Atrial cardiomyopathy: An entity of emerging interest in the clinical setting.

Since 1995, the concept of atrial cardiomyopathy (ACM) has been associated with myocardial fibrosis. Despite a consensus document in 2016, ACM's definition primarily relies on histopathological findings. The focus on diagnostic criteria for ACM is driven by the potential link to thromboembolic events even independently on atrial fibrillation (AF). The complexity of the mutual relationships between ACM and AF makes difficult any assessment of the thromboembolic risk associated to ACM per se. ACM's thrombogenicity is a multifaceted clinical phenomenon involving electrical, functional, and structural modifications. Factors such as cardiovascular risk factors (e.g., hypertension), common cardiac comorbidities (e.g., heart failure), and extracardiac conditions (e.g., neuromuscular disorders) can promote atrial derangement, triggering atrial fibrillation (AF) and increasing the risk of thromboembolic events. Several diagnostic methods are available to detect the key features of ACM, including electrical changes assessed by surface and intracavitary ECG, and structural and functional alterations evaluated through echocardiography and cardiac magnetic resonance (CMR). These methods can be complemented by electro-anatomical mapping (EAM) to enhance the accuracy of myocardial tissue characterization and assessment of atrial fibrosis. Although certain clinical conditions (e.g., atrial high-rate episodes, AHREs; embolic stroke of undetermined source, ESUS) often exhibit atrial alterations in their thromboembolic presentations, recent randomized trials have failed to demonstrate the benefits of oral anticoagulation in patients with ACM without AF. However, ACM constitutes the substrate for the development of AF, as proposed in the AF European guidelines under the 4S-AF scheme. This review emphasizes the lack of a diagnostic gold standard and the need for clinical criteria for ACM, aiming to better understand the potential therapeutic implications of atrial structural and functional derangements, even in the absence of clinical evidence of AF.