Key result
Mathematical modeling demonstrates that stretch activation of cation-nonselective ion channels causes ectopic excitation and functional conduction block, potentially triggering ventricular arrhythmias.
Computational modeling demonstrates that stretch activation of cation-nonselective ion channels during ventricular repolarization can trigger and sustain ventricular arrhythmias.
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Computational models link stretch-activated channels to ventricular ectopy and block; leaves open clinical relevance and therapeutic targeting.
Garny et al. (2004) studied Ventricular arrhythmia. Mechanical stimulation and stretch activation of ion channels was evaluated on Ectopic excitation and functional block of conduction. Mathematical modeling demonstrates that stretch activation of cation-nonselective ion channels causes ectopic excitation and functional conduction block, potentially triggering ventricular arrhythmias.
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