title: Characterization of atrial histopathological and electrophysiological             changes in a mouse model of aging.
abstract: The detailed mechanisms of age-related atrial structural and electrophysiological             changes remain elusive. Small animal models have recently been used for the investigation             of atrial tachyarrhythmia. In this study, we investigated the hypothesis that             atrial structural and electrical characterization with aging provides a substrate             for 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 surface             electrocardiogram and sinus node recovery time (SNRT) were recorded at baseline.             Atrial fibrillation (AF) inducibility and duration were measured by a transesophageal             electrode catheter. Collagen content was assessed by the collagen volume fraction.             Whole cell configuration using the patch clamp technique was performed for the             transient outward potassium (Ito) and ultra-rapid delayed rectifier potassium             (Ikur) currents. P-wave duration, SNRT and rate-corrected SNRT were longer in             the aged group than in the remaining 2 groups, paralleled by inducibility significantly             being increased in the aged group. The right atrium had significantly higher levels             of fibrosis than the left atrium in all the groups (P<0.05), whereas the extent             of fibrosis in the left atrium had a higher positive correlation with age relative             to the right atrium (P<0.05). Moreover, in old age, the dispersion of left             relative to right atrium repolarization and augmented Ito currents contributed             to vulnerability to AF. Nevertheless, Ikur currents in the atrial myocytes showed             no age-related changes. The present study demonstrates that in addition to the             structural alterations, aging can also cause integrative and cellular electrophysiological             changes in a mouse model of aging, facilitating AF initiation and maintenance.
authors.affiliation: Graduate School of Medicine, Tianjin Medical University, Tianjin, PR China.
authors.forename: Tao
authors.initials: T
authors.lastname: Luo
authors.forename: Cui-Xian
authors.initials: CX
authors.lastname: Chang
authors.forename: Xin
authors.initials: X
authors.lastname: Zhou
authors.forename: Shi-Kui
authors.initials: SK
authors.lastname: Gu
authors.forename: Tie-Ming
authors.initials: TM
authors.lastname: Jiang
authors.forename: Yu-Ming
authors.initials: YM
authors.lastname: Li
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology; D004562:Electrocardiography / Q000379:methods; D055724:Electrophysiological Phenomena; D006325:Heart Atria / Q000033:anatomy & histology* / Q000503:physiopathology; D006339:Heart Rate / Q000502:physiology; D008297:Male; D051379:Mice; D023421:Models, Animal; D032383:Myocytes, Cardiac / Q000473:pathology*; D011188:Potassium / Q000502:physiology
chemical_list: D011188:Potassium