The Role of Genetically Determined Polymorphic Drug Metabolism in the Beta-Blockade Produced by Propafenone

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Abstract
Propranolol and the sodium-channel–blocking antiarrhythmic agent propafenone share structural features. Although propafenone's beta-blocking actions are readily demonstrable in vitro, clinically significant beta-blockade occurs inconsistently in vivo. In this study, we tested the hypothesis that genetically determined variations in the biotransformation of propafenone to its 5-hydroxy metabolite account for variations in the drug's beta-blocking action.