 0.001). Lastly, higher NYHA class was indicative of lower RV efficiency and higher oxygen consumption (p = 0.013). Conclusion: Right ventricular total power output can be accurately estimated directly from pulmonary hemodynamics and right coronary perfusion during PAH. This model highlights the increased vulnerability of PAH patients with compromised right coronary flow coupled with high afterload.
KW - pulmonary arterial hypertension
KW - right heart failure
KW - right ventricular energetics
UR - http://www.scopus.com/inward/record.url?scp=85130160532&partnerID=8YFLogxK
U2 - https://doi.org/10.14814/phy2.15136
DO - https://doi.org/10.14814/phy2.15136
M3 - Article
C2 - 35582996
SN - 2051-817X
VL - 10
JO - Physiological reports
JF - Physiological reports
IS - 10
M1 - e15136
ER -