Key result
Computational modeling demonstrated that mechano-electric feedback plays a major role in the occurrence of fibrillation and defibrillation in the absence of structural cardiac damage.
Why the study?
The study aimed to investigate the role of mechano-electric feedback in healthy cardiac cycles and cardiac arrhythmia using human ventricular models.
Answers are grounded in this paper and cite their sources.
Computational modeling demonstrates that mechano-electric feedback is a key driver of arrhythmogenesis and defibrillation even without structural heart damage.
The current study aims to investigate the role of mechano-electric feedback (MEF) in healthy cardiac cycles and in cardiac arrhythmia using human ventricular models. The numerical formulation of stretch-activated channels (SACs) in terms of the fibre stretch of the myocardium is incorporated into the modified Hill model that describes the myocardium as an electro-visco-active material. Additionally, we propose models of SACs formulated in terms of the rate of stretch along fibre direction and the stretch along sheet direction. We analyze the effect of the three different models for SACs and different material properties on the regular cycles by using electrocardiogram and volume-time curves, and show that the each model of SACs has regionally different influences on the heart model. Moreover, we simulate 'commotio cordis' and 'precordial thump' and demonstrate that MEF plays a major role in the occurrence of fibrillation and defibrillation in the absence of the structural cardiac damage. Furthermore, we study the role of MEF in premature ventricular contraction when the blood pressure is disturbed.
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Lee et al. (2022) studied Cardiac arrhythmia. Computational modelling of mechano-electric feedback (MEF) was evaluated on Effect on electrocardiogram, volume-time curves, and occurrence of fibrillation/defibrillation. Computational modeling demonstrated that mechano-electric feedback plays a major role in the occurrence of fibrillation and defibrillation in the absence of structural cardiac damage.
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