January 1, 2006Circulation JournalOpen Access

Arrhythmogenesis in the Short-QT Syndrome Associated With Combined HERG Channel Gating Defects

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Structured PICO

Population

Simulation model of ventricular action potentials using the Markov model of KCNH2 channel integrated into the Luo-Rudy theoretical model of cardiac ventricular cells

Intervention

Simulated N588K mutation of KCNH2 channel with combined gating defects (gain of function and accelerated deactivation)

Comparator

Simulated wild-type (WT) KCNH2 channel

Outcome

Action potential duration (APD) and occurrence of early after-depolarizations (EADs)surrogate

In a simulation model of short-QT syndrome, arrhythmogenesis (EADs) requires both a gain of function and accelerated deactivation of the HERG channel, rather than gain of function alone.

Limitations

Simulation studies are generally simplified
Conducted in isolated cell models rather than multicellular tissue with complex interactions

Discussion

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Implication

Questions single-parameter HERG models of short-QT arrhythmogenesis; leaves open translation to human disease and targeted therapies.

Cite This Study

Itoh et al. (2006) studied this question.

synapsesocial.com/papers/6a745aa84d9108bbdbdb62a7 https://doi.org/10.1253/circj.70.502

View Full Paper

Ask AI

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Arrhythmogenesis in the Short-QT Syndrome Associated With Combined HERG Channel Gating Defects

Structured PICO

Limitations

Discussion

Implication

Cite This Study

Arrhythmogenesis in the Short-QT Syndrome Associated With Combined HERG Channel Gating Defects

Structured PICO

Limitations

Discussion

Implication

Cite This Study

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