After CRT D implantation the QRS

After CRT-D implantation, the QRS duration decreased to 122ms (Fig. 2), and the cardiac dyssynchrony improved. However, 5 days after implantation, atrial flutter (AFL) and electrical storm presenting as frequent VT were seen. As shown in Fig. 3A, the VT was initiated by a premature ventricular complex. The CRT-D intracardiac tracing showed both AFL and VT. Appropriate shocks were delivered, and both the AFL and VT were terminated (Fig. 3B); however, incessant VT developed after restoration of sinus rhythm. A total of 9 VT zone shocks were delivered. Biventricular pacing was discontinued, and intravenous administration of amiodarone was initiated to inhibit VT. The VT abated within 1 week, and CRT was restarted. Oral amiodarone was administered to prevent VT recurrence. To determine the risk of ventricular arrhythmia, we evaluated the corrected recovery time (RTc) dispersion and Tpeak-end dispersion on a signal-averaged vector-projected 187-channel electrocardiogram (SAVP-ECG). RTc and Tpeak-end dispersion increased during the period of electrical storm (average, 15ms and 48ms, respectively; Fig. 4A). These findings suggest that transmural dispersion of repolarization increased in our patient, leading to ventricular proarrhythmia. Two years after implantation of CRT-D, follow-up SAVP-ECG showed decreased augmentation of RTc dispersion and Tpeak-end dispersion (17ms and 13ms, respectively; Fig. 4B). It remains unclear whether this improvement was the result of time or the administration of amiodarone. We halved the dose of amiodarone before withdrawing the drug altogether. No VT recurrence occurred despite discontinuation of the antiarrhythmic agent.
Discussion Proarrhythmic events after CRT have been reported in 5–10% of CRT recipients [1–4]. Gasparini et al. investigated the incidence of electrical storm in patients with Amyloid Beta-Peptide (1-40) failure treated with CRT and reported an increased incidence in patients with nonischemic cardiomyopathy in whom a CRT-D was implanted for secondary prevention [5]. In most cases, the arrhythmia can be managed by administration of an antiarrhythmic agent and/or discontinuation of LV pacing within 1 month after implantation of the CRT system. Kantharia et al. reported a case of electrical storm induced by CRT. The VT did not disappear even after extraction of the LV lead, and catheter ablation was performed to control the VT [6]. In another case, VT was induced by biventricular pacing and controlled by triple-site biventricular pacing and atrioventricular node ablation [7]. In contrast, CRT has been reported to suppress arrhythmias in some cases [8–10]. These reports suggest that the suppression is not due to the effects of pacing itself. Rather, reverse remodeling with CRT can decrease the AFL burden and frequency of ventricular arrhythmias. The mechanism underlying the proarrhythmic effect of CRT is not well understood. One explanation is that transmural dispersion of repolarization increases with LV pacing. Bai et al. studied the effects of LV epicardial pacing and biventricular pacing in a canine model of dilated cardiomyopathy [11] and showed that both LV epicardial pacing and biventricular pacing prolonged the ventricular repolarization time and increased transmural dispersion of repolarization. Prolonged transmural dispersion occurred parallel to augmentation in the Tpeak-end interval. According to Scott et al., CRT with transseptal endocardial LV pacing (in comparison with epicardial LV pacing) reduced QTc and Tpeak-end dispersion, and these authors concluded that transseptal LV pacing may be less arrhythmogenic [12]. Barbhaiya et al. looked at the relationship between ventricular arrhythmia, the QT interval, and Tpeak-end dispersion and found that increases in Tpeak-end dispersion and Tpeak-end/QT ratio were associated with an increased incidence of ventricular arrhythmia in patients with a CRT-D [13]. Another group also reported an association between Tpeak-end dispersion and major arrhythmic events [14].