Charles Antzelevitch

发表

Ionic bases for electrophysiological distinctions among epicardial, midmyocardial, and endocardial myocytes from the free wall of the canine left ventricle.

C Antzelevitch, G. Gintant, C. Antzelevitch, 1993, Circulation research.

Electrical heterogeneity, cardiac arrhythmias, and the sodium channel.

C. Antzelevitch, Charles Antzelevitch, 2000, Circulation research.

I(NaCa) contributes to electrical heterogeneity within the canine ventricle.

C Antzelevitch, C. Antzelevitch, R. Goodrow, 2000, American journal of physiology. Heart and circulatory physiology.

Ionic Mechanisms Responsible for the Electrocardiographic Phenotype of the Brugada

J. Towbin, R. Dumaine, V. Nesterenko, 1999 .

High [Ca2+]o-induced electrical heterogeneity and extrasystolic activity in isolated canine ventricular epicardium. Phase 2 reentry.

J. M. Di Diego, C. Antzelevitch, J. Diego, 1994, Circulation.

Sodium channel block produces opposite electrophysiological effects in canine ventricular epicardium and endocardium.

C. Antzelevitch, S. Krishnan, Charles Antzelevitch, 1991, Circulation research.

J-wave syndromes. from cell to bedside.

Charles Antzelevitch, Gan-Xin Yan, 2011, Journal of electrocardiology.

Cellular and ionic mechanisms responsible for the Brugada syndrome.

C. Antzelevitch, G. Yan, Charles Antzelevitch, 2000, Journal of electrocardiology.

Induced pluripotent stem cells as a model for accelerated patient- and disease-specific drug discovery.

C. Antzelevitch, M. Doss, A. Sachinidis, 2010, Current medicinal chemistry.

Quinidine-induced action potential prolongation, early afterdepolarizations, and triggered activity in canine Purkinje fibers. Effects of stimulation rate, potassium, and magnesium.

C. Antzelevitch, J. Davidenko, R. Goodrow, 1989, Circulation.

I(to) and action potential notch are smaller in left vs. right canine ventricular epicardium.

C Antzelevitch, J. M. Di Diego, C. Antzelevitch, 1996, The American journal of physiology.

Transethnic Genome-Wide Association Study Provides Insights in the Genetic Architecture and Heritability of Long QT Syndrome

T. Werge, P. Ellinor, S. Priori, 2020, Circulation.

Effects of a K(+) channel opener to reduce transmural dispersion of repolarization and prevent torsade de pointes in LQT1, LQT2, and LQT3 models of the long-QT syndrome.

C. Antzelevitch, W. Shimizu, W. Shimizu, 2000, Circulation.

Transethnic genome-wide association study provides insights in the genetic architecture and heritability of long QT syndrome Running title: Genome-wide association study in long QT syndrome

T. Werge, P. Ellinor, S. Priori, 2020 .

Cellular basis for long QT, transmural dispersion of repolarization, and torsade de pointes in the long QT syndrome.

C. Antzelevitch, W. Shimizu, Charles Antzelevitch, 1999, Journal of electrocardiology.

Phenotypical Manifestations of Mutations in the Genes Encoding Subunits of the Cardiac Voltage–Dependent L-Type Calcium Channel

C. Napolitano, C. Antzelevitch, Charles Antzelevitch, 2011, Circulation research.

Brugada syndrome: report of the second consensus conference: endorsed by the Heart Rhythm Society and the European Heart Rhythm Association.

I. Gussak, H. Lemarec, K. Nademanee, 2005, Circulation.

Minimum Information about a Cardiac Electrophysiology Experiment (MICEE): Standardised Reporting for Model Reproducibility, Interoperability, and Data Sharing

Gary R. Mirams, TA Quinn, S Granite, 2011, Progress in biophysics and molecular biology.

Cellular and ionic mechanisms underlying erythromycin-induced long QT intervals and torsade de pointes.

C Antzelevitch, C. Antzelevitch, G. Yan, 1996, Journal of the American College of Cardiology.

Therapy for the Brugada syndrome.

J. Fish, C. Antzelevitch, Charles Antzelevitch, 2006, Handbook of experimental pharmacology.

Common variants at SCN5A-SCN10A and HEY2 are associated with Brugada syndrome, a rare disease with high risk of sudden cardiac death

R. Redon, E. Behr, D. Roden, 2013, Nature Genetics.