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Charles Antzelevitch

Researcher at Lankenau Institute for Medical Research

Publications -  527
Citations -  58069

Charles Antzelevitch is an academic researcher from Lankenau Institute for Medical Research. The author has contributed to research in topics: Brugada syndrome & Repolarization. The author has an hindex of 118, co-authored 515 publications receiving 54661 citations. Previous affiliations of Charles Antzelevitch include University of Southern California & Main Line Health.

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Atrial-Selective Sodium Channel Block Strategy to Suppress Atrial Fibrillation: Ranolazine versus Propafenone

TL;DR: Propafenone and ranolazine both suppress AF, but ranolazines, unlike propafen one, does it with minimal effects on ventricular myocardium, suggesting a reduced potential for promoting ventricular arrhythmias.
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Torsades de pointes following acute myocardial infarction: evidence for a deadly link with a common genetic variant.

TL;DR: The data suggest that the common K897T polymorphism is associated with an increased risk of TdP developing in the subacute phase of MI and provide the first line of evidence in support of the hypothesis that a common polymorphism may increase the risk of life-threatening arrhythmias in a much more prevalent cardiac disease such as myocardial infarction.
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A CACNA1C variant associated with reduced voltage-dependent inactivation, increased CaV1.2 channel window current, and arrhythmogenesis.

TL;DR: The combined effects of the CACNA1C variant to diminish voltage-dependent inactivation of CaV1.2 and increase window current expand the appreciation of mechanisms by which a gain of function of Ca V1.
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Ionic and Cellular Mechanisms Underlying the Development of Acquired Brugada Syndrome in Patients Treated with Antidepressants

TL;DR: Antidepressant‐Induced Brugada Syndrome is a syndrome in which the central nervous system is affected by an antidepressant and the individual’s self-esteem is affected.
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Atrial-selective sodium channel block for the treatment of atrial fibrillation.

TL;DR: This review summarizes the available data relative to current therapies, focusing on understanding of the actions of atrial selective sodium channel blockers in suppressing and preventing the induction of AF and electrophysiological properties that confer atrial-selectivity to these antifibrillatory drugs.