title: Transient hemodynamic changes upon changing a BCPA into a TCPC in staged Fontan operation: a computational model study.
abstract: The clinical benefits of the Fontan operation in treating single-ventricle defects have been well documented. However, perioperative mortality or morbidity remains a critical problem. The purpose of the present study was to identify the cardiovascular factors that dominate the transient hemodynamic changes upon the change of a bidirectional cavopulmonary (Glenn) anastomosis (BCPA) into a total cavopulmonary connection (TCPC). For this purpose, two computational models were constructed to represent, respectively, a single-ventricle circulation with a BCPA and that with a TCPC. A series of model-based simulations were carried out to quantify the perioperative hemodynamic changes under various cardiovascular conditions. Obtained results indicated that the presence of a low pulmonary vascular resistance and/or a low lower-body vascular resistance is beneficial to the increase in transpulmonary flow upon the BCPA to TCPC change. Moreover, it was found that ventricular diastolic dysfunction and mitral valve regurgitation, despite being well-known risk factors for poor postoperative outcomes, do not cause a considerable perioperative reduction in transpulmonary flow. The findings may help physicians to assess the perioperative risk of the TCPC surgery based on preoperative measurement of cardiovascular function.
authors: SJTU-CU International Cooperative Research Center, School of Naval Architecture, Ocean and Civil Engineering, Shanghai Jiao Tong University, 800 Dongchuan Road, Shanghai 200240, China.
authors: Fuyou
authors: F
authors: Liang
authors: Hideaki
authors: H
authors: Senzaki
authors: Zhaofang
authors: Z
authors: Yin
authors: Yuqi
authors: Y
authors: Fan
authors: Koichi
authors: K
authors: Sughimoto
authors: Hao
authors: H
authors: Liu
mesh_terms: D018729:Fontan Procedure / Q000009:adverse effects* / Q000379:methods; D018610:Heart Bypass, Right / Q000009:adverse effects* / Q000379:methods; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D008944:Mitral Valve Insufficiency / Q000209:etiology / Q000503:physiopathology; D008954:Models, Biological; D011652:Pulmonary Circulation / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology; D016276:Ventricular Function / Q000502:physiology