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- W2059142008 abstract "The characterization of single gene disorders has provided important insights into the molecular pathogenesis of cardiac arrhythmias. Primary electricalal diseases including long-QT syndrome, short-QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia have been associated with mutations in a variety of ion channel subunit genes that promote arrhythmogenesis. Pathological remodeling of ionic currents and network properties of the heart critical for normal electrical propagation plays a critical role in the initiation and maintenance of acquired arrhythmias. This review focuses on the molecular and cellular basis of electrical activity in the heart under normal and pathophysiological conditions to provide insights into the fundamental mechanisms of inherited and acquired cardiac arrhythmias. Improved understanding of the basic biology of cardiac arrhythmias holds the promise of identifying new molecular targets for the treatment of cardiac arrhythmias." @default.
- W2059142008 created "2016-06-24" @default.
- W2059142008 creator A5009404984 @default.
- W2059142008 creator A5023584164 @default.
- W2059142008 creator A5083609472 @default.
- W2059142008 date "2005-10-18" @default.
- W2059142008 modified "2023-10-12" @default.
- W2059142008 title "Molecular Basis of Arrhythmias" @default.
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- W2059142008 doi "https://doi.org/10.1161/circulationaha.104.494476" @default.
- W2059142008 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16230503" @default.
- W2059142008 hasPublicationYear "2005" @default.
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