During AF alterations of the electrophysiological properties of the atria occur, evidenced by progressive shortening in the refractory periods and loss of normal rate adaptation response[
9,
25]. Previous studies have shown that a critical number of existing wavelets is essential for AF to be sustained. Since the length of the wavelet is the product of myocardial conduction velocity and refractory period, a decrease in either conduction velocity or a decrease of the refractory period will lead to an increase in the maximum number of wavelets that can be accommodated in a constant area. Similarly, a larger number of circulating wavelets can exist on the surface of larger atria[
26,
27]. During the recovery period, following conversion to SR, the atria have a heightened predilection of AF recurrence[
9,
12,
25]. Atria exhibiting a short wavelength have been shown to be more vulnerable to arrhythmia induction[
24]. This is in agreement with observations that the ease of initiation and probability of maintenance of AF are related to the fibrillatory cycle length[
27,
28]. The time-course of restoration of normal atrial electrophysiology is poorly understood, but appears to be partially dependent on the duration of the arrhythmia before cardioversion. Studies suggest that atrial effective refractory period reverts to normal within three days of cardioversion of long-standing AF[
14]. It has been postulated that electrical remodeling is partially due to intracellular calcium overload since verapamil attenuates the process[
11,
12,
15]. Pre-treatment with verapamil may reduce[
6,
7,
29] and that digoxin[
30] delays reversal of electrical remodeling, which may have an impact on the incidence of early AF recurrence. Moreover, AF also leads to progressive mechanical dysfunction[
31], seen as post cardioversion atrial stunning. A recent study has shown a relationship between transmitral peak A wave velocity and relapse into AF[
32]. Left atrial dilation in patients with AF may be caused by underlying cardiovascular and valvular disease, but progressive dilatation is also a consequence of the arrhythmia itself[
33,
34]. Conversely, left atrial diameter decreases after successful cardioversion to sinus rhythm[
35]. Atrial dilation increases the predilection to AF, and to its post-cardioversion recurrence, probably by impeding intra-atrial conduction and by increasing the atrial area in which multiple wavelet re-entry can occur.