Cellular basis for atrial fibrillation in an experimental model of short QT1: Implications for a pharmacological approach to therapy
- 19 October 2009
- journal article
- research article
- Published by Elsevier in Heart Rhythm
- Vol. 7 (2) , 251-257
Abstract
No abstract availableKeywords
This publication has 39 references indexed in Scilit:
- How Do Atrial-Selective Drugs Differ From Antiarrhythmic Drugs Currently Used in the Treatment of Atrial Fibrillation?Journal of Atrial Fibrillation, 2008
- The pharmacological response of ischemia-related atrial fibrillation in dogs: Evidence for substrate-specific efficacyCardiovascular Research, 2007
- Disopyramide is an effective inhibitor of mutant HERG K+ channels involved in variant 1 short QT syndromeJournal of Molecular and Cellular Cardiology, 2006
- Catheter Ablation of Long‐Lasting Persistent Atrial Fibrillation: Critical Structures for TerminationJournal of Cardiovascular Electrophysiology, 2005
- Further Insights into the Effect of Quinidine in Short QT Syndrome Caused by a Mutation in HERGJournal of Cardiovascular Electrophysiology, 2005
- Identification of a KCNE2 Gain-of-Function Mutation in Patients with Familial Atrial FibrillationThe American Journal of Human Genetics, 2004
- Transmembrane action potential heterogeneity in the canine isolated arterially perfused right atrium: effect ofIKrandIKur/ItoblockAmerican Journal of Physiology-Heart and Circulatory Physiology, 2004
- Sudden Death Associated With Short-QT Syndrome Linked to Mutations in HERGCirculation, 2004
- Ionic mechanisms of electrical remodeling in human atrial fibrillationCardiovascular Research, 1999
- Ionic Mechanisms of Regional Action Potential Heterogeneity in the Canine Right AtriumCirculation Research, 1998