Wide QRS Complex Tachycardia Change to Narrow QRS Complex Tachycardia After β-Blocker Administration

Class Ic AADs, such as propafenone and flecainide, are widely used for the treatment of AF. One-to-one AFL is recognized as a proarrhythmic complication of class Ic AADs.⁵ These mechanisms could include the following: (1) a prolongation in the atrial flutter cycle length occurs due to drug-induced depression of atrial conduction velocity; or (2) due to the lack of inhibition of AV node conduction, 1:1 AV conduction occurs when the atrial rate slows enough. On the other hand, class Ic AADs may cause bizarre aberrant conduction during SVT, which may mimic VT.^6,7 The possible explanation is the occurrence of rate-dependent conduction slowing in the ventricular muscle and marked prolongation of the QRS duration. That is, the faster the ventricular rate, the greater the effect of drug-induced slowing down of ventricular conduction and the wider the QRS interval. In the current case, esmolol slowed conduction through the AV node, which attenuated the effect of propafenone on ventricular conduction and thus shortened the QRS duration. Therefore, in the presence of class Ic AADs, AFL with 1:1 AV conduction may manifest as wide complex tachycardia, which is a challenge for differential diagnosis. The conduction delay due to class Ic AADs has been known to be more pronounced in the ventricular myocardium than in the His-Purkinje system, leaving the initial part of the QRS complex less affected. Based on this, Kim et al⁸ proposed an algorithm to diagnose fascicular VT from RBBB pattern SVT. They found the RS/QRS ratio in lead V₆ was significantly lower in SVT than in VT. A cutoff value of the RS/QRS ratio greater than 0.41 differentiated VT from SVT (specificity, 89.7%; sensitivity, 97.2%). In the current case, the RS/QRS ratio in lead V₆ was 0.35 (<0.41) (Figure, A). This supported the diagnosis of SVT.