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Biomechanical Modeling to Inform Pulmonary Valve Replacement in Tetralogy of Fallot Patients After Complete Repair
M. Gusseva, T. Hussain, CH. Friesen, P. Moireau, A. Tandon, C. Patte, M. Genet, K. Hasbani, G. Greil, D. Chapelle, R. Chabiniok
Language English Country Great Britain
Document type Journal Article, Observational Study, Research Support, Non-U.S. Gov't
Grant support
WT 203148/Z/16/Z
Wellcome
- MeSH
- Models, Biological * MeSH
- Heart Valve Prosthesis Implantation methods MeSH
- Adult MeSH
- Tetralogy of Fallot surgery MeSH
- Hemodynamics physiology MeSH
- Pulmonary Valve Insufficiency congenital diagnosis surgery MeSH
- Cardiac Surgical Procedures methods MeSH
- Humans MeSH
- Magnetic Resonance Imaging, Cine MeSH
- Abnormalities, Multiple * MeSH
- Follow-Up Studies MeSH
- Pulmonary Valve abnormalities diagnostic imaging surgery MeSH
- Reoperation MeSH
- Retrospective Studies MeSH
- Heart Ventricles diagnostic imaging physiopathology MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Observational Study MeSH
- Research Support, Non-U.S. Gov't MeSH
BACKGROUND: A biomechanical model of the heart can be used to incorporate multiple data sources (electrocardiography, imaging, invasive hemodynamics). The purpose of this study was to use this approach in a cohort of patients with tetralogy of Fallot after complete repair (rTOF) to assess comparative influences of residual right ventricular outflow tract obstruction (RVOTO) and pulmonary regurgitation on ventricular health. METHODS: Twenty patients with rTOF who underwent percutaneous pulmonary valve replacement (PVR) and cardiovascular magnetic resonance imaging were included in this retrospective study. Biomechanical models specific to individual patient and physiology (before and after PVR) were created and used to estimate the RV myocardial contractility. The ability of models to capture post-PVR changes of right ventricular (RV) end-diastolic volume (EDV) and effective flow in the pulmonary artery (Qeff) was also compared with expected values. RESULTS: RV contractility before PVR (mean 66 ± 16 kPa, mean ± standard deviation) was increased in patients with rTOF compared with normal RV (38-48 kPa) (P < 0.05). The contractility decreased significantly in all patients after PVR (P < 0.05). Patients with predominantly RVOTO demonstrated greater reduction in contractility (median decrease 35%) after PVR than those with predominant pulmonary regurgitation (median decrease 11%). The model simulated post-PVR decreased EDV for the majority and suggested an increase of Qeff-both in line with published data. CONCLUSIONS: This study used a biomechanical model to synthesize multiple clinical inputs and give an insight into RV health. Individualized modeling allows us to predict the RV response to PVR. Initial data suggest that residual RVOTO imposes greater ventricular work than isolated pulmonary regurgitation.
References provided by Crossref.org
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- $a BACKGROUND: A biomechanical model of the heart can be used to incorporate multiple data sources (electrocardiography, imaging, invasive hemodynamics). The purpose of this study was to use this approach in a cohort of patients with tetralogy of Fallot after complete repair (rTOF) to assess comparative influences of residual right ventricular outflow tract obstruction (RVOTO) and pulmonary regurgitation on ventricular health. METHODS: Twenty patients with rTOF who underwent percutaneous pulmonary valve replacement (PVR) and cardiovascular magnetic resonance imaging were included in this retrospective study. Biomechanical models specific to individual patient and physiology (before and after PVR) were created and used to estimate the RV myocardial contractility. The ability of models to capture post-PVR changes of right ventricular (RV) end-diastolic volume (EDV) and effective flow in the pulmonary artery (Qeff) was also compared with expected values. RESULTS: RV contractility before PVR (mean 66 ± 16 kPa, mean ± standard deviation) was increased in patients with rTOF compared with normal RV (38-48 kPa) (P < 0.05). The contractility decreased significantly in all patients after PVR (P < 0.05). Patients with predominantly RVOTO demonstrated greater reduction in contractility (median decrease 35%) after PVR than those with predominant pulmonary regurgitation (median decrease 11%). The model simulated post-PVR decreased EDV for the majority and suggested an increase of Qeff-both in line with published data. CONCLUSIONS: This study used a biomechanical model to synthesize multiple clinical inputs and give an insight into RV health. Individualized modeling allows us to predict the RV response to PVR. Initial data suggest that residual RVOTO imposes greater ventricular work than isolated pulmonary regurgitation.
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- $a Hussain, Tarique $u Division of Pediatric Cardiology, Department of Pediatrics, UT Southwestern Medical Center, Dallas, Texas, USA
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- $a Chabiniok, Radomír $u Inria, Palaiseau, France; LMS, École Polytechnique, CNRS, Institut Polytechnique de Paris, Palaiseau, France; Division of Pediatric Cardiology, Department of Pediatrics, UT Southwestern Medical Center, Dallas, Texas, USA; School of Biomedical Engineering & Imaging Sciences, St Thomas' Hospital, King's College London, London, United Kingdom; Department of Mathematics, Faculty of Nuclear Sciences and Physical Engineering, Czech Technical University in Prague, Prague, Czech Republic. Electronic address: radomir.chabiniok@UTSouthwestern.edu
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