C
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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High [Ca2+]o-induced electrical heterogeneity and extrasystolic activity in isolated canine ventricular epicardium. Phase 2 reentry.
TL;DR: The data suggest that increased intracellular calcium activity, as occurs during ischemia and reperfusion, may contribute to the development of electrical inhomogeneity in the ventricle and thus to the genesis of ventricular arrhythmias through a mechanism other than triggered activity, namely, phase 2 reentry.
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Atrial Fibrillation and Brugada Syndrome
TL;DR: The presence of a prominent transient outward current in atria and the observation that episodes of AF are triggered by closely coupled atrial extrasystoles point to the possibility that a substrate similar to that responsible for ventricular arrhythmogenesis underlies the development of AF in patients with Brugada syndrome.
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A transient outward potassium current activator recapitulates the electrocardiographic manifestations of Brugada syndrome
Kirstine Calloe,Jonathan M. Cordeiro,José M. Di Diego,Rie Schultz Hansen,Morten Grunnet,Søren-Peter Olesen,Charles Antzelevitch +6 more
TL;DR: It is suggested that a genetic defect leading to a gain of function of I(to) could explain variants of BrS, in which ST-segment elevation or J-waves are evident in both right and left ECG leads.
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Drug-induced afterdepolarizations and triggered activity occur in a discrete subpopulation of ventricular muscle cells (M cells) in the canine heart: quinidine and digitalis.
TL;DR: Differences in the electrophysiology and pharmacology of three functionally distinct myocardial cell types found in the canine ventricle are highlighted, including those capable of inducing EADs and DADs.
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Arrhythmogenic mechanisms of QT prolonging drugs: is QT prolongation really the problem?
TL;DR: It is demonstrated that prolongation of the QT interval is not the sole determinant of the potential of a drug to cause TdP; agents that do not increase transmural dispersion of repolarization have little or no potential to induce the arrhythmia despite their ability to prolong theQT interval.