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.