LAUSR

Atrial fibrillation is uncommon in healthy young individuals. Diverse pathologies, including hypertension, valvular disease, obesity, excessive alcohol consumption, cancer and aging are associated with increased risk of atrial fibrillation (AF). Why? Recent studies have shown that atrial remodeling in response to hemodynamic and/or metabolic stresses, or as a result of genetic predisposition, contributes to the development of atrial dysfunction that can increase both the incidence and persistence of AF. A recent global consensus document focused on better understanding the mechanisms and risk factors that contribute to atrial dysfunction— now termed atrial cardiomyopathy, which can be the end result of the disparate mechanisms that promote atrial dysfunction.1 Atrial cardiomyopathy has been defined as “Any complex of structural, architectural, contractile, or electrophysiological changes affecting the atria with the potential to produce clinically relevant manifestations.1” Atrial cardiomyopathy encompasses a broad range of pathways, some of which are modifiable and some of which are not (eg, genetic variants, sex, age).