Eur J Heart Fail. 2026 Aug 19:xuag268. doi: 10.1093/ejhf/xuag268. Online ahead of print.
ABSTRACT
Atrial cardiomyopathy (AtCM) encompasses all forms of electrical atrial dysfunction in combination with mechanical atrial dysfunction, atrial enlargement and/or excessive atrial fibrosis. A growing body of evidence suggests that AtCM not only represents a consequence of ventricular and valvular heart disease but, critically, serves as the substrate driving atrial fibrillation (AF) and independently contributes to thromboembolic risk and heart failure (HF). Recent advances in cardiac imaging, electrocardiography, and electroanatomic mapping have enabled characterisation of AtCM and quantification of its severity, defining a continuum from atrial health to overt atrial failure. This framework creates an opportunity for targeted interventions that may reverse AtCM and prevent progression to clinical disease. This scientific statement summarises contemporary evidence regarding the natural history, determinants, and therapeutic modification of AtCM. We describe how targeted management of relevant lifestyle factors and comorbidities may prevent or attenuate AtCM progression and report the response of AtCM to pharmacological and structural interventions for HF and valve disease. Recognition of the bidirectional relationship between AtCM and AF has provided important insights into arrhythmia-mediated remodelling and generated the strongest evidence to date for reverse atrial remodelling following successful rhythm-control strategies. We also review emerging atrial-directed therapies targeting fibrosis, inflammation, metabolic dysfunction, and infiltrative disease. While AtCM appears to be, at least in part, a modifiable disease process, current evidence remains largely observational or mechanistic. We therefore highlight key evidence gaps and future research priorities to identify potentially reversible disease, develop targeted therapies, and translate state-of-the-art atrial phenotyping into improved patient outcomes.
PMID:42617069 | DOI:10.1093/ejhf/xuag268