Abstract: Long QT syndrome type 1 (LQT1) is caused by muta- tions that impair the function of the slow delayed rectifier potassium (IK s ) channels. Most LQT1 patients experience arrhythmic events during beta-adrenergic stimulation (β- AS). A full description of the ionic mechanisms underlying arrhythmogenecity in LQT1 patients and their relation to β-AS is still lacking. In this study we constructed a set of stochastic human ventricular cell models reproducing ex- perimental AP properties at baseline and following ionic inhibitions. Using the constructed models, we showed that AP duration, morphology and beat-to-beat variability in LQT1 are highly specific of the underlying ionic character- istics. Likewise, the response of individual IK s -deficient cells to β-AS can range from negligible to as much as 200% increase in AP temporal variability, recognized as a marker of arrhythmogenesis in the setting of LQT1. By partial correlation analysis, major ionic factors driving AP changes associated with LQT1 and β-AS were ascer- tained.

Idioma: Inglés

Año: 2017

En: Computing in Cardiology (2017, Rennes, France)

Financiación: info:eu-repo/grant/Agreement/ES/MINECO TIN2013-41998-R
Financiación: info:eu-repo/grant/Agreement/ES/MINECO DPI2016-75458-R
Financiación: info:eu-repo/grant/Agreement/EU/ERC-2014-StG-638284

Creative Commons You must give appropriate credit, provide a link to the license, and indicate if changes were made. You may do so in any reasonable manner, but not in any way that suggests the licensor endorses you or your use.


Este artículo se encuentra en las siguientes colecciones:
Communications and papers



 Record created 2018-05-30, last modified 2018-05-30


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