Key result
In ventricular myocyte models, the occurrence of phase-3 early afterdepolarizations requires a substantial increase of L-type Ca2+ and slow delayed rectifier K+ currents, thresholds for which are greatly reduced by the presence of T-type Ca2+ current.
Why the study?
Although phase-2 EADs have been widely observed, phase-3 EADs and triggered activities are much more arrhythmogenic but have rarely been demonstrated in isolated ventricular myocytes.
Population
Three widely used ventricular action potential models
Comparison
Presence vs absence of T-type Ca2+ current
Design
Computer simulation study
Authors
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Phase-3 EADs may propagate readily as triggered activity; leaves open their dominance in clinical arrhythmogenesis.
Computational modeling reveals that T-type calcium currents, present in failing myocytes, significantly lower the threshold for highly arrhythmogenic phase-3 early afterdepolarizations.
Zhang et al. (2021) studied Cardiac arrhythmias (Phase-3 early afterdepolarizations). T-type Ca2+ current (ICa,T) presence and ion channel conductance variations vs. Absence of ICa,T and baseline ion channel conductances was evaluated on Occurrence and mechanisms of phase-3 early afterdepolarizations and triggered activities. In ventricular myocyte models, the occurrence of phase-3 early afterdepolarizations requires a substantial increase of L-type Ca2+ and slow delayed rectifier K+ currents, thresholds for which are greatly reduced by the presence of T-type Ca2+ current.
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