Atrial Cardiomyopathy Through the Pathologist’s Lens: From Tissue Remodeling to Clinical Expression

Atrial cardiomyopathy (ACM) provides a useful framework for understanding structural, architectural, contractile, and electrophysiological disease of the atria. ACM and atrial fibrillation (AF) are closely linked but are not interchangeable: ACM favors arrhythmogenesis, whereas sustained AF can accelerate atrial injury. This review considers ACM from the pathologist's perspective, encompassing primary atrial disease and secondary remodeling associated with valvular disease and classical cardiomyopathies. The histologic spectrum includes cardiomyocyte hypertrophy and myocytolysis, interstitial and replacement fibrosis, endocardial fibroelastosis, adipose and inflammatory infiltration, vascular injury, and amyloid deposition. Structural remodeling is regionally heterogeneous, and appendage specimens may underrepresent abnormalities elsewhere in the atrium. Histologic interpretation requires attention to intrinsic regional architecture, associated lesions, previous interventions, and methods of quantification. At the molecular and cellular level, genetic susceptibility and acquired stressors converge on cardiomyocyte dysfunction, inflammation, fibroblast activation, and extracellular-matrix remodeling. Correlating these tissue changes with mapping, imaging, biomarkers, and clinical outcomes will be necessary to validate noninvasive phenotypes and identify clinically meaningful disease subsets. At present, ACM should prompt etiologic investigation and risk assessment but does not by itself constitute an indication for specific therapy.