Key result
Modified ten Tusscher-Panfilov model reproduces LQTS-associated phase-2 EADs driven by spontaneous sarcoplasmic reticulum calcium release.
Why the study?
Early afterdepolarizations cause lethal ventricular arrhythmias in LQTS, but the dynamical mechanisms of their formation in human ventricular myocytes remained to be clarified.
Population
ten Tusscher and Panfilov human ventricular myocyte mathematical model
Design
Mathematical modeling and numerical simulation study
Authors
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Hypothesis-generating for phase-2 EAD triggers in LQTS models; leaves open any clinical translation or therapeutic targeting.
This mathematical modeling study provides theoretical insights into the mechanisms of early afterdepolarizations in long QT syndrome, highlighting the role of spontaneous SR Ca2+ release.
Kurata et al. (2019) studied Long QT syndrome (LQTS). Modified ten Tusscher-Panfilov mathematical model vs. Original ten Tusscher-Panfilov model was evaluated on Dynamical mechanisms of early afterdepolarization (EAD) formation. A modified version of the ten Tusscher-Panfilov model with accelerated ICaL inactivation reproduced phase-2 EADs in long QT syndrome type 1 and 2 cardiomyocytes, partially attributable to spontaneous sarcoplasmic reticulum Ca2+ releases.
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