J
Jonathan M. Cordeiro
Researcher at University of Calgary
Publications - 90
Citations - 6564
Jonathan M. Cordeiro is an academic researcher from University of Calgary. The author has contributed to research in topics: Brugada syndrome & Repolarization. The author has an hindex of 35, co-authored 87 publications receiving 6143 citations. Previous affiliations of Jonathan M. Cordeiro include University of Western Ontario & University of Guadalajara.
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Journal ArticleDOI
Loss-of-Function Mutations in the Cardiac Calcium Channel Underlie a New Clinical Entity Characterized by ST-Segment Elevation, Short QT Intervals, and Sudden Cardiac Death
Charles Antzelevitch,Guido D. Pollevick,Jonathan M. Cordeiro,Oscar Casis,Michael C. Sanguinetti,Yoshiyasu Aizawa,Alejandra Guerchicoff,Ryan Pfeiffer,Antonio Oliva,Bernd Wollnik,Philip Gelber,Elias P. Bonaros,Elena Burashnikov,Yuesheng Wu,John D. Sargent,Stefan Schickel,Ralf Oberheiden,Atul Bhatia,Li Fern Hsu,Michel Haïssaguerre,Rainer Schimpf,Martin Borggrefe,Christian Wolpert +22 more
TL;DR: This is the first report of loss-of-function mutations in genes encoding the cardiac L-type calcium channel to be associated with a familial sudden cardiac death syndrome in which a Brugada syndrome phenotype is combined with shorter-than-normal QT intervals.
Journal ArticleDOI
Sudden death associated with short-QT syndrome linked to mutations in HERG.
Ramon Brugada,Kui Hong,Robert Dumaine,Jonathan M. Cordeiro,Fiorenzo Gaita,Martin Borggrefe,Teresa M. Menendez,Josep Brugada,Guido D. Pollevick,Christian Wolpert,Elena Burashnikov,Kiyotaka Matsuo,Yue Sheng Wu,Alejandra Guerchicoff,Francesca Bianchi,Carla Giustetto,Rainer Schimpf,Pedro Brugada,Charles Antzelevitch +18 more
TL;DR: The genetic basis for a new clinical entity characterized by sudden death and short-QT intervals in the ECG is described and a novel genetic and biophysical mechanism responsible for sudden death in infants, children, and young adults caused by mutations in KCNH2 is demonstrated.
Journal ArticleDOI
Electrophysiological effects of ranolazine, a novel antianginal agent with antiarrhythmic properties.
Charles Antzelevitch,Luiz Belardinelli,Andrew C. Zygmunt,Alexander Burashnikov,José M. Di Diego,Jeffrey M. Fish,Jonathan M. Cordeiro,George Thomas +7 more
TL;DR: The actions of ranolazine to suppress EADs and reduce TDR suggest that, in addition to its antianginal actions, the drug may possess antiarrhythmic activity.
Journal ArticleDOI
Ionic and Cellular Basis for the Predominance of the Brugada Syndrome Phenotype in Males
José M. Di Diego,Jonathan M. Cordeiro,Robert J. Goodrow,Jeffrey M. Fish,Andrew C. Zygmunt,Guillermo J. Pérez,Fabiana S. Scornik,Charles Antzelevitch +7 more
TL;DR: The results suggest that the predominance of the Brugada phenotype in males is a result of the presence of a more prominent Ito in males versus females.
Journal ArticleDOI
Functional effects of KCNE3 mutation and its role in the development of Brugada syndrome.
Eva Delpón,Jonathan M. Cordeiro,Lucía Núñez,Poul Erik Bloch Thomsen,Alejandra Guerchicoff,Guido D. Pollevick,Yuesheng Wu,Jørgen K. Kanters,Carsten Toftager Larsen,Jacob Hofman-Bang,Elena Burashnikov,Michael Christiansen,Charles Antzelevitch +12 more
TL;DR: These results provide definitive evidence for a functional role of KCNE3 in the modulation of Ito in the human heart and suggest that mutations in KC NE3 can underlie the development of the Brugada syndrome.