Pulsed Field Ablation of Atrial Fibrillation: An Initial Australian Single-Centre Experience.

BACKGROUND: Pulsed field ablation (PFA) is a newer ablation energy source with the potential to reduce complications and improve efficacy compared to conventional thermal atrial fibrillation (AF) ablation. This study aimed to present an initial single-centre Australian experience of PFA for AF ablation. METHODS: Initial consecutive patients undergoing PFA for paroxysmal or persistent AF at a single centre were included. Baseline patient characteristics, procedural data and clinical outcomes were collected prospectively at the time of the procedure. Patients were followed up at 3 months and 6-monthly thereafter. RESULTS: In total, 100 PFA procedures were performed in 97 patients under general anaesthesia. All pulmonary veins (403 of 403) were successfully isolated acutely. Median follow-up was 218 days (range, 16-343 days), and the Kaplan-Meier estimate for freedom from atrial arrhythmias at 180 days was 87% (95% confidence interval 79%-95%). Median procedure time was 74 minutes (range, 48-134 minutes). Median fluoroscopy dose-area product was 345 µGym2 (interquartile range, 169-685 µGym2). Two (2%) pseudoaneurysm vascular access complications occurred. There were no cases of thromboembolic complications, stroke, phrenic nerve palsy, pulmonary vein stenosis, atrio-oesophageal fistula, or pericardial tamponade. CONCLUSIONS: Pulsed field ablation can be performed safely and efficiently, with encouraging efficacy in early follow-up. Further data and clinical trials will be required to assess the comparative utility of PFA in contemporary AF ablation practice.

Freedom from atrial arrhythmia and other clinical outcomes at 5 years and beyond after catheter ablation of atrial fibrillation: a systematic review and meta-analysis.

AIMS: Catheter ablation of atrial fibrillation (AF) is now a mainstream procedure although long-term outcomes are uncertain. We performed a systematic review and meta-analysis of procedural outcomes at 5 years and beyond. METHODS AND RESULTS: We searched PubMed and Embase and after the screening, identified 73 studies (67 159 patients) reporting freedom from atrial arrhythmia, all-cause death, stroke, and major bleeding at ≥5 years after AF ablation. The pooled mean age was 59.7y, 71.5% male, 62.2% paroxysmal AF, and radiofrequency was used in 78.1% of studies. Pooled incidence of freedom from atrial arrhythmia at 5 years was 50.6% (95%CI 45.5-55.7%) after a single ablation and 69.7% [95%CI (confidence interval) 63.8-75.3%) after multiple procedures. The incidence was higher among patients with paroxysmal compared with non-paroxysmal AF after single (59.7% vs. 33.3%, p = 0.002) and multiple (80.8% vs. 60.6%, p < 0.001) ablations but was comparable between radiofrequency and cryoablation. Pooled incidences of other outcomes were 6.0% (95%CI 3.2-9.7%) for death, 2.4% (95%CI 1.4-3.7%) for stroke, and 1.2% (95%CI 0.8-2.0%) for major bleeding at 5 years. Beyond 5 years, freedom from arrhythmia recurrence remained largely stable (52.3% and 64.7% after single and multiple procedures at 10 years), while the risk of stroke and bleeding increased over time. CONCLUSION: Nearly 70% of patients having multiple ablations remained free from atrial arrhythmia at 5 years, with the incidence slightly decreasing beyond this period. Risk of death, stroke, and major bleeding at 5 years were low but increased over time, emphasizing the importance of long-term thromboembolism prevention and bleeding risk management.

Is Digital Tomosynthesis on Par With Computed Tomography for the Detection and Measurement of Pulmonary Nodules?

Chest digital tomosynthesis (DT) has potential advantages compared to computed tomography (CT) such as radiation dose reduction. However, the role of DT in pulmonary nodule management remains investigative. We compared DT against CT for pulmonary nodule detection and size measurement. A clinical population comprising 54 nodules from 30 patients and a screening population comprising 42 nodules from 52 patients were included. Scans were independently read by two radiologists. Agreement in nodule measurements between readers and between modalities was assessed by Bland-Altman analysis using a 95% level of significance. The DT true positive fraction for the two readers was 0.44 and 0.39 in the clinical population, and 0.10 and 0.05 in the screening population. No significant inter-modality bias was observed between DT and CT measurements of nodule size, but the range of variation between modalities was approximately 30%. Inter-reader DT measurements also showed no significant bias, with a range of variation of approximately 15%. We conclude that DT has poor nodule detection sensitivity compared to CT. However, DT showed good measurement reproducibility and may be useful for monitoring growth of existing pulmonary nodules.

The ß3 -adrenoceptor agonist mirabegron increases human atrial force through ß1 -adrenoceptors: an indirect mechanism?

BACKGROUND AND PURPOSE: Mirabegron has been classified as a ß3 -adrenoceptor agonist approved for overactive bladder syndrome. We investigated possible cardiac effects of mirabegron in the absence or presence of ß-adrenoceptor subtype antagonists. In view of its phenylethanolamine structure, we investigated whether mirabegron has indirect sympathomimetic activity by using neuronal uptake blockers. EXPERIMENTAL APPROACH: Right atrial trabeculae, from non-failing hearts, were paced and contractile force measured at 37°C. Single concentrations of mirabegron were added in the absence or presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), ß3 (L-748,337), ß1 (CGP 20712A), ß2 (ICI 118,551) -adrenoceptor antagonists, neuronal uptake inhibitors desipramine or phenoxybenzamine. KEY RESULTS: Mirabegron significantly increased contractile force in human right atrium (1 µM, 7.6 ± 2.6%, n = 7; 10 µM, 10.2 ± 1.5%, n = 22 compared with (-)-isoprenaline P < 0.05). In the presence of IBMX, mirabegron (10 µM) caused a greater contraction. L-748,337 (100 nM) had no effect on the increase in contractile force caused by mirabegron (10 µM). In contrast, mirabegron (10 µM) reduced contractile force in the presence of CGP 20712A, which was not affected by L-748,337 (100 nM) or ICI 118,551 (50 nM). Mirabegron (10 µM) also reduced contractile force in the presence of desipramine or phenoxybenzamine. CONCLUSIONS AND IMPLICATIONS: Mirabegron increases human atrial force through ß1 - but not ß3 -adrenoceptors. Desipramine and phenoxybenzamine block neuronal uptake and conceivably prevent mirabegron from releasing noradrenaline. A non-specific cardiodepressant effect is not mediated through ß3 (or ß2 )-adrenoceptors, consistent with lack of ß3 -adrenoceptor function on human atrial contractility.