Drug-induced ventricular tachycardia in a patient with atrial flutter: a clinical case

Abstract

Introduction. Atrial flutter (AFL) often persists in the absence of appropriate therapy and carries a high risk of thromboembolism. Flecainide, a class IC antiarrhythmic, is effective and safe in patients without structural heart disease but may cause proarrhythmic effects in the presence of predisposing factors. Objective(s). To present the clinico-paraclinical aspects of an episode of monomorphic ventricular tachycardia (VT) in a patient with AFL and to highlight the proarrhythmic effect of Flecainide. Materials and methods. A 45-year-old woman known with AFL for approximately 1 year. Chronic treatment: Flecainide 200 mg/day, Bisoprolol 5 mg/day, Apixaban 5 mg twice/day. ECG: Typical counterclockwise AFL 4:1 with HR 75 bpm. Laboratory tests: unremarkable. During preparation for electrical cardioversion, the patient experienced an episode of rapid palpitations. Results. ECG - monomorphic VT with a heart rate of 200 bpm, superior axis, and a QRS duration of 160 ms exhibiting a left bundle branch block morphology, with a transition zone in leads V5, V6. External electrical cardioversion at 150 J, under midazolam sedation, restored sinus rhythm. ECHO: non-dilated cardiac chambers and preserved LV EF. Coronary angiography revealed no significant stenotic lesions. Electrophysiological study with up to 6 atrial and 4 ventricular extrastimuli induced no arrhythmias. Cavotricuspid isthmus ablation achieved bidirectional block. Conclusion(s). Monomorphic VT was likely triggered by the pro-arrhythmic effect of Flecainide. Sinus rhythm and hemodynamic stability were achieved through electrical defibrillation. Cavotricuspid isthmus ablation with confirmed bidirectional block prevented atrial flutter recurrence.