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Beta-adrenergic Modulation of Arrhythmogenesis and Identification of Targeted Sites of Antiarrhythmic Therapy in Timothy (LQT8) Syndrome: A Theoretical Study
Heart And Circulatory Physiology, 11/06/09
Sung RJ et al. – G406R Cav1.2 channel mutation confers not only a trigger but also a substrate for lethal ventricular arrhythmias which can be exaggerated by BAS. It is suggested that, besides beta–adrenergic blockers and ICa,L channel blockers, an agent aimed at reduction of IUP may provide additional antiarrhythmic effect in patients with TS.
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