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- W2095958303 abstract "Introduction: Gain‐of‐function mutations within Scn5a , including the ΔKPQ 1505‐1507 deletion in the inactivation domain compromising myocardial repolarization, are implicated in human long QT 3 syndrome (LQT3), associated with ventricular arrhythmogenesis and sudden death. Methods and Results: Patch clamp studies on isolated ventricular Scn5a +/Δ myocytes from ΔKPQ mice produced by homologous recombination in embryonic stem (ES) cells confirmed such altered electrophysiological properties of the mutant channel. Programmed electrical stimulation (PES) with decremental pacing from the basal right ventricular epicardial surface and paced electrogram fractionation analysis (PEFA) of electrograms recorded from the basal left ventricular epicardial surface of Langendorff‐perfused whole heart preparations demonstrated ventricular tachycardia (VT) in 8 of 9 Scn5a +/Δ mutant (but no Scn5a +/+ (wild‐type (WT)) controls; n = 17), with increased electrogram durations (EGD) and more dispersed conduction curves. Isoproterenol (100 nM) was without effect on tachycardic Scn5a +/Δ hearts (n = 9) yet propranolol (1 μM) prevented VT in all isoproterenol‐infused WT control (n = 4) but no Scn5a +/Δ hearts (n = 4). Furthermore propranolol itself increased EGD and dispersion in Scn5a +/Δ hearts. In contrast, mexiletine (10 μM) suppressed VTs in 4 of 5 Scn5a +/Δ hearts without altering EGD or dispersion. Conclusion: β‐adrenoreceptor blockade does not confer an antiarrhythmic effect and may even enhance arrhythmogenesis by increasing reentrant substrate in Scn5a +/Δ hearts while mexiletine protects against VT without modifying conduction characteristics. Together these findings permit a scheme where VT in LQT3 is initiated by triggered mechanisms but propagated by reentry." @default.
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- W2095958303 date "2005-12-01" @default.
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- W2095958303 title "Paced Electrogram Fractionation Analysis of Arrhythmogenic Tendency in ΔKPQ <i>Scn5a</i> Mice" @default.
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- W2095958303 doi "https://doi.org/10.1111/j.1540-8167.2005.00200.x" @default.
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