TY - JOUR
T1 - Prediction of hemodynamics after atrial septal defect closure using a framework of circulatory equilibrium in dogs
AU - Uike, Kiyoshi
AU - Saku, Keita
AU - Nishikawa, Takuya
AU - Yamamura, Kenichiro
AU - Nagata, Hazumu
AU - Muraoka, Mamoru
AU - Ohga, Shouichi
AU - Tsutsui, Hiroyuki
AU - Sunagawa, Kenji
N1 - Funding Information:
This work was supported by Research and Development of Supportive Device Technology for Medicine using Information and Communication Technology from Japan Agency for Medical Research and Development (JP18he1102003), Development of Advanced Measurement and Analysis Systems from Japan Agency for Medical Research and Development (JP18hm0102041), Mirai-iryou from Japan Agency for Medical Research and Development (JP18he1902003), Actelion Academia Prize 2015, the Japan Society for the Promotion of Science (18K15893, 19K17605), and the Japan Foundation for Applied Enzymology (VBIC: Vascular Biology of Innovation).
Funding Information:
K. Saku and K. Sunagawa received research funding from Omron Healthcare Co. K. Saku received honoraria from Japan Abiomed. H. Tsutsui received honoraria from Otsuka, Takeda Pharmaceuticals, Mitsubishi-Tanabe Pharma, Daiichi Sankyo, Nippon Boehringer, Bayer Yakuhin, Pfizer, Novartis Pharma, Ono Pharmaceutical, MSD, Teijin Pharma, Bristol-Myers Squibb, and Astellas Pharma; manuscript fees from Medical View and Nippon Rinsho; and research funding from Nippon Boehringer, Mitsubishi-Tanabe Pharma, Japan Tobacco, Daiichi Sankyo, IQVIA Services Japan, Takeda Pharmaceutical, Bayer Yakuhin, Sanofi, Acterion Pharmaceuticals Japan, and MSD. None of the other authors has any conflicts of interest, financial or otherwise, to disclose.
Publisher Copyright:
Copyright © 2020 the American Physiological Society
PY - 2020/10/15
Y1 - 2020/10/15
N2 - In patients with heart failure, atrial septal defect (ASD) closure has a risk of inducing life-threatening acute pulmonary edema. The objective of this study was to develop a novel framework for quantitative prediction of hemodynamics after ASD closure. The generalized circulatory equilibrium comprises right and left cardiac output (CO) curves and pulmonary and systemic venous return surfaces. We incorporated ASD into the framework of circulatory equilibrium by representing ASD shunt flow (QASD) by the difference between pulmonary flow (QP) and systemic flow (QS). To examine the accuracy of prediction, we created ASD in six dogs. Four weeks after ASD creation, we measured left atrial pressure (PLA), right atrial pressure (PRA), QP, and Qs before and after ASD balloon occlusion. We then predicted postocclusion hemodynamics from measured preocclusion hemodynamics. Finally, we numerically simulated hemodynamics under various ASD diameters while changing left and right ventricular function. Predicted postocclusion PLA, PRA, and QS from preocclusion hemodynamics matched well with those measured [PLA: coefficient of determination (r2) = 0.96, standard error of estimate (SEE) = 0.89 mmHg, PRA: r2 = 0.98, SEE = 0.26 mmHg, QS: r2 = 0.97, SEE = 5.6 mL·min-1·kg-1]. A simulation study demonstrated that ASD closure increases the risk of pulmonary edema in patients with impaired left ventricular function and normal right ventricular function, indicating the importance of evaluation for the balance between right and left ventricular function. ASD shunt incorporated into the generalized circulatory equilibrium accurately predicted hemodynamics after ASD closure, which would facilitate safety management of ASD closure. NEW & NOTEWORTHY We developed a framework to predict the impact of atrial septal defect (ASD) closure on hemodynamics by incorporating ASD shunt flow into the framework of circulatory equilibrium. The proposed framework accurately predicted hemodynamics after ASD closure. Patient-specific prediction of hemodynamics may be useful for safety management of ASD closure.
AB - In patients with heart failure, atrial septal defect (ASD) closure has a risk of inducing life-threatening acute pulmonary edema. The objective of this study was to develop a novel framework for quantitative prediction of hemodynamics after ASD closure. The generalized circulatory equilibrium comprises right and left cardiac output (CO) curves and pulmonary and systemic venous return surfaces. We incorporated ASD into the framework of circulatory equilibrium by representing ASD shunt flow (QASD) by the difference between pulmonary flow (QP) and systemic flow (QS). To examine the accuracy of prediction, we created ASD in six dogs. Four weeks after ASD creation, we measured left atrial pressure (PLA), right atrial pressure (PRA), QP, and Qs before and after ASD balloon occlusion. We then predicted postocclusion hemodynamics from measured preocclusion hemodynamics. Finally, we numerically simulated hemodynamics under various ASD diameters while changing left and right ventricular function. Predicted postocclusion PLA, PRA, and QS from preocclusion hemodynamics matched well with those measured [PLA: coefficient of determination (r2) = 0.96, standard error of estimate (SEE) = 0.89 mmHg, PRA: r2 = 0.98, SEE = 0.26 mmHg, QS: r2 = 0.97, SEE = 5.6 mL·min-1·kg-1]. A simulation study demonstrated that ASD closure increases the risk of pulmonary edema in patients with impaired left ventricular function and normal right ventricular function, indicating the importance of evaluation for the balance between right and left ventricular function. ASD shunt incorporated into the generalized circulatory equilibrium accurately predicted hemodynamics after ASD closure, which would facilitate safety management of ASD closure. NEW & NOTEWORTHY We developed a framework to predict the impact of atrial septal defect (ASD) closure on hemodynamics by incorporating ASD shunt flow into the framework of circulatory equilibrium. The proposed framework accurately predicted hemodynamics after ASD closure. Patient-specific prediction of hemodynamics may be useful for safety management of ASD closure.
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U2 - 10.1152/AJPHEART.00098.2020
DO - 10.1152/AJPHEART.00098.2020
M3 - Article
C2 - 32886004
AN - SCOPUS:85093538955
SN - 0363-6135
VL - 319
SP - H938-H947
JO - American Journal of Physiology
JF - American Journal of Physiology
IS - 5
ER -