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The role of mechano-electric feedbacks and hemodynamic coupling in scar-related ventricular tachycardia

Mechano-electric feedbacks (MEFs), which model how mechanical stimuli are transduced into electrical signals, have received sparse investigation by considering electromechanical simulations in simplified scenarios. In this paper, we study the effects of different MEFs modeling choices for myocardial...

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Published in:Computers in biology and medicine 2022-03, Vol.142, p.105203-105203, Article 105203
Main Authors: Salvador, Matteo, Regazzoni, Francesco, Pagani, Stefano, Dede', Luca, Trayanova, Natalia, Quarteroni, Alfio
Format: Article
Language:English
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Summary:Mechano-electric feedbacks (MEFs), which model how mechanical stimuli are transduced into electrical signals, have received sparse investigation by considering electromechanical simulations in simplified scenarios. In this paper, we study the effects of different MEFs modeling choices for myocardial deformation and nonselective stretch-activated channels (SACs) in the monodomain equation. We perform numerical simulations during ventricular tachycardia (VT) by employing a biophysically detailed and anatomically accurate 3D electromechanical model for the left ventricle (LV) coupled with a 0D closed-loop model of the cardiocirculatory system. We model the electromechanical substrate responsible for scar-related VT with a distribution of infarct and peri-infarct zones. Our mathematical framework takes into account the hemodynamic effects of VT due to myocardial impairment and allows for the classification of their hemodynamic nature, which can be either stable or unstable. By combining electrophysiological, mechanical and hemodynamic models, we observe that all MEFs may alter the propagation of the transmembrane potential. In particular, we notice that the presence of myocardial deformation in the monodomain equation may change the VT basis cycle length and the conduction velocity but do not affect the hemodynamic nature of the VT. Finally, nonselective SACs may affect VT stability, by possibly turning a hemodynamically stable VT into a hemodynamically unstable one. •We perform comprehensive electromechanical simulations of ventricular tachycardia (VT).•Our model reproduces both hemodynamically stable and hemodynamically unstable VT.•We unravel the electric and hemodynamic impact of mechano-electric feedbacks on VT.•Results show that deformation affects VT cycle length but does not change stability.•Stretch-activated channels may affect the hemodynamics associated with VT.
ISSN:0010-4825
1879-0534
DOI:10.1016/j.compbiomed.2021.105203