Outcome of slow pathway modulation for atrioventricular nodal reentrant tachycardia with 50 versus 30 watts-more power, more effect?

PURPOSE: Slow pathway modulation is the treatment of choice in patients with atrioventricular nodal reentrant tachycardia (AVNRT). No comparative data on ablation strategies exist. Therefore, we sought to compare two common ablation approaches. METHODS: We analyzed prospective ablation databases of two high-volume tertiary centers (> 1000 ablations/year) using either 30 or 50 W for slow pathway modulation from 2012 to 2013. We analyzed procedural characteristics as well as short- and long-term outcomes. Mean follow-up was 36 ± 9 months. RESULTS: Six hundred thirty-four patients (50 W center: n = 342, 30 W center: n = 292) were ablated. Slow pathway modulation was successful in 99% in both groups (p = ns). Periprocedural AV block occurred in nine patients (2.6%) in the 50 W and five patients (1.7%) in the 30 W group (p = 0.59), respectively. We documented no permanent higher-degree AV block. The number of RF lesions and seconds of RF delivery was significantly less in the 50 W group (p = 0.04 for number of lesions; p < 0.001 for seconds). AVNRT recurrence was similar (p = 0.23). In males, significantly fewer recurrences accrued in the 50 W group (p = 0.04), while in females less transient AV blocks occurred during the procedure with 30 W (p = 0.07). CONCLUSIONS: The 30 and 50 W target power approaches for slow pathway modulation are highly effective and safe. Significantly, fewer RF duration was necessary to modulate the slow pathway with higher power output (50 W). Our subgroup analysis suggests that males and females might benefit most from different modulation approaches.

Novel non-pharmacological approaches for antiarrhythmic therapy of atrial fibrillation.

Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice. Its prevalence is increasing in our ageing population, and it has a soaring impact on health systems. It can cause thrombo-embolism, heart failure, and hospitalizations, and is associated with a two-fold increase in all-cause mortality. There have been great advances in understanding the mechanism of AF that are currently being translated into new therapeutic concepts. Experimental studies demonstrated that AF-induced electrical and structural remodelling of the fibrillating atria perpetuate AF ('AF begets AF'). Furthermore, there is growing understanding that the atria are an endocrine organ expressing angiotensin and thrombogenic substances. Clinical, electrophysiological studies have identified automatic triggers, often in the pulmonary veins, that initiate paroxysmal AF. Electrical isolation of the pulmonary veins by circular ablation abolishes these triggers. Whereas isolation of the pulmonary veins often maintains sinus rhythm in patients with paroxysmal AF, additional ablation strategies are used in persistent and permanent AF to modify the more complex electrical and structural atrial changes. The 'role model' for extensive ablation in the left atrium is the surgical MAZE procedure that abolishes long-standing AF by cutting and sewing the atria into complex pieces. New surgical approaches of AF therapy use radiofrequency or other sources for an easy ablation during open-heart surgery. A lot of effort has also been put in the development of device therapy for the treatment of AF, with mixed effects on maintenance of sinus rhythm, but unexpected insights into the development of asymptomatic AF recurrences. This review aims to provide an overview of these non-pharmacological treatment options of AF in the context of potential pathophysiological processes.