Continuing anticoagulation in patients with resolved atrial fibrillation – is there a clear evidence?
I read with interest the article by Adderley et. al.  on the risk of stroke in patients with resolved atrial fibrillation (AF) and congratulate authors for their effort and agree that the patients with resolved-AF remain at higher risk of stroke than patients without history of AF, but respectfully question their conclusions and recommendation to update guidelines to advocate continued use of anticoagulants in patients with resolved-AF.
Atrial fibrillation (AF) and carotid atherosclerosis or carotid artery stenosis (CAS) share several risk factors and often coexist in the same patient, and carotid atherosclerosis often antedates AF . The ARIC study showed that carotid atherosclerosis plays an important role in the cause of stroke in patients with AF  and is associated with increased risk of ischemic stroke in these patients . Similarly, Lehtola et al  in FibStroke registry also found that concomitant CAS in patients with AF doubles the risk of recurrent stroke, and in a multivariate analysis CAS was shown to be an independent risk factor for stroke in patients with AF, and anticoagulation in these patients with AF and CAS did not reduce the rate of stroke recurrence.
It is interesting that in the current study, authors did not assess the degree of carotid atherosclerosis or stenosis, when there were significant baseline differences, with almost 1.5 to 2 times higher prevalence of cardiovascular risk factors (hypertension, diabetes, ischemic heart disease and heart failure) among patients with resolved atrial fibrillation compared to patients without a history of atrial fibrillation. Authors presume that the underlying mechanism of stroke in patients with resolved-AF was possibly cardioembolic thereby recommending, to update guidelines for continuing anticoagulation in patients with resolved-AF when it is unclear whether the underlying mechanism was cardioembolic or not.
The efficacy of anticoagulation in the prevention of AF-related stroke is well established, however, anticoagulation has not been found to be beneficial than antiplatelet therapy in the secondary prevention of non-cardioembolic stroke [5,6]. Hence, it is unclear if continuing anticoagulation in these patients would reduce stroke and is premature to make such strong recommendations when the major factor contributing to stroke, even in patients with atrial fibrillation, is not evaluated in this study.
1. Adderley NJ, Nirantharakumar K, Marshall T: Risk of stroke and transient ischemic attack in patients with a diagnosis of resolved atrial fibrillation: retrospective cohort studies. BMJ 2018;360:k1717.
2. Willeit K, Pechlaner R, Eggar G, et al. Carotid atherosclerosis and incident atrial fibrillation. Arterioscler Thromb Vasc Biol 2013; 33(11):2660-5.
3. Bekwelem W, Jensen PN, Norby FL, et al. Carotid Atherosclerosis and Stroke in Atrial Fibrillation: The Atherosclerosis Risk in Communities Study. Stroke 2016; 47:1643-46.
4. Lehtola H, Airaksinen KEJ, Hartikainen P, Hartikainen JEK, Palomaki A, Nuotio I, Yitalo A, Kiviniemi T and Mustonen P. Stroke recurrence in patients with atrial fibrillation: concomitant carotid artery stenosis doubles the risk. European Journal of Neurology 2017; 24:719-25
5. Hart RG, Pearce LA, Miller VT, et al. Cardioembolic vs noncardioembolic strokes in atrial fibrillation: frequency and effect of antithrombotic agents in the stroke prevention in atrial fibrillation studies. Cerebrovasc Diseases 2000; 10:39-43.
6. Chimowitz MI, Lynn MJ, Howlett-Smith H, et al. Comparison of warfarin and aspirin for symptomatic intracranial arterial stenosis. N Engl J Med 2005; 352:1305-16.
Competing interests: No competing interests