Oral anticoagulation after catheter ablation of atrial fibrillation: caught in the attribution trap?

Catheter ablation procedures are performed in 5-10% of patients suffering from atrial fibrillation (AF). 3 While the main reason for undertaking AF ablation is because the patient is suffering from symptomatic AF, those who undergo AF ablation are younger and ‘generally healthier’ than patients who do not undergo ablation treatment, 6 as reflected by lower stroke risk scores, but also driven by confounders that will inform the clinical decision to submit a patients to catheter ablation procedures. Manipulation in the left atrium, wound healing, and scar formation in the atria, along with other factors, generate a thrombogenic milieu in the atria of patients undergoing AF ablation. Therefore, all ablation patients require continuous oral anticoagulation during and for at least 3 months after an AF ablation procedure. The indication for long-term anticoagulation should be based on clinical stroke risk factors thereafter. Karasoy and colleagues have now reported on a cohort of 4050 patients (59.5 years, 74% men) who underwent a first catheter ablation for AF in Denmark from 2000 to 2011. Approximately half of the patients had clinically documented AF recurrence (measured by hospitalization or reablation) and each patient received 1.5 AF ablation procedureson average, very much in linewith published outcomes after catheter ablation. The authors furthermore analysed thrombo-embolic events [(ischaemic stroke, transient ischaemic attack (TIA), and peripheral artery embolism] and severe bleeding events in this cohort over a mean follow-up time of .3 years. This information is valuable because of the comprehensive capture of information in a population-based sample. Consistent with other data, early thrombo-embolic events after ablation were common (20 thrombo-embolic events in the first 2 weeks after the first ablation, corresponding to an estimated yearly incidence of 12.9% per year; figure 2 in Karasoy et al.). It is conceivable that changes in practice, e.g. continued oral anticoagulation during AF ablation procedures, prevent some ischaemic strokes during AF ablation. Clearly, there is an unmet need to better protect the brain against ischaemic damage during AF ablation. Half of the patients received oral anticoagulation for at least 1 year after catheter ablation, including patients without a clear indication for continued anticoagulation (56% of CHA2DS2VASC 1⁄4 0 patients, 67% of CHA2DS2VASC 1⁄4 1 patients). As expected, bleeding events were higher in patients who remained on anticoagulation after AF ablation [hazard ratio (HR) 2.05; figure 4 in Karasoy et al.]. There were 103 clinically documented thrombo-embolic events during follow-up (annualized rate 0.8%, wide confidence intervals), numerically a bit lower than expected. In part, this lower rate is probably explained by the low intensity follow-up, where patients with ‘subclinical’ strokes and TIAs that are managed as outpatients or not brought to medical attention will not be captured on national databases, while controlled trials will pick up such events. Furthermore, permanent ‘silent brain emboli’ which are found in AF and can be triggered by catheter ablation are not reflected in this analysis, although they may contribute to cognitive decline. Nonetheless, the stroke rate in a matched cohort of Danish patients receiving cardioversions or antiarrhythmic drug therapy during the same period was higher (1.77% per year). Our hypothetical figure summarizes these observation in a speculative manner (Figure 1).