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Wide Complex Tachycardia and Flecainide

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A patient in their 70s with a history of paroxysmal atrial fibrillation and a structurally normal heart was prescribed flecainide, 100 mg twice a day, for rhythm control. The patient presented to the emergency department with complaints of dizziness. Their blood pressure was 60/44 mm Hg, heart rate was 166 beats/min, and oxygen saturation was 100% on ambient air. Serum sodium level was 138 mEq/L; serum potassium level, 4.4 mEq/L; and serum creatinine level, 0.86 mg/dL. The electrocardiogram (ECG) at presentation (Figure 1) showed a regular monomorphic wide complex tachycardia (WCT) at a rate of 160 beats/min.

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Flecainide is an antagonist of cardiac sodium channel α-subunit-5 used for the treatment of supraventricular arrhythmias in patients without structural heart disease. It slows the velocity of membrane depolarization without affecting repolarization, resulting in prolongation of the P-wave duration, PR segment, and QRS. Flecainide binds primarily to activated/open sodium channels; therefore, the block is further increased during faster rates (use dependence). Consequently, myocardial conduction is depressed, especially during higher heart rates, giving rise to a bizarre-looking WCT, mimicking VT. Flecainide slows conduction through the atrial tissue more than it prolongs refractoriness, which enables organized atrial activity and promotes atrial flutter.1 Sometimes, the atrial rate slows enough to enable 1:1 conduction through the AV node, resulting in very high heart rate, which can potentially degenerate into life-threatening arrhythmias. Therefore, patients taking flecainide also need an AV nodal-blocking agent to mitigate this risk.2 Alternatively, flecainide itself can induce VT by creation of areas of functional conduction block promoting reentry.3 This case highlights the limitations of WCT diagnostic criteria in clinical practice. The Brugada algorithm was tested in patients without antiarrhythmic drug treatment.4 The use of class I antiarrhythmic drugs results in a low specificity of the second Brugada criterion.5 Alternatively, the ventricular activation velocity ratio (vi/vt) has several advantages in this setting. To apply, measure the total vertical distance covered by the final 40 milliseconds of the QRS. If this is equal to or more than the vertical distance covered by the first 40 milliseconds of the QRS, VT is diagnosed. The concept is that with aberration, ventricular activation during the first portion of the QRS is mediated by the His-Purkinje system, whereas in VT, the His-Purkinje system is engaged later in the QRS complex.6 The use of antiarrhythmic drugs that impair conduction in the His-Purkinje system and ventricular myocardium (such as class I drugs) would be expected to decrease the vi and vt approximately to the same degree. Thus, the vi/vt ratio will not change substantially. When confronted with a WCT, it is crucial to integrate both the clinical and the ECG information and not rely exclusively on ECG algorithms. Furthermore, extended rhythm monitoring and multiple ECGs often provide critical information that can facilitate the diagnosis of challenging rhythms.

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Article Information

Corresponding Author: Carlos Ruben Lopez Perales, MD, Department of Cardiology, Miguel Servet University Hospital, Isabel la Católica 1-3, Zaragoza 50009, Spain (caruben89@gmail.com).

Published Online: August 1, 2022. doi:10.1001/jamainternmed.2022.2940

Conflict of Interest Disclosures: None reported.

References
1.
Courand  PY , Sibellas  F , Ranc  S , Mullier  A , Kirkorian  G , Bonnefoy  E .  Arrhythmogenic effect of flecainide toxicity.   Cardiol J. 2013;20(2):203-205.PubMedGoogle ScholarCrossref
2.
Comelli  I , Pigna  F , Cervellin  G .  1:1 Atrial flutter induced by flecainide, whilst the patient was at rest.   Am J Emerg Med. 2018;36(11):2131.e3-2131.e5.PubMedGoogle ScholarCrossref
3.
Banavalikar  B , Shenthar  J , Padmanabhan  D .  Unusual wide complex tachycardia during rhythm control for atrial fibrillation.   Circulation. 2018;138(5):537-539.PubMedGoogle ScholarCrossref
4.
Brugada  P , Brugada  J , Mont  L , Smeets  J , Andries  EW .  A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex.   Circulation. 1991;83(5):1649-1659.PubMedGoogle ScholarCrossref
5.
Alberca  T , Almendral  J , Sanz  P , Almazan  A , Cantalapiedra  JL , Delcán  JL .  Evaluation of the specificity of morphological electrocardiographic criteria for the differential diagnosis of wide QRS complex tachycardia in patients with intraventricular conduction defects.   Circulation. 1997;96(10):3527-3533.PubMedGoogle ScholarCrossref
6.
Kashou  AH , Noseworthy  PA , DeSimone  CV , Deshmukh  AJ , Asirvatham  SJ , May  AM .  Wide complex tachycardia differentiation.   J Am Heart Assoc. 2020;9(11):e016598.PubMedGoogle Scholar
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