QTc compared to JTc for monitoring drug-induced repolarization changes in the setting of ventricular pacing.

BACKGROUND: QT prolongation is a risk factor for proarrhythmia when beginning antiarrhythmic drug therapy (AAD). However, there are no data regarding monitoring repolarization changes during a ventricular paced (VP) rhythm. OBJECTIVE: The purpose of this study was to compare serial changes in corrected QT and JT intervals, during native conduction (NC) and VP rhythms when initiating Class III AADs. METHODS: Twenty-two patients (73% men; mean age 65 ± 11 years) with an implantable device and with <10% VP were monitored during AAD initiation (16 sotalol, 6 dofetilide). QTc and JTc were measured from ECGs obtained during NC and VP at baseline (pre-AAD) and then after each AAD dose. RESULTS: During AAD loading, mean QTc increased significantly during NC (431 ± 28 ms to 463 ± 33 ms, P = .002) but not with VP (520 ± 48 ms to 538 ± 45 ms, P = .07). Mean percent increase in peak QTc during NC was significantly greater than during VP (12% vs 7%, P = .003). In contrast, peak JTc during AAD loading was not significantly different between NC and VP (P = .67). CONCLUSION: When initiating AAD, the change in QTc during VP does not correlate with the change in QTc during NC; thus, the VP QTc is inadequate for monitoring repolarization changes. However, VP JTc correlates well with JTc during NC. When initiating Class III AADs in patients with VP rhythms, the JTc, and not the QTc, interval is the useful marker for assessing repolarization.

Verapamil-sensitive left posterior fascicular ventricular tachycardia after myocardial infarction.

Verapamil-sensitive fascicular ventricular tachycardia (VT) of right bundle branch block (RBBB) and superior axis pattern is typically seen in young patients with structurally normal hearts and considered "idiopathic". Recently, involvement of the Purkinje system in post-infarction monomorphic VT that mimics such idiopathic fascicular VT has been described. In this report we describe a case of a patient who following myocardial infarction developed left posterior fascicular Purkinje reentrant VT that was sensitive to verapamil. The VT was successfully treated by radiofrequency ablation guided by three dimensional electroanatomical CARTO mapping. Our case highlights that involvement of Purkinje fibers should be considered in post infarction patients with VT of narrow QRS duration, RBBB morphology and superior axis. Recognition of such VT is clinically important, as this arrhythmia is amenable to curative catheter ablation.