Computational Modeling of Right Ventricular Motion and Intracardiac Flow in Repaired Tetralogy of Fallot

Author(s):  
Yue-Hin Loke ◽  
Francesco Capuano ◽  
Elias Balaras ◽  
Laura J. Olivieri
2018 ◽  
Vol 315 (6) ◽  
pp. H1691-H1702 ◽  
Author(s):  
Pia Sjöberg ◽  
Johannes Töger ◽  
Erik Hedström ◽  
Per Arvidsson ◽  
Einar Heiberg ◽  
...  

Intracardiac hemodynamic forces have been proposed to influence remodeling and be a marker of ventricular dysfunction. We aimed to quantify the hemodynamic forces in patients with repaired tetralogy of Fallot (rToF) to further understand the pathophysiological mechanisms as this could be a potential marker for pulmonary valve replacement (PVR) in these patients. Patients with rToF and pulmonary regurgitation (PR) > 20% ( n = 18) and healthy control subjects ( n = 15) underwent MRI, including four-dimensional flow. A subset of patients ( n = 8) underwent PVR and MRI after surgery. Time-resolved hemodynamic forces were quantified using 4D-flow data and indexed to ventricular volume. Patients had higher systolic and diastolic left ventricular (LV) hemodynamic forces compared with control subjects in the lateral-septal/LV outflow tract ( P = 0.011 and P = 0.0031) and inferior-anterior ( P < 0.0001 and P < 0.0001) directions, which are forces not aligned with blood flow. Forces did not change after PVR. Patients had higher RV diastolic forces compared with control subjects in the diaphragm-right ventricular (RV) outflow tract (RVOT; P < 0.001) and apical-basal ( P = 0.0017) directions. After PVR, RV systolic forces in the diaphragm-RVOT direction decreased ( P = 0.039) to lower levels than in control subjects ( P = 0.0064). RV diastolic forces decreased in all directions ( P = 0.0078, P = 0.0078, and P = 0.039) but were still higher than in control subjects in the diaphragm-RVOT direction ( P = 0.046). In conclusion, patients with rToF and PR had LV hemodynamic forces less aligned with intraventricular blood flow compared with control subjects and higher diastolic RV forces along the regurgitant flow direction in the RVOT and that of tricuspid inflow. Remaining force differences in the LV and RV after PVR suggest that biventricular pumping does not normalize after surgery. NEW & NOTEWORTHY Biventricular hemodynamic forces in patients with repaired tetralogy of Fallot and pulmonary regurgitation were quantified for the first time. Left ventricular hemodynamic forces were less aligned to the main blood flow direction in patients compared with control subjects. Higher right ventricular forces were seen along the pulmonary regurgitant and tricuspid inflow directions. Differences in forces versus control subjects remain after pulmonary valve replacement, suggesting that altered biventricular pumping does not normalize after surgery.


2018 ◽  
Vol 34 (10) ◽  
pp. 1369.e9-1369.e11 ◽  
Author(s):  
Pamela Moceri ◽  
Maxime Sermesant ◽  
Delphine Baudouy ◽  
Emile Ferrari ◽  
Nicolas Duchateau

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Suellen M Yin ◽  
Laura M Mercer-rosa ◽  
Jungwon Min ◽  
Elizabeth Goldmuntz ◽  
Victoria L Vetter

Introduction: Electrical-mechanical interactions contribute to arrhythmias, sudden cardiac death, and right ventricular remodeling in repaired tetralogy of Fallot (TOF). Hypothesis: There are significant changes in electrocardiographic properties and electrical-mechanical interactions that occur over time after complete TOF repair and with pulmonary valve replacement (PVR). Methods: This retrospective cohort study of 177 patients, initially recruited for a cross-sectional research protocol, underwent complete TOF repair at 0.3±0.9 years with 21.5±4.2 years of clinical follow-up. We assessed ECG, Holter, cardiopulmonary exercise testing (CPET), and MRI data. We used linear mixed effects models to examine QRS duration (QRSd) and its rate of change over time, associations between comparable ECG and MRI, Holter and MRI, ECG and Holter, ECG and CPET, and pre-PVR and post-PVR results. Results: QRSd increased after TOF repair, but the rate of change decreased from 5.2 ms/year 1 year post-operatively to 1.7 ms/year 20 years post-operatively. Twenty years from TOF repair, post-operative arrhythmias included ventricular ectopy: ventricular tachycardia (4 of 20 patients) on Holter and premature ventricular contractions (14 of 19 patients) on CPET. QRSd was positively associated with right ventricular (RV) volumes, RV:left ventricular (LV) end-diastolic volume ratio, and complex ventricular ectopy on Holter; and negatively associated with RV ejection fraction (EF). The association between QRSd and RV volumes was weaker post-PVR. QRSd and its rate of change were associated with increased LV volume post-PVR. Complex ventricular ectopy was associated with lower LV EF, and significant atrial ectopy was associated with higher LV mass-to-volume ratio. Conclusions: Substantial ventricular ectopy occurs in adolescents and young adults after repair of TOF. Electrophysiologic changes included QRSd prolongation that progressively slowed. QRSd and its rate of change were associated with published risk factors for arrhythmia and sudden cardiac death, and with indications for PVR. Our ongoing research aims to identify an optimal threshold of pre-PVR QRSd and its rate of change that preserves bi-ventricular electrical-mechanical coupling post-PVR.


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