Why the study?
Do N588K and L532P KCNH2 mutations increase vulnerability to atrial arrhythmia in a 3D electrophysiological model?
Do N588K and L532P KCNH2 mutations increase vulnerability to atrial arrhythmia in a 3D electrophysiological model?
Computational modeling demonstrates that N588K and L532P KCNH2 mutations shorten action potential duration and increase atrial vulnerability to re-entry and fibrillation.
No immediate change to patient care indicated; leaves open the arrhythmogenic role of these mutations pending human validation.
BACKGROUND: gene cause atrial arrhythmia. METHODS: The N588K and L532P mutations were induced in the Courtemanche-Ramirez-Nattel (CRN) cell model, which was subjected to two-dimensional and three-dimensional simulations to compare the electrical conduction patterns of the wild-type and mutant-type genes. RESULTS: In contrast to the early self-termination of the wild-type conduction waveforms, the conduction waveform of the mutant-type retained the reentrant wave (N588K) and caused a spiral break-up, resulting in irregular wave generation (L532P). CONCLUSION: gene mutation increases the vulnerability of the atrial tissue for arrhythmia.
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Heikhmakhtiar et al. (2020) studied this question.
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