“…This time course of the development of CSNRT prolongation suggests that not only electrophysiological changes but also additional structural changes might be involved in the sinus node dysfunction in long‐term AF. In the clinical setting, postmortem studies showed deficiency of the nodal cell, fibrosis, and infiltration of fat in and around the sinus node in patients with bradycardia‐tachycardia syndrome 4,7 and long‐term AF 5,8 . A recent study reported a change in the nature of sinus pacemaker activity with loss of the normal multicentric pattern of activation, suggesting loss of automatic pacemaker cells and widespread impairment of sino‐atrial conduction 6 .…”