Key result
Mathematical modeling demonstrated that cardiac tissue deformation significantly influences the formation of virtual electrodes and that strain-activated channels in t-tubules react strongly to transverse stretching.
This computational model elucidates the mechanisms of mechanoelectric feedback in cardiac tissue, demonstrating how specific mechanical deformations alter electrical propagation and ion channel activation.
Extracellular conductivity dilutes deformation effects on myocardial excitability; leaves open mechanoelectric feedback's role in arrhythmia mechanisms.
Mechanoelectric feedback manifests itself in a change in myocardial conductivity and in the appearance of additional transmembrane currents associated with strain-activated ion channels. Modeling of the effect of changes in intracellular conductivity on electrical processes in the myocardium is considered. When the excitation wave propagates in the myocardium, the influence of the deformation is diluted by the extracellular conductivity, which is weakly dependent on the deformation. Deformation has a much greater influence on those effects where the intracellular and extracellular media play more independent roles. One of these effects is the formation of virtual electrodes as areas of depolarization and hyperpolarization that occur when an electric current is applied to the myocardium in a small area. Two variants of deformation are considered: tension along the fibers and shear parallel to the fibers. In the case of shear, the virtual electrodes may rotate towards the main deformation axes. Another task is to polarize a strip of cardiac tissue with isolated boundaries and fibers approaching them at an angle when an electric current flows along it. Here, an exact analytical solution can be obtained for both an undeformed and a uniformly deformed strip. A model of channel activation under complex deformation is constructed, based on the assumption that these channels respond to a local increase in the area of the membrane section. Two options for the location of activated channels are considered: uniform distribution on the outer surface of the cell and uniform distribution in t-tubules, that is special invaginations of the cell membrane located perpendicular to the lateral surface. The proportion of membrane regions in the state of stretching, where the channels can be activated, has been found.
No takes yet. Share an insight, caveat, or question.
Vasserman et al. (2022) studied Myocardial mechanoelectric feedback (theoretical model). Cardiac tissue deformation (mathematical model) vs. Undeformed state was evaluated on Formation of virtual electrodes and activation of strain-activated ion channels. Mathematical modeling demonstrated that cardiac tissue deformation significantly influences the formation of virtual electrodes and that strain-activated channels in t-tubules react strongly to transverse stretching.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: