Pulmonary vein isolation alone versus pulmonary vein isolation with additional extensive ablation for paroxysmal and persistent atrial fibrillation.

Background: The value of additional ablation beyond pulmonary vein isolation for atrial fibrillation (AF) ablation is unclear, especially for persistent AF. It is uncertain whether substrate modification with additional extensive ablation improves outcomes. We reviewed our experience to determine whether pulmonary vein isolation with additional extensive ablation (PVIEA) improves outcomes compared to pulmonary vein isolation alone (PVIA) for AF ablation. Methods: Consecutive cases of patients with PVIA versus PVIEA were compared between September 9, 2013 and December 12, 2020. Procedural data collected include radiofrequency ablation delivery time (RADT) and arrhythmia inducibility. Clinical data collected include sinus rhythm maintenance post-procedure. Results: A total of 235 patients were studied (67 PVIA and 168 PVIEA). RADT was shorter when comparing ablation with PVIA versus PVIEA (32 vs. 40 min; p = .04). More arrhythmias were inducible with PVIEA (p < .01). There was no difference in sinus rhythm maintenance by Kaplan-Meier survival analysis (log-rank test p = .75), after 3 or 12 months between groups overall, and when stratified by AF type (paroxysmal and persistent), left atrial volume, CHA2DS2-VASc score, left ventricular ejection fraction, or catheter ablation setting (high-power short-duration, standard-power standard-duration, temperature-controlled non-contact-force). Conclusion: AF ablation with PVIA or PVIEA produces similar sinus rhythm maintenance overall and when stratified by catheter setting and AF type. PVIA reduced procedure times and less arrhythmias were inducible post-ablation.

High-power short-duration versus standard-power standard-duration settings for repeat atrial fibrillation ablation.

INTRODUCTION: High-power short-duration (HPSD) ablation is a novel strategy using contact force-sensing catheters optimized for radiofrequency ablation for atrial fibrillation (AF). No study has directly compared HPSD versus standard-power standard-duration (SPSD) contact force-sensing settings in patients presenting for repeat ablation with AF recurrence after initial ablation. METHODS: We studied consecutive cases of patients with AF undergoing repeat ablation with SPSD or HPSD settings after their initial pulmonary vein isolation (PVI) with temperature controlled non-contact force, SPSD or HPSD settings between 6/23/14 and 3/4/20. Procedural data collected included radiofrequency ablation delivery time (RADT). Clinical data collected include sinus rhythm maintenance post-procedure. RESULTS: A total of 61 patients underwent repeat ablation (36 SPSD, 25 HPSD). A total of 51 patients (83.6%) were found to have pulmonary vein reconnections necessitating repeat isolation, 10 patients (16.4%) had durable PVI and ablation targeted non-PV sources. RADT was shorter when comparing repeat ablation using HPSD compared to SPSD (22 vs 35 min; p = 0.01). There was no difference in sinus rhythm maintenance by Kaplan-Meier survival analysis (log rank test p = 0.87), after 3 or 12-months between groups overall, and when stratified by AF type, left atrial volume index, CHA2DS2-VASc score, or left ventricular ejection fraction. CONCLUSION: We demonstrated that repeat AF ablation with HPSD reduced procedure times with similar sinus rhythm maintenance compared to SPSD in those presenting for repeat ablation.

Comparison of clinical and procedural outcomes between high-power short-duration, standard-power standard-duration, and temperature-controlled noncontact force guided ablation for atrial fibrillation.

INTRODUCTION: High-power short-duration (HPSD) ablation is a novel strategy using contact force-sensing catheters optimized for power-controlled radiofrequency ablation for atrial fibrillation (AF). This study investigates the outcomes of HPSD (50 W delivered for up to 15 s, Lesion Size Index of 5-6) compared to standard-power standard-duration (SPSD) (20-25 W until 400-500 gram seconds, up to 60 s) and temperature-controlled noncontact (TCNC) (20-40 W up to 60 s of ablation) settings. METHODS: We studied consecutive cases of patients with AF undergoing pulmonary vein isolation with TCNC, SPSD, and HPSD between January 7th, 2013 and January 11th, 2019. Procedural data collected include time to isolate the left (LPVT) and right pulmonary veins (RPVT), total ablation time (TAT), and radiofrequency ablation delivery time (RADT). Clinical data collected include sinus rhythm maintenance postprocedure. RESULTS: One hundred and seventy-one patients were studied (44 TCNC, 51 SPSD, 76 HPSD). RADT was shorter when comparing HPSD to SPSD (25 vs. 41 min; p < .01), HPSD to TCNC (25 vs. 76 min; p < .01), and SPSD to TCNC groups (41 vs. 76 min; p < .01). TAT, LPVT, and RPVT were reduced between HPSD versus SPSD, HPSD versus TCNC, and SPSD versus TCNC groups, respectively (p < .01). There was no difference in sinus rhythm maintenance by Kaplan-Meier survival analysis (log rank test p = .12), after 3 or 12 months between groups overall, and when stratified by AF type, left atrial volume, CHA2 DS2 -VASc score, or left ventricular ejection fraction. CONCLUSION: AF ablation with HPSD reduced procedure times with similar sinus rhythm maintenance compared to SPSD and TCNC.

Ablation of Foxl1-Cre-labeled hepatic progenitor cells and their descendants impairs recovery of mice from liver injury.

BACKGROUND & AIMS: Foxl1(+) hepatic progenitor cells (HPCs) differentiate into cholangiocytes and hepatocytes after liver injury. We investigated the requirement for Foxl1(+) HPCs in recovery from liver injury in mice. METHODS: We developed mice in which we could trace and delete Foxl1-expressing HPCs and their descendants (Foxl1-Cre;Rosa(YFP/iDTR)-inducible diphtheria toxin receptor [iDTR] mice). Foxl1-Cre-negative mice were used as controls. Liver damage was induced in male mice by placing them on choline-deficient, ethionine-supplemented (CDE) diets for 15 days; mice then were placed on normal diets and allowed to recover. Liver damage was induced in female mice by placing them on 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-containing diets, followed by a recovery period. Some mice were given injections of diphtheria toxin during the recovery phase to delete Foxl1-Cre-marked HPCs and their descendants. Livers were collected from all mice and analyzed by immunofluorescence, quantitative reverse-transcription polymerase chain reaction, flow cytometry, and histologic analyses. RESULTS: Foxl1-Cre-marked HPCs were required for the development of cholangiocytes and hepatocytes in livers after CDE diet-induced injury. A smaller percentage of yellow fluorescent protein-positive (YFP(+)) hepatocytes contained markers of oxidative stress, DNA damage, or cell death than YFP-negative hepatocytes, indicating that YFP(+) hepatocytes are newly formed cells. Injection of diphtheria toxin deleted YFP(+) cells from Foxl1-Cre;Rosa(YFP/iDTR) mice and prevented the resolution of hepatic steatosis. In mice recovering from DDC diet-induced injury, most cholangiocytes arose from Foxl1-Cre-marked HPCs. Deletion of YFP(+) cells did not alter levels of markers of liver injury or liver function. CONCLUSIONS: Based on studies of Foxl1-Cre;Rosa(YFP/iDTR) mice, Foxl1(+) HPCs and/or their descendants are required for the development of cholangiocytes and hepatocytes in liver after CDE diet-induced injury.