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

Abstract

Background. Atrial flutter (AFL) often persists in the absence of appropriate therapy and carries a high risk of thromboembolism. Flecainide, IC class antiarrhythmic drug, 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 clinical and 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 preparing for electrical cardioversion, the patient provoked an episode of rapid palpitations. Results. ECG showed monomorphic ventricular tachycardia 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, have restored sinusal rhythm. Echocardiography demonstrated non-dilated cardiac chambers and preserved left ventricular ejection fraction. 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 ventricular tachycardia was likely triggered by the proarrhythmic effect of Flecainide. Sinusal rhythm and hemodynamic stability were achieved through electrical defibrillation. Cavotricuspid isthmus ablation with confirmed bidirectional block prevented atrial flutter recurrence.