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An Unusual Case of Flecainide‐induced QT Prolongation Leading to Cardiac Arrest
Author(s) -
Oguayo Kevin N.,
Oyetayo Ola O.,
Costa Steven M.,
Mixon Timothy A.
Publication year - 2014
Publication title -
pharmacotherapy: the journal of human pharmacology and drug therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.227
H-Index - 109
eISSN - 1875-9114
pISSN - 0277-0008
DOI - 10.1002/phar.1403
Subject(s) - flecainide , medicine , cardiology , torsades de pointes , ventricular tachycardia , qt interval , ventricular fibrillation , sotalol , sodium channel blocker , prolongation , anesthesia , repolarization , atrial fibrillation , sodium channel , sodium , electrophysiology , chemistry , organic chemistry
Flecainide is recommended as a first‐line antiarrhythmic drug to maintain normal sinus rhythm in patients with atrial fibrillation ( AF ) who have structurally normal hearts or hypertension without left ventricular hypertrophy. Flecainide is a sodium channel blocker with minimal effects expected on ventricular repolarization. We describe the case of a 32‐year‐old man with a structurally normal heart and persistent AF who was started on diltiazem and flecainide 50 mg twice/day approximately a year prior to presentation. Due to persistent and bothersome symptoms, his dose was increased to 150 mg twice/day, which was associated with a progressive lengthening of his corrected QT interval. On the day of presentation, he underwent an exercise test as part of his job requirements. While running, he felt lightheaded and experienced a syncopal event and cardiac arrest. An automated external defibrillator was available that displayed polymorphic ventricular tachycardia. The patient was successfully resuscitated. Although rare, this case suggests that flecainide can induce QT prolongation leading to torsades de pointes. Clinicians should be aware and consider periodic evaluations with electrocardiograms.