Perspective:

The impact of sustained AF on atrial electrical and structural remodeling has been previously well described. Animals and humans with sustained AF have shorter action potential duration and effective atrial refractory period, which makes them vulnerable to AF initiation. Additionally, AF causes slowing in atrial conduction, activation of inflammation, fibrosis, and left atrial dilation. In the present study, the authors show that sustained AFL shortens atrial refractory period and action potential duration similar to that caused by AF, along with significantly enhanced vulnerability to atrial tachyarrhythmia induction by atrial extrasystoles, but it does not result in the slowing of atrial conduction, activation of inflammation, and fibrosis. Thus, AFL does not contribute to the perpetuation of future AF episodes. Additional inference from these data are that conduction disturbances and fibrosis in AFL patients are likely caused by the primary atrial cardiomyopathy, not AFL itself. Interventions targeting inflammatory signaling to prevent fibrosis caused by AF are likely to have a major impact on the disease management.