Why the study?
Does a reduced dose of encainide suppress ventricular tachycardia in a patient with severe renal dysfunction?
Does a reduced dose of encainide suppress ventricular tachycardia in a patient with severe renal dysfunction?
Patients with severe renal dysfunction may require significantly lower doses of encainide than standard recommendations to achieve therapeutic effects and avoid toxicity, highlighting the need for therapeutic drug monitoring.
May support reduced encainide dosing with monitoring in severe renal dysfunction; hypothesis-generating and should not yet change practice.
Dosage of encainide for patients with lethal ventricular arrhythmias is based on pharmacodynamic effects and efficacy of arrhythmia suppression, coupled with metabolizer phenotype and extent of renal and hepatic dysfunction. Decreased clearance in patients with renal dysfunction necessitates a reduction in dosage to avoid toxic and dose-related proarrhythmic effects. This case represents a patient with severe renal dysfunction and sustained ventricular tachycardia who achieved electrophysiologically guided suppression of induced ventricular tachycardia at a steady-state encainide dose of only 25 mg daily, significantly lower than package insert or compendial recommendations for initial dosage in patients with renal insufficiency. Documented "therapeutic" metabolite concentrations correlated to electrophysiologic response. Literature review illustrates the complexity of encainide dosage in such individuals and underscores the need for therapeutic drug monitoring to individualize dosage.
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Fronc et al. (1992) studied this question.
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