br Discussion CRT has become an established

Discussion CRT has become an established adjunctive treatment to optimal pharmacological therapy in patients with advanced CHF, diminished LV function, and intra-ventricular conduction delay [8]. Despite the benefits of CRT including improvements in exercise capacity, functional class, and ventricular hemodynamics, a pro-arrhythmic effect is less clear. The incidence of pro-arrhythmia reported in a limited single series was low, ranging from 3.4% to 4% during the first few days, with a predominance for ischemic cardiomyopathy patients [7–9]. Tachyarrhythmia was observed as MMVT, mostly in ischemic cardiomyopathy patients, or as polymorphic ventricular tachycardia (PMVT) or TdP, as seen in our case. Most MMVTs seen in ischemic cardiomyopathy patients are caused by reentry and involve complex circuits in the LV [10]. The induction of a reentrant VT may be site specific, and can be facilitated by pacing at or near these circuits [11]. Reentry is the mechanism responsible for MMVT in CRT-implanted patients. Normally, ventricular activation starts at the endocardium via the subendocardial Purkinje network and spreads across the ventricular wall. Although the epicardium is activated last, it repolarizes first because of its shorter mobile game duration. This produces a repolarization sequence opposite to activation [12]. On ECG, this activation and repolarization sequence produces an upright T wave with the same polarity as the QRS [12]. LV epicardial pacing via the coronary sinus route abolishes normal repolarization of the LV by prolonging the QT interval, JT interval, and transmural dispersion of repolarization. First defined in 2003 by Medina-Ravell et al. [5], pacing site-dependent changes in ventricular repolarization potentially constitute the mechanism of TdP. Prolongation of ventricular repolarization time, the same circumstance as in long QT syndromes, makes the ventricle vulnerable to ventricular extrasystoles that result in R on T phenomenon and TdP. With BVP mode, the patient׳s QTc interval was prolonged from 521ms to 536ms, the JTc interval was prolonged from 305ms to 360ms, and the T peak–T end interval was prolonged from 120ms to 190ms. All markers of myocardial dispersion of repolarization were prolonged with LV epicardial pacing, and BVP was followed by ventricular extrasystole over the T wave resulting in TdP. Despite amiodarone infusion, 12 appropriate CRT-D defibrillations occurred (Fig. 3). As noted above, switching off the BVP mode stopped the electrical storm of TdP.
Conclusion
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Acknowledgments
Introduction Idiopathic ventricular arrhythmias (VAs) have become curable as improved knowledge and ablative techniques have been established. However, VA originating from the left ventricular outflow tract (LVOT) remains a challenge because of the complexity of the involved anatomic structures and the unique electrophysiological properties of the region. The unique feature is not fully understood, although some reports suggest a possible link between the aortomitral continuity (AMC) and the conduction system [1]. We present a case of LVOT-VT that demonstrated the missing link between the AMC and the conduction system.
Case report A 60-year-old man was referred for examination and treatment of a documented VT during exercise (Fig. 1a). The VT showed a right bundle branch block with an inferior axis pattern, but without a precordial transition. In addition, lead I showed an rS pattern, but an apparent S-wave was not observed in V6, suggesting that the focus of the VT is located on the left coronary cusp, not beneath the aortic valve [2]. An electrophysiological study was performed, in which quadripolar electrode catheters were attached in the high right atrium and right ventricular apex by using a decapolar electrode for recording the His bundle electrogram and a 3.5-mm Navistar ThermoCool Catheter (Biosense-Webster, Diamond Bar, CA, USA) for LVOT recording. The clinical VA was inducible by isoproterenol infusion (0.02μg/[kgmin]). A pacemap, obtained at the bottom of left coronary cusp (LCC), showed a near-perfect match (11/12; Fig. 1a). During the VA, a spiked presystolic potential (PP) preceded the onset of the QRS complex (Vo) by −16ms, and a QS pattern was demonstrated in the unipolar recordings. Several radiofrequency catheter ablation (RFCA) attempts in haploid region (up to 25W) yielded only partial success. Subsequently, we examined the endocardial side of the AMC and found a highly preceding PP relative to the onset of the QRS complex (PP-Vo=68ms) of the VA (Figs. 1b and 2a). The unipolar recordings showed a qrS activation pattern that corresponded to the PP and VAs. A near perfect pacemap was obtained at this earliest activation (Fig. 1a). Soon after the RF application, non-sustained VT occurred and turned into the bigeminy of a single ventricular premature complex (VPC). The PP-Vo interval was gradually prolonged during RFCA, followed by the disappearance of the VA, with a PP-VPC block (Fig. 2a). However, the sinus-PP bigeminy remained even after the disappearance of the VA. In addition, a late potential (LP), recorded immediately after the ventricular potential of the sinus beats, disappeared simultaneously with the elimination of the VPC (Fig. 2a). After five more applications, the VA was totally eliminated, whereas the sinus-PP, bigeminal rhythm remained. It is interesting that the PP rates were dependent on the rates of the preceding sinus rhythm and the coupling intervals of the sinus-PP bigeminy were constant (Fig. 2b).