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2016 Nov;42(5):31627

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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]

In addition, amiodarone blocks sodium and calcium channels and inhibits the effects of alpha- and beta-adrenoceptors, thereby possessing properties of all four Vaughan Williams classes of antiarrhythmic agents

Its natural occurrence in the body also means established metabolic pathways for processing and elimination