A Fully-Coupled Electro-Mechanical Whole-Heart Computational Model: Influence of Cardiac Contraction on the ECG

Abstract

The ECG is one of the most commonly used non-invasive tools to gain insights into the electrical functioning of the heart. It has been crucial as a foundation in the creation and validation of in silico models describing the underlying electrophysiological processes. However, so far, the contraction of the heart and its influences on the ECG have mainly been overlooked in in silico models. As the heart contracts and moves, so do the electrical sources within the heart responsible for the signal on the body surface, thus potentially altering the ECG. To illuminate these aspects, we developed a human 4-chamber electro-mechanically coupled whole heart in silico model and embedded it within a torso model. Our model faithfully reproduces measured 12-lead ECG traces, circulatory characteristics, as well as physiological ventricular rotation and atrioventricular valve plane displacement. We compare our dynamic model to three non-deforming ones in terms of standard clinically used ECG leads (Einthoven and Wilson) and body surface potential maps (BSPM). The non-deforming models consider the heart at its ventricular end-diastatic, end-diastolic and end-systolic states. The standard leads show negligible differences during P-Wave and QRS-Complex, yet during T-Wave the leads closest to the heart show prominent differences in amplitude. When looking at the BSPM, there are no notable differences during the P-Wave, but effects of cardiac motion can be observed already during the QRS-Complex, increasing further during the T-Wave. We conclude that for the modeling of activation (P-Wave/QRS-Complex), the associated effort of simulating a complete electro-mechanical approach is not worth the computational cost. But when looking at ventricular repolarization (T-Wave) in standard leads as well as BSPM, there are areas where the signal can be influenced by cardiac motion of the heart to an extent that should not be ignored.

Abnormal Diastolic Hemodynamic Forces: A Link Between Right Ventricular Wall Motion, Intracardiac Flow, and Pulmonary Regurgitation in Repaired Tetralogy of Fallot

“…There was inconsistent timing of exercise stress test in RTOF patients, although the time interval between CMR and stress tests were still within recommended surveillance guidelines of RTOF patients ( 45 ) and unlikely to alter results based on previous longitudinal studies ( 46 , 47 ). As the RV kinematic reconstruction is driven by imaging, the current methodology does not couple electrical propagation with mechanical contraction ( 48 , 49 ), which may explain the lack of correlation between HDF and QRS duration. Most importantly, we did not interpret the systolic HDF in this cohort – this was partly due to concern that subtle deviations in feature tracking during early systole were amplified by second order effects contributing to systolic discrepancies shown in Figure 8 .…”

Comparison of Propagation Models and Forward Calculation Methods on Cellular, Tissue and Organ Scale Atrial Electrophysiology

“…In our simulation setup, we did not consider motion and contraction of the atria for the sake of reducing model complexity and computational cost. Moss et al showed that a fully coupled electro-mechanical model does not have any influence on simulation results regarding atrial activation and that resulting P waves exhibit negligible differences to the ones computed on a non-deforming model [56]. However, the atrial repolarization results of our study might be affected to a larger extent by the lack of a coupled model as previous studies reported a substantial impact of mechanical feedback on electrophysiological behavior in the ventricles [57], [58], especially during the repolarization phase [56], [59].…”

How drugs modulate the performance of the human heart

“…The O'Hara Rudy model also serves as the consensus base model for the Comprehensive in Vitro Proarrhythmia Assay initiative established to develop a new paradigm for assessing proarrhythmic risk [58,59]. Despite its use as the consensus base model, novel updates to this model have recently been proposed which report dynamic drug-IKr interactions and a re-assessment of the myocardial pro-arrhythmic sensitivity to I Kr blockage [60,61], sex differences in drug-sensitive cardiomyocyte ion channel current densities [7], and apico-basal heterogeneity in the slow delayed rectifying potassium channel conductance [62]. These aspects might affect the critical drug concentration at which arrhythmia start developing in this study.…”