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The detailed mechanisms of age-related atrial structural and electrophysiologicalchanges remain elusive. Small animal models have recently been used for the investigationof atrial tachyarrhythmia. In this study, we investigated the hypothesis thatatrial structural and electrical characterization with aging provides a substratefor atrial fibrillation using a mouse model of aging. Male Kunming mice aged 2(young), 12 (middle-aged) and 24 months (aged) were used in this study. A surfaceelectrocardiogram and sinus node recovery time (SNRT) were recorded at baseline.Atrial fibrillation (AF) inducibility and duration were measured by a transesophagealelectrode catheter. Collagen content was assessed by the collagen volume fraction.Whole cell configuration using the patch clamp technique was performed for thetransient outward potassium (Ito) and ultra-rapid delayed rectifier potassium(Ikur) currents. P-wave duration, SNRT and rate-corrected SNRT were longer inthe aged group than in the remaining 2 groups, paralleled by inducibility significantlybeing increased in the aged group. The right atrium had significantly higher levelsof fibrosis than the left atrium in all the groups (P&lt;0.05), whereas the extentof fibrosis in the left atrium had a higher positive correlation with age relativeto the right atrium (P&lt;0.05). Moreover, in old age, the dispersion of leftrelative to right atrium repolarization and augmented Ito currents contributedto vulnerability to AF. Nevertheless, Ikur currents in the atrial myocytes showedno age-related changes. The present study demonstrates that in addition to thestructural alterations, aging can also cause integrative and cellular electrophysiologicalchanges in a mouse model of aging, facilitating AF initiation and maintenance.

Characterization of atrial histopathological and electrophysiological changes in a mouse model of aging