Atrial Myopathy

Highlights • The authors discuss the concept of atrial myopathy; its relationship to aging, electrophysiological remodeling, and autonomic remodeling; the interplay between atrial myopathy, AF, and stroke; and suggest how to identify patients with atrial myopathy and how to incorporate atrial myopathy into decisions about anticoagulation. • Atrial myopathy seen in animal models of AF and in patients with AF is the result of a combination of factors that lead to electrical and structural remodeling in the atrium. Although AF may lead to the initiation and/or progression of this myopathy, the presence of AF is by no means essential to the development or the maintenance of the atrial myopathic state. • Methods to identify atrial myopathy include atrial electrograms, tissue biopsy, cardiac imaging, and certain serum biomarkers. A promising modality is 4-dimensional flow cardiac magnetic resonance. The concept of atrial myopathy may help guide oral anticoagulant therapy in selected groups of patients with AF, particularly those with low to intermediate risk of strokes and those who have undergone successful AF ablation. This review highlights the need for prospective randomized trials to test these hypotheses.
Summary This paper discusses the evolving concept of atrial myopathy by presenting how it develops and how it affects the properties of the atria. It also reviews the complex relationships among atrial myopathy, atrial fibrillation (AF), and stroke. Finally, it discusses how to apply the concept of atrial myopathy in the clinical setting—to identify patients with atrial myopathy and to be more selective in anticoagulation in a subset of patients with AF. An apparent lack of a temporal relationship between episodes of paroxysmal AF and stroke in patients with cardiac implantable electronic devices has led investigators to search for additional factors that are responsible for AF-related strokes. Multiple animal models and human studies have revealed a close interplay of atrial myopathy, AF, and stroke via various mechanisms (e.g., aging, inflammation, oxidative stress, and stretch), which, in turn, lead to fibrosis, electrical and autonomic remodeling, and a pro-thrombotic state. The complex interplay among these mechanisms creates a vicious cycle of ever-worsening atrial myopathy and a higher risk of more sustained AF and strokes. By highlighting the importance of atrial myopathy and the risk of strokes independent of AF, this paper reviews the methods to identify patients with atrial myopathy and proposes a way to incorporate the concept of atrial myopathy to guide anticoagulation in patients with AF.
Central Illustration