Aged atria: electrical remodeling conducive to atrial fibrillation.

The incidence of atrial fibrillation (AF) increases with age. Alterations in structure and function of atrial ion channels associated with aging provide the substrate for AF. In this review we provide an overview of current knowledge regarding these age-related changes in atria, focusing on intrinsic ion channel function, impulse initiation and conduction. Studies on the action potentials (APs) of atria have shown that the AP contour is altered with age and the dispersion of AP parameters is increased with age. However, studies using human tissues are not completely consistent with experimental animal studies, since specimens from humans have been obtained from hearts with concomitant cardiovascular diseases and/or that are under the influence of pharmacologic agents. Ionic current studies show that while there are no age-related changes in sodium currents in atrial tissue, the calcium current is reduced and the transient outward and sustained potassium currents are increased in aged cells. While sinoatrial node firing is reduced with age, enhanced impulse initiation may occur in aged atrial cells, for example in the pulmonary veins and coronary sinus. Fibrous tissue is increased in aged atria, which is associated with an increased likelihood of abnormal electrical conduction. Thus, age-related AF involves alterations in the substrate as well as in the passive properties of aged atria.