Background-Left atrioesophageal fistula is a devastating complication of atrial fibrillation ablation. There is no standard approach for avoiding this complication, which is caused by thermal injury during ablation. The objectives of this study were to evaluate the course of the esophagus and the temperature within the esophagus during pulmonary vein antrum isolation (PVAI) and correlate these data with esophagus tissue damage. Methods and Results-Eight-one patients presenting for PVAI underwent esophagus evaluation that included temperature probe placement. Esophagus course was obtained with computed tomography, 3D imaging (NAVX), or intracardiac echocardiography. For each lesion, the power, catheter and esophagus temperature, location, and presence of microbubbles were recorded. Lesion location and esophagus course were defined with 6 predetermined left atrial anatomic segments. Endoscopy evaluated tissue changes during and after PVAI. Of 81 patients, the esophagus coursed near the right pulmonary veins in 23 (28.4%), left pulmonary veins in 31 (38.3%), and mid-posterior wall in 27 (33%

Pre-existent LAS in patients undergoing PVAI for AF is a powerful, independent predictor of procedural failure. Left atrial scarring is associated with a lower EF, larger LA size, and increased inflammatory markers.

Ventricular fibrillation in ICM is triggered by monomorphic PVCs originating from the scar border zone with preceding PLPs; targeting these PVCs may prevent VF recurrence. In the absence of PVCs, both substrate mapping and ablation appear to be equally effective.

The SVC harbors the majority of non-PV triggers of AF. SVCI is feasible, safe, and may be considered as an adjunctive strategy to PVAI for ablation of AF. The long-term favorable outcome of this hybrid approach remains to be evaluated in a larger series of patients.

Background-The role of pulmonary vein (PV) isolation in ablative treatment of atrial fibrillation (AF) has been debated in conflicting reports. We sought to compare PV conduction in patients who had no AF recurrence (group I), patients who could maintain sinus rhythm on antiarrhythmic medication (group II), and patients who had recurrent AF despite antiarrhythmic medication (group III) after PV antrum isolation (PVAI). Methods and Results-PV conduction was examined in consecutive patients undergoing second PVAI for AF recurrence.We also recruited some patients cured of AF to undergo a repeat, limited electrophysiological study at Ͼ3 months after PVAI. All patients underwent PVAI with an intracardiac echocardiography (ICE)-guided approach with complete isolation of all 4 PV antra (PVA). The number of PVs with recurrent conduction and the shortest atrial to PV (A-PV) conduction delay was measured with the use of consistent Lasso positions defined by ICE. Late AF recurrence was defined as AF Ͼ2 months after PVAI with the patient off medications. Patients in groups I (nϭ26), II (nϭ37), and III (nϭ44) did not differ at baseline (38% permanent AF; ejection fraction 53Ϯ6%). Recurrence of PV-left atrial (LA) conduction was seen in 1.7Ϯ0.8 and 2.2Ϯ0.8 PVAs for groups II and III but only in 0.2Ϯ0.4 for group I (Pϭ0.02). In patients with recurrent PV-LA conduction, the A-PV delay increased from the first to second procedure by 69Ϯ47% for group III, 267Ϯ110% for group II, and 473Ϯ71% for group I (PϽ0.001). When pacing was at a faster rate, A-PV block developed in all 5 of the group I patients with recurrent PV-LA conduction. Conclusions-The majority of patients with drug-free cure show no PV-LA conduction recurrence. Substantial A-PV delay is seen in patients able to maintain sinus rhythm on antiarrhythmic medication or cured of AF compared with patients who fail PVAI. (Circulation. 2005;112:627-635.)

Successful ablation sites of hemodynamically stable, monomorphic VTs post-MI are often located in the scar border zone as defined by substrate voltage mapping. However, in a sizable minority, ablation sites are located within endocardial scar, epicardially, and even in normal myocardium.

VF is the causative arrhythmia for a sizable proportion of patients with ES. The initial ICD indication, coronary artery disease, and amiodarone therapy are predictors of the causative arrhythmias in ES. There does not appear to be any mortality difference between ES patients with VT and VF, but mortality is increased in patients with ES versus control ICD patients without ES.

Extensive ablation during PVAI does not cause deterioration in LA function, and may cause long-term improvement, especially in patients with higher AF burden.