Jackson J. Liang

Aims Ablation of outflow tract ventricular arrhythmias may be limited by a deep intramural location of the arrhythmogenic source. This study evaluates the acute and long-term outcomes of patients undergoing ablation of intramural outflow tract premature ventricular complexes (PVCs). Methods and results This multicenter series included patients with structurally normal heart or nonischemic cardiomyopathy and intramural outflow tract PVCs defined by: (a) ≥ 2 of the following criteria: (1) earliest endocardial or epicardial activation < 20ms pre-QRS; (2) Similar activation in different chambers; (3) no/transient PVC suppression with ablation at earliest endocardial/epicardial site; or (b) earliest ventricular activation recorded in a septal coronary vein. Ninety-two patients were included, with a mean PVC burden of 21.5±10.9%. Twenty-six patients had had previous ablations. All PVCs had inferior axis, with LBBB pattern in 68%. In 29 patients (32%) direct mapping of the intramural septum was performed using an insulated wire or multielectrode catheter, and in 13 of these cases the earliest activation was recorded within a septal vein. Most patients required special ablation techniques (one or more), including sequential unipolar ablation in 73%, low-ionic irrigation in 26%, bipolar ablation in 15% and ethanol ablation in 1%. Acute PVC suppression was achieved in 75% of patients. Following the procedure, the PVC burden was reduced to 5.8±8.4%. The mean follow-up was 15±14 months and 16 patients underwent a repeat ablation. Conclusion Ablation of intramural PVCs is challenging; acute arrhythmia elimination is achieved in 3/4 patients, and non-conventional approaches are often necessary for success.

Introduction Incidental left atrial appendage (LAA) isolation may occur during radiofrequency ablation of persistent atrial fibrillation (AF). The study aims to describe the mechanisms and long‐term thromboembolic risk related to incidental LAA isolation. Methods Patients who experienced incidental LAA isolation after AF ablation were included. Culprit sites where ablation resulted in LAA isolation were identified. Thromboembolic risk despite oral anticoagulation (OAC) was compared to that in a propensity‐matched control group without LAA isolation. Results Forty‐one patients with LAA isolation, and 82 matched patients without LAA isolation were included. The patient age, ejection fraction, LA diameter, and CHA 2 DS 2 ‐VASc score were 64 ± 11 years, 55 ± 12%, 45.0 ± 7 mm and 2.62 ± 1.5, respectively. Culprit sites included the LAA base, mitral isthmus, inferior LA, Bachmann′s bundle, coronary sinus, and Marshall vein. After 4.2 ± 3.6 years follow‐up, thromboembolism occurred in 7 of 41 patients (17%) with LAA isolation versus 3 of 82 patients (4%) without isolation (log rank p < .009, HR 5.14, 95% CI [1.32–19.94], p = .02). Patients with and without thromboembolism had similar CHA 2 DS 2 ‐VASc scores (2.65 ± 1.3 vs. 2.71 ± 0.76, p = .89). Thromboembolism occurred during noncompliance with or temporary discontinuation of OAC in four of the seven patients. Conclusions Incidental LAA isolation may occur during ablation of atrial arrhythmias in the vicinity of, or even at sites remote from the appendage. Patients with incidental LAA isolation had higher rates of thromboembolism compared to patients without isolation. Since thromboembolism may occur despite prescription for OAC, the risks of LAA isolation must be weighed against clinical benefit and appendage occlusion devices should be considered in vulnerable patients.