persistently rapid rate of atrial excitation produces a progressive shortening of the atrial effective refractory period and promotes the perpetuation of atrial fibrillation (AF); 1,2 however, most paroxysmal AF terminates spontaneously within a few days despite the presence of atrial remodeling. Termination of human AF with class I antiarrhythmic drugs is preceded by an increase in fibrillation cycle length (FCL), and a failure to increase the FCL correlates with a failure to terminate the AF with medication. 3 In canine models of AF, the mapping data suggest that the increase in FCL induced by antiarrhythmic drugs may relate to fusion of wavelets, an increase in the size of reentry circuits, a decrease in circuit number and finally, termination of AF. 4 Compared with drug-induced termination, the mechanism of spontaneous termination of human AF is still unclear. It is difficult to obtain intracardiac recordings just prior to spontaneous termination of paroxysmal AF for analysis of the fibrillation waves because spontaneous