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Modelling and imaging cardiac repolarization abnormalities.

Y Rudy
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Abstract

Repolarization abnormalities, including those induced by the congenital or acquired long QT (LQT) syndrome, provide a substrate for life-threatening cardiac arrhythmias. In this article, we use computational biology to link HERG mutations mechanistically to the resulting abnormalities of the whole-cell action potential. We study how the kinetic properties of I(Ks) (the slow delayed rectifier) that are conferred by molecular subunit interactions, facilitate its role in repolarization and 'repolarization reserve'. A new noninvasive imaging modality (electrocardiographic imaging) is shown to image cardiac repolarization on the epicardial surface, suggesting its possible role in risk stratification, diagnosis and treatment of LQT syndrome.

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Action PotentialsAdaptation, PhysiologicalAnimalsArrhythmias, CardiacComputer SimulationDisease Models, AnimalERG1 Potassium ChannelElectrocardiographyEther-A-Go-Go Potassium ChannelsGuinea PigsHeartLong QT SyndromeMarkov ChainsMolecular ConformationMutationPhenotypePotassium ChannelsRisk AssessmentJournal ArticleResearch Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov't

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Y Rudy. 2006. Modelling and imaging cardiac repolarization abnormalities.. https://doi.org/10.1111/j.1365-2796.2005.01586.x

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