Background: Recent randomized controlled trials (RCT) suggest that ablation is superior to antiarrhythmic drugs (AAD) as an initial therapy for paroxysmal atrial fibrillation (pAF) to prevent arrhythmia recurrences. We performed an updated meta-analysis of RCTs, to include recent data from cryoballoon-based ablation, and to compare arrhythmia-free survival and adverse events between ablation and AAMs. Methods: We searched MEDLINE and EMBASE from inception to December 2020. We included RCT comparing patients with pAF undergoing ablation or receiving AADs as an initial therapy. We combined data using the random-effects model to calculate hazards ratio (HR) for arrhythmia-free survival and odds ratio (OR) for adverse events. Results: Five studies from 2005-2020 involving 985 patients were included (495 patients and 490 patients underwent ablation and medication as initial therapy, respectively). Patients who underwent ablation had higher freedom from atrial tachyarrhythmias (AT) during the 12-24 months follow-up period (pooled HR=0.48, 95% CI:0.40-0.59, p<0.001) (Figure 2). In a subgroup analysis of ablation method used, both cryoablation group (pooled HR=0.49, 95% CI:0.38-0.64, p<0.001) (Figure 2A) and radiofrequency ablation group (pooled HR=0.47, 95%CI:0.35-0.64, p<0.001) (Figure 2B) showed reduction in AT recurrence compared to AAD group. There were no differences in adverse events including cerebrovascular accident, pericardial effusion or tamponade, pulmonary vein stenosis, acute coronary syndrome, deep vein thrombosis and pulmonary embolism, and bradycardia requiring a pacemaker. Conclusion: Catheter ablation (both cryoablation and radiofrequency ablation) is superior to AAD as an initial therapy for pAF in efficacy for reducing AT recurrences without a compromise in adverse events.

Background: Multiple strategies have advocation for power titration and catheter movement during atrial fibrillation (AF) ablation. Comparative favoring evidence regarding the efficacy, logistics, and safety of a higher power, shorter duration (HPSD) ablation strategy compared to a lower power, longer duration (LPLD) ablation strategy is insubstantial. We performed a meta-analysis to compare arrhythmia-free survival, procedure times, and complication rates between the two strategies. Methods: We searched MEDLINE, EMBASE and Cochrane Library from inception to April 2020. We included studies comparing patients underwent HPSD and LPLD strategies for AF ablation and reporting either of the following outcomes: freedom from atrial tachyarrhythmia (AT) including AF and atrial flutter, procedure time, or periprocedural complications. We combined data using the random-effects model to calculate odds ratio (OR) and weight mean difference (WMD) with 95% confidence interval (CI). Results: Nine studies from 2006-2020 involving 2,282 patients were included (1,369 patients underwent HPSD strategy and 853 patients underwent LPLD strategy). HPSD strategy was not associated with an increased freedom from AT at 12-month follow-up (OR= 1.41, 95%CI:0.90-2.21). There was a significant reduction in the HPSD group for total procedure (WMD=49.60, 95%CI:29.76-69.44) and ablation (WMD=17.92, 95%CI:13.63-22.22) times, but not for fluoroscopy time (WMD=1.15, 95%CI:-0.67-2.97). HPSD was not associated with a reduction in esophageal ulcer/atrioesophageal fistula (OR=0.35, 95%CI:0.12-1.06) or pericardial effusion/cardiac tamponade rates (OR=0.96, 95%CI:0.24-3.79). Conclusions: When compared to a LPLD strategy, HPSD strategy does not improve recurrent AT nor reduce periprocedural complication risks. However, a HPSD strategy can significantly reduce total procedure and ablation times.

Introduction: Brugada syndrome is associated with ventricular arrhythmia leading to sudden cardiac death. Risk stratification is challenging, as major arrhythmic events (MAE) are rare. We assessed the utility of drug challenge testing in Brugada syndrome by a systematic review and meta-analysis. Methods and results: We comprehensively searched the databases of MEDLINE and EMBASE from inception to May 2019. Included studies compared the incidence of MAE between spontaneous and drug challenge induced Type-1. Data were combined using the random-effects, generic inverse variance method, to calculate pooled incidence and odds ratio (OR). Mixed-effects Poisson regression was used to calculated incidence rate ratio (IRR). Eighteen studies from 2006 to 2018 were included (4,099 patients, mean follow-up 4.5 years). Pooled annual incidences of MAE in spontaneous, drug challenge induced (regardless of symptoms), asymptomatic drug challenge induced, and symptomatic drug challenge induced Type-1 were 23.8 (95% confidence interval [CI]: 19.8-27.8), 6.5 (95% CI: 3.9-9.1), 2.1 (95% CI: -0.3-4.4), and 19.6 (95% CI: 9.9-29.3) per 1,000 person-years respectively. The incidence of MAE between symptomatic drug challenge induced and asymptomatic spontaneous Type-1 was not statistically different (IRR=1.0, 95%CI: 0.6-1.7). The presence of ventricular tachyarrhythmia during drug challenge testing was a predictor of MAE (OR=3.73, 95% CI: 1.77-7.86, p=0.001). Conclusions: The incidence of MAE in drug challenge induced Type-1 in asymptomatic patients is low. The incidence of MAE between symptomatic drug challenge induced and asymptomatic spontaneous Type-1 was similar. Ventricular tachyarrhythmia during drug challenge testing could be a useful risk marker for MAE in Brugada syndrome.