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Biotransformation Antiarrhythmic drugs (AADs) undergo metabolism in the liver through CYP450 isoenzymes, resulting in active metabolites that either block sodium (Na+) channels (such as mexiletine and propafenone), extend action potential duration (APD) [for instance, N-acetylprocainamide (NAPA)], or cause central nervous system (CNS) toxicity (as seen with lidocaine) (11)

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Long-acting formulations extending beyond once-weekly dosing could improve adherence further