By Masayasu Hiraoka, International Congress on Electrocardiol

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Extra resources for Advances in Electrocardiology 2004: Proceedings of the 31th International Congress on Electrocardiology (Advances in Electrocardiography)

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Bobkowski, A. Nowak, J. Zuchwieja, B. Mrozinski and A. Siwinska 17 Modeling of Cardiac Electrical Activity 796 80 1 805 Reflections on T Waves A. van Oosterom 807 Electrocardiographic Imaging (ECGI): Validation and Application in Humans Y. Rudy 816 Whole Heart Model and ECG/MCG Inverse Problem Y. Okamoto 817 Changes in Rabbit Heart Vulnerability during Phase 1A of Acute Global Ischemia 818 N. Trayanova and B. Rodriguez Simulated Epicardial Potential Maps with a Membrane-Based Bidomain Model of the Human Heart 827 M.

25. Splawski I, Shen J, Timothy KW, et al: Spectrum of mutations in long-QT syndrome genes. KVLQT1, HERG, SCNSA, KCNE1, and KCNE2. Circulation 2000;102:1178-1185. 26. Moss AJ, Zareba W, Kaufman ES, et al: Increased risk of arrhythmic events in long-QT syndrome with mutations in the pore region of the human ether-a-go-go-related gene potassium channel. Circulation 2002; 105:794-799. 27. Schwartz PJ, Priori SG, Spazzolini C, et al: Genotype-phenotype correlation in the long-QT syndrome: gene-specific triggers for life-threatening arrhythmias.

The most widely accepted mechanism of AF is reentry (multiple wavelets or single reentry such as “mother rotor”). However, recently attention has been focused on the mechanisms of AF initiation and maintenance. HaYssaguerre and colleagues [ 11 studied the mechanism of paroxysmal AF in patients and found that AF is initiated by premature focal activity originating mainly in the pulmonary veins (PVs) and that radiofrequency ablation of these foci can successhlly eliminate AF. In addition, in patients with drug-refractory chronic AF and structural heart diseases, following cardioversion, the PVs are 26 27 also the dominant trigger reinitiating AF [2].

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