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Background: Atrioventricular nodal reentrant tachycardia (AVNRT) is treatable by catheter ablation. Advances in mapping‐system technology permit fluoroless workflow during ablations. As national practice trends toward fluoroless approaches, easily obtained, reproducible methods of slow‐pathway identification, and ablation become increasingly important. We present a novel method of slow‐pathway identification and initial ablation results from this method. Methods and Results: We examined AVNRT ablations performed at our institution over a 12‐month period. In these cases, the site of the slow pathway was predicted by latest activation in the inferior triangle of Koch during sinus rhythm. Ablation was performed in this region. Proximity of the predicted site to the successful ablation location, complication rates, and patient outcomes were recorded. Junctional rhythm was seen in 40/41 ablations (98%) at the predicted site (mean, 1.3 lesions and median, 1 lesion per case). One lesion was defined as 5 mm of ablation. The initial ablation was successful in 39/41 cases (95%); in two cases, greater or equal to 2 echo beats were detected after the initial ablation, necessitating further lesion expansion. In 8/41 cases (20%), greater than one lesion was placed during initial ablation before attempted reinduction. Complications included one transient heart block and one transient PR prolongation. During follow‐up (median, day 51), one patient had lower‐extremity deep‐vein thrombosis and pulmonary embolus, and one had a lower‐extremity superficial venous thrombosis. There was one tachycardia recurrence, which prompted a redo ablation. Conclusions: Mapping‐system detection of late‐activation, low‐amplitude voltage during sinus rhythm provides an objective, and fluoroless means of identifying the slow pathway in typical AVNRT. [ABSTRACT FROM AUTHOR]

Introduction: Ventricular fibrillation and ventricular flutter (cycle length ≤230 msec) induced at electrophysiologic studies are thought to be nonspecific findings in patients presenting with syncope of unknown origin. However, there are limited data on the prognosis of these patients in long-term follow-up. Methods and Results: We followed 274 consecutive patients with coronary artery disease presenting with syncope or presyncope who underwent electrophysiologic studies from January 1992 to June 1999 and assessed the risk of subsequent arrhythmias stratified by the electrophysiologic result at the time of their presentation with syncope. Ventricular fibrillation was induced in 23 patients (8%); ventricular flutter in 24 (9%), sustained ventricular tachycardia in 41 (15%); and nonsustained ventricular tachycardia 42 (15%). In 37 ± 25 months of follow-up, there have been ventricular arrhythmias in 34 patients, including 3 (13%) of 23 who had induced ventricular fibrillation, and 7 (30%) of 24 with induced ventricular flutter, compared to 13 (32%) of 41 with sustained ventricular tachycardia, 7 (17%) of 42 with nonsustained ventricular tachycardia, and only 4 (3%) of 144 noninducible patients (P < 0.001 for induced ventricular fibrillation and ventricular flutter vs noninducible patients). The inducibility of ventricular fibrillation and ventricular flutter were independent risk factors for arrhythmia occurrence in follow-up. Conclusion: Ventricular fibrillation and ventricular flutter induced at electrophysiologic studies have prognostic significance for arrhythmia occurrence in patients presenting with syncope. These induced arrhythmias may not be as nonspecific as previously thought and treatment should be considered for these patients. [ABSTRACT FROM AUTHOR]