Background-The aim was to relate distinct scar distributions found in nonischemic cardiomyopathy with ventricular tachycardia (VT) morphology, late potential distribution, ablation strategy, and outcome. Methods and Results-Eighty-seven patients underwent catheter ablation for drug-refractory VT. Based on endocardial unipolar voltage, 44 were classified as predominantly anteroseptal and 43 as inferolateral. Anteroseptal patients more frequently fulfilled diagnostic criteria for dilated cardiomyopathy (64% versus 36%), associated with more extensive endocardial unipolar scar (41 [22-83] versus 9 [1-29] cm 2 ; P<0.001). Left inferior VT axis was predictive of anteroseptal scar (positive predictive value, 100%) and right superior axis for inferolateral (positive predictive value, 89%). Late potentials were infrequent in the anteroseptal group (11% versus 74%; P<0.001). Epicardial late potentials were common in the inferolateral group (81% versus 4%; P<0.001) and correlated with VT termination sites (κ=0.667; P=0.014), whereas no anteroseptal patient had an epicardial VT termination (P<0.001). VT recurred in 44 patients (51%) during a median follow-up of 1.5 years. Anteroseptal scar was associated with higher VT recurrence (74% versus 25%; log-rank P<0.001) and redo procedure rates (59% versus 7%; log-rank P<0.001). After multivariable analysis, clinical predictors of VT recurrence were electrical storm (hazard ratio, 3.211; P=0.001) and New York Heart Association class (hazard ratio, 1.608; P=0.018); the only procedural predictor of VT recurrence was anteroseptal scar pattern (hazard ratio, 5.547; P<0.001). Conclusions-Unipolar low-voltage distribution in nonischemic cardiomyopathy allows categorization of scar pattern as inferolateral, often requiring epicardial ablation mainly based on late potentials, and anteroseptal, which frequently involves an intramural septal substrate, leading to a higher VT recurrence. (Circ Arrhythm Electrophysiol. 2014;7:414-423.)

Background-The mechanism of cardiac resynchronization therapy (CRT)-induced proarrhythmia remains unknown. We postulated that pacing from a left ventricular (LV) lead positioned on epicardial scar can facilitate re-entrant ventricular tachycardia. The aim of this study was to investigate the relationship between CRT-induced proarrhythmia and LV lead location within scar. Methods and Results-Twenty-eight epicardial and 63 endocardial maps, obtained from 64 CRT patients undergoing ventricular tachycardia ablation, were analyzed. A positive LV lead/scar relationship, defined as a lead tip positioned on scar/border zone, was determined by overlaying fluoroscopic projections with LV electroanatomical maps. CRTinduced proarrhythmia occurred in 8 patients (12.5%). They all presented early with electrical storm (100% versus 39% of patients with no proarrhythmia; P<0.01), requiring temporary biventricular pacing discontinuation in half of cases. They more frequently presented with heart failure/cardiogenic shock (50% versus 7%; P<0.01), requiring intensive care management. Ventricular tachycardia was re-entrant in all. The LV lead location within epicardial scar was significantly more frequent in the proarrhythmia group (60% versus 9% P=0.03 on epicardial bipolar scar, 80% versus 17% P=0.02 on epicardial unipolar scar, and 80% versus 17% P=0.02 on any-epicardial scar). Ablation was performed within epicardial scar, close to the LV lead, and allowed CRT reactivation in all patients. Conclusions-CRT-induced proarrhythmia presented early with electrical storm and was associated with an LV lead positioning within epicardial scar. Catheter ablation allowed for resumption of biventricular stimulation in all patients. (Circ Arrhythm Electrophysiol. 2014;7:1064-1069.)

Atrial fibrillation (AF) is the most common clinically relevant cardiac arrhythmia. AF poses patients at increased risk of thromboembolism, in particular ischemic stroke. The CHADS2 and CHA2DS2-VASc scores are useful in the assessment of thromboembolic risk in nonvalvular AF and are utilized in decision-making about treatment with oral anticoagulation (OAC). However, OAC is underutilized due to poor patient compliance and contraindications, especially major bleedings. The Virchow triad synthesizes the pathogenesis of thrombogenesis in AF: endocardial dysfunction, abnormal blood stasis, and altered hemostasis. This is especially prominent in the left atrial appendage (LAA), where the low flow reaches its minimum. The LAA is the remnant of the embryonic left atrium, with a complex and variable morphology predisposing to stasis, especially during AF. In patients with nonvalvular AF, 90% of thrombi are located in the LAA. So, left atrial appendage occlusion could be an interesting and effective procedure in thromboembolism prevention in AF. After exclusion of LAA as an embolic source, the remaining risk of thromboembolism does not longer justify the use of oral anticoagulants. Various surgical and catheter-based methods have been developed to exclude the LAA. This paper reviews the physiological and pathophysiological role of the LAA and catheter-based methods of LAA exclusion.

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