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The atria provide an important contribution to cardiac function.1,2 Besides their impact on ventricular filling, they serve as a volume reservoir, host pacemaker cells and important parts of the cardiac conduction system (e.g. sinus node, AV node), and secrete natriuretic peptides like atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) that regulate fluid homeostasis. Atrial myocardium is affected by many cardiac and non-cardiac conditions3 and is, in some respects, more sensitive than ventricular.4 The atria are activated, besides the three specialized intermodal tracts,5,6 through working cardiomyocytes, so that any architectural or structural change in the atrial myocardium may cause significant electrophysiological disturbances. In addition, atrial cells (both cardiomyocytes and non-cardiomyocyte elements like fibroblasts, endothelial cells, and neurons) react briskly and extensively to pathological stimuli3 and are susceptible to a range of genetic influences.7 Responses include atrial cardiomyocyte hypertrophy and contractile dysfunction, arrhythmogenic changes in cardiomyocyte ion-channel and transporter function, atrial fibroblast proliferation, hyperinnervation, and thrombogenic changes.2 Thus, atrial pathologies have a substantial impact on cardiac performance, arrhythmia occurrence, and stroke risk.1,8Ventricular cardiomyopathies have been well classified; however, a …

EHRA/HRS/APHRS/SOLAECE expert consensus on Atrial cardiomyopathies: Definition, characterisation, and clinical implication