It can be counterintuitive for patients with atrial fibrillation (AF) to understand the evidence-based recommendation to receive anticoagulation therapy despite successful suppression of their arrhythmia with an antiarrhythmic drug. After all, the general teaching is that the heightened risk of stroke and systemic thromboemboli occurs due to the stasis of blood in the left atrial appendage produced during rapid and disorganized fibrillation of atrial tissue. And yet, randomized clinical trial data have shown that cessation of anticoagulation given maintenance of sinus rhythm may be harmful and that the benefit of AF suppression can be achieved only when anticoagulation is maintained. How can this be? One potential explanation is that the AF is an epiphenomenon, serving as a marker of an underlying atrial myopathy, or atrial cardiopathy, and not necessarily causal. If true, this would suggest that the optimal selection of patients for anticoagulation might not rely solely on evidence of AF, but rather on other biomarkers of atria prone to forming thrombi.
