Shih‐Lin Chang

BACKGROUND: Current American and European guidelines emphasize the importance of rate-control treatments in treating atrial fibrillation with a Class I recommendation, although data on the survival benefits of rate control are lacking. The goal of the present study was to investigate whether patients receiving rate-control drugs had a better prognosis compared with those without rate-control treatment. METHODS AND RESULTS: This study used the National Health Insurance Research Database in Taiwan. There were 43 879, 18 466, and 38 898 patients with atrial fibrillation enrolled in the groups receiving β-blockers, calcium channel blockers, and digoxin, respectively. The reference group consisted of 168 678 subjects who did not receive any rate-control drug. The clinical end point was all-cause mortality. During a follow-up of 4.9±3.7 years, mortality occurred in 88 263 patients (32.7%). After adjustment for baseline differences, the risk of mortality was lower in patients receiving β-blockers (adjusted hazard ratio=0.76; 95% confidence interval=0.74-0.78) and calcium channel blockers (adjusted hazard ratio=0.93; 95% confidence interval=0.90-0.96) compared with those who did not receive rate-control medications. On the contrary, the digoxin group had a higher risk of mortality with an adjusted hazard ratio of 1.12 (95% confidence interval=1.10-1.14). The results were observed consistently in subgroup analyses and among the cohorts after propensity matching. CONCLUSIONS: In this nationwide atrial fibrillation cohort, the risk of mortality was lower for patients receiving rate-control treatment with β-blockers or calcium channel blockers, and the use of β-blockers was associated with the largest risk reduction. Digoxin use was associated with greater mortality. Prospective, randomized trials are necessary to confirm these findings.

INTRODUCTION: The mechanisms of late (<1 year after the ablation) and very late (>1 year after the ablation) recurrences of paroxysmal atrial fibrillation (AF) after catheter ablation have not been reported. METHODS AND RESULTS: Fifty consecutive patients undergoing a repeated electrophysiologic study to investigate the recurrence of paroxysmal AF after the first ablation were included. Group 1 consisted of 12 patients with very late (26 +/- 13 months) and group 2 consisted of 38 patients with late (3 +/- 3 months) recurrence of paroxysmal AF. In the baseline study, group 1 had a lower incidence of AF foci from the pulmonary veins (PVs) (67% vs 92%, P = 0.048) and a higher incidence of AF foci from the right atrium (50% vs 13%, P = 0.014) than group 2. In the repeated study, group 1 had a higher incidence of AF foci from the right atrium (67% vs 3%, P < 0.001) and a lower incidence of AF foci from the left atrium (50% vs 97%, P < 0.001), including a lower incidence of AF foci from the PVs (50% vs 79%, P = 0.07) and from the left atrial free wall (0% vs 29%, P = 0.046) than group 2. Furthermore, most of these AF foci (64% of group 1, 65% of group 2) were from the previously targeted foci. CONCLUSION: The right atrial foci played an important role in the very late recurrence of AF, whereas the left atrial foci (the majority were PVs) were the major origin of the late recurrence of AF after the catheter ablation of paroxysmal AF.

INTRODUCTION: We aimed to clarify the effect of vein of Marshall (VOM) ethanol infusion for treating VOM triggers and/or mitral flutter after first-attempt endocardial ablation in patients with nonparoxysmal atrial fibrillation (AF). METHODS AND RESULTS: Of the 254 consecutive patients (age, 56 ± 10 years; 221 male) undergoing catheter ablation for drug-refractory nonparoxysmal AF, 32 (12.6%) received VOM ethanol infusion. The patients were stratified into group 1 (pulmonary vein isolation [PVI], substrate modification, VOM ethanol infusion), group 2 (PVI, substrate modification), and group 3 (PVI alone). Propensity-matched analysis (N = 128) of long-term outcomes (3.9 ± 0.5 years) revealed a higher AF recurrence risk in group 2 (hazard ratio [HR], 4.17; 95% confidence interval [95% CI], 1.63-10.69; P = .003) and group 3 (HR, 1.82; 95% CI, 1.09-3.04; P = .021) than in group 1, as well as a higher atrial arrhythmia recurrence risk in group 2 than in group 1 (HR, 2.42; 95% CI, 1.16-5.03; P = .018). A higher procedural termination rate was observed in group 1 than groups 2 and 3 (41.7% vs 17.2% vs 18.8%; P = .042). On multivariate analysis, VOM ethanol injection was an independent predictor of freedom from recurrence of AF (HR, 0.20; 95% CI, 0.08-0.52; P = .001) and atrial arrhythmia (HR, 0.35; 95% CI, 0.17-0.74; P = .005), whereas a left atrial diameter >45 mm and hypertension were independent risk factors for recurrence. Periprocedural complications rates were comparable among the groups. CONCLUSION: Adjunctive VOM ethanol infusion is effective and safe for treating nonparoxysmal AF in patients with VOM triggers and/or refractory mitral flutter, providing good long-term freedom from AF and atrial arrhythmia.

INTRODUCTION: The left atrial appendage (LAA) has been proven to be the most important site of thrombus formation in patients with atrial fibrillation (AF). However, the information regarding the morphometric alteration of the LAA related to the outcome of AF ablation is still lacking. Thus, we evaluated the long-term changes of the LAA morphology in patients undergoing catheter ablation of AF using magnetic resonance angiography (MRA). METHODS AND RESULTS: Group 1 included 15 controls without any AF history. Group 2 included 40 patients with drug-refractory paroxysmal AF. They were divided into two subgroups: group 2a included 30 patients without AF recurrence after pulmonary vein (PV) ablation. Group 2b included 10 patients with late recurrence of AF. The LAA morphology before and after (20 +/- 11 months) ablation was evaluated by three-dimensional MRA. The group 2 patients had a larger baseline LAA size (including the LAA orifice, neck, and length) and less eccentric LAA orifice and neck. After the AF ablation, there was a significant reduction in the LAA size in the group 2a patients, and the morphology of the LAA neck became more eccentric during the follow-up period. In group 2b, the LAA size increased and no significant change in the eccentricity of the orifice and neck could be noted. CONCLUSIONS: The morphometric remodeling of the LAA in the AF patients could be reversed after a successful ablation of the AF. Progressive dilation of the LAA was noted in the patients with AF recurrence. These structural changes in the LAA may play a role in reducing the potential risk of cerebrovascular accidents.