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Characterization of the biophysical properties of the mutated channels and their response to sympathetic activity has helped to identify the importance of EADs and sympathetic stimulation as proarrhythmic triggers, providing the scientific basis for beta-blocker therapy (or left cardiac sympathetic denervation) as a mainstay of antiarrhythmic therapy in LQTS [29]

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While animal studies and short-term human use have not revealed concerning signals, effects from years of use remain entirely unknown