Antithrombotic therapy after successful catheter ablation for atrial fibrillation: toward a risk-stratified and strategy-based approach

Catheter ablation has become a cornerstone therapy for atrial fibrillation (AF), offering effective rhythm control and symptomatic improvement. However, whether successful ablation sufficiently reduces thromboembolic risk to allow modification of long-term antithrombotic therapy remains uncertain. Current guidelines consistently recommend that decisions regarding anticoagulation after AF ablation be based on baseline stroke risk rather than procedural success, reflecting concerns regarding asymptomatic AF recurrence and the persistence of thromboembolic risk (1,2).

The OCEAN trial provides important randomized evidence addressing this issue. In this study, patients with at least one stroke risk factor who remained free of AF recurrence for at least one year after catheter ablation were randomized to rivaroxaban or aspirin and followed for 3 years (3). The primary composite outcome of stroke, systemic embolism, or covert cerebral infarction occurred at very low rates in both groups, with no significant difference between treatments (3). These findings suggest that, in selected patients after apparently successful ablation, the residual thromboembolic risk may be substantially lower than traditionally assumed.

However, these results should be interpreted in the context of the study population. Despite inclusion criteria based on stroke risk, the OCEAN cohort represents a relatively low-risk group. The mean CHA₂DS₂-VASc score was modest (approximately 2.2), a large proportion of patients had paroxysmal AF, and structural remodeling appeared limited, with a mean left atrial diameter of approximately 40 mm (3). Taken together, these features suggest a population with relatively preserved atrial substrate, likely to respond favorably to ablation, with a lower probability of asymptomatic AF recurrence and, consequently, a reduced thromboembolic risk. Accordingly, the remarkably low event rates observed in OCEAN—approximately 0.3 to 0.6 events per 100 patient-years—may reflect, at least in part, favorable patient selection rather than a universal effect of ablation. This distinction is clinically important, as patients with persistent AF, enlarged atria, or advanced atrial cardiomyopathy may have substantially higher residual risk, limiting the generalizability of these findings.

On the other hand, the key clinical question extends beyond whether anticoagulation can be discontinued. Rather, it becomes how antithrombotic therapy should be tailored after AF ablation across different risk profiles.

Randomized studies of post-ablation antithrombotic management have explored two distinct therapeutic strategies: de-escalation or discontinuation of anticoagulation, and alternative approaches aimed at maintaining stroke prevention. The OCEAN trial represents a pharmacological de-escalation strategy, demonstrating very low event rates despite inclusion of both clinical and subclinical cerebrovascular events. Similarly, the ALONE-AF trial reported low stroke rates following discontinuation of anticoagulation in patients without recurrent atrial arrhythmia, although the study was underpowered and limited by early termination (4). Importantly, interpretation of these findings requires consideration of endpoint definitions. The OCEAN trial uniquely incorporated covert cerebral infarction detected by brain magnetic resonance imaging into its primary endpoint, thereby capturing subclinical events that would not have been identified in most prior trials. Despite this broader and more sensitive endpoint, event rates remained low, suggesting that thromboembolic risk after successful ablation may be attenuated, but not eliminated.

De-escalation strategies, however, represent only one component of the therapeutic landscape. In higher-risk populations, alternative approaches aimed at maintaining stroke protection have been evaluated. In the OPTION trial, left atrial appendage (LAA) occlusion was non-inferior to continued anticoagulation in patients with a higher mean CHA₂DS₂-VASc score of approximately 3.5 (5). Similarly, the PRAGUE-17 trial demonstrated non-inferiority of LAA closure compared with direct oral anticoagulants in high-risk AF patients (6). These studies primarily evaluated clinically overt thromboembolic events, in contrast to the broader endpoint used in OCEAN.

Taken together, these findings define a spectrum of post-ablation antithrombotic strategies: de-escalation or discontinuation in lower-risk patients and sustained or alternative stroke prevention in higher-risk populations. Across this spectrum, thromboembolic event rates remain low but consistently non-zero, regardless of whether management is pharmacological or mechanical occlusion. This pattern suggests that contemporary strategies—including rhythm control, anticoagulation, and LAA exclusion—may reduce stroke risk to a similar range, but do not eliminate it.

Another important unresolved issue is the relationship between AF burden and stroke risk. Catheter ablation reduces AF burden but does not necessarily eliminate arrhythmia. Although emerging evidence suggests that AF burden may influence thromboembolic risk, current clinical risk stratification tools do not incorporate this parameter. In addition, continuous rhythm monitoring was not mandated in OCEAN, and asymptomatic AF recurrence may have been underestimated. These limitations highlight the need for improved risk stratification strategies that integrate rhythm status, atrial substrate, and clinical risk factors.

Importantly, these uncertainties warrant caution when considering discontinuation of anticoagulation, even in patients who appear to be at relatively low risk after successful ablation. The absence of documented AF recurrence should not be equated with elimination of thromboembolic risk, particularly given the limitations of intermittent rhythm surveillance. Furthermore, both AF and stroke risk are dynamic processes. Patients may develop recurrent arrhythmia years after ablation and may simultaneously accumulate additional CHA₂DS₂-VASc risk factors over time. In addition, persistent atrial cardiomyopathy may contribute to thromboembolic risk independently of clinically detected AF. As highlighted by Junarta et al., the concept of “zero-burden AF” should not necessarily be interpreted as “zero-risk AF” (7). Therefore, decisions regarding long-term anticoagulation should be individualized and accompanied by continued reassessment of rhythm status and evolving clinical risk profiles rather than being based solely on apparent procedural success.

From a clinical perspective, the implications of these findings are nuanced. The OCEAN trial does not support routine discontinuation of anticoagulation in all patients after AF ablation. Instead, it suggests that, in selected low-risk patients, thromboembolic risk is low and de-escalation strategies may be considered. Conversely, in patients with higher stroke risk or more advanced structural heart disease, continued anticoagulation or alternative approaches such as LAA occlusion should be strongly considered.

Future research should focus on refining patient selection for different antithrombotic strategies. This will likely require integration of advanced rhythm monitoring, imaging-based assessment of atrial disease, and potentially biomarker-guided risk stratification. In parallel, further randomized trials comparing pharmacological and device-based strategies across diverse risk populations will be essential.

In conclusion, the OCEAN trial provides important evidence that thromboembolic risk after successful AF ablation may be lower than previously assumed in selected patients. However, the absence of documented AF recurrence should not be interpreted as elimination of thromboembolic risk, given the dynamic nature of both AF progression and stroke risk over time. When considered alongside data from higher-risk cohorts, including trials of LAA occlusion, these results support a risk-stratified and strategy-based approach to post-ablation antithrombotic therapy. Continued reassessment of rhythm status and evolving clinical risk factors will be essential for optimizing long-term treatment decisions.

Acknowledgments

None.

Footnote

Provenance and Peer Review: This article was commissioned by the editorial office, Journal of Thoracic Disease. The article has undergone external peer review.

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Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1353/coif). The authors have no conflicts of interest to declare.

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