Submit Manuscript | http://medcraveonline.com When a premature atrial depolarization encounters a period of incomplete recovery of excitability its conduction velocity diminishes. The conduction velocity and the effective refractory period (ERP) are the determinants in the genesis of reentrant arrhythmias according to the wavelength theory [12][13][14]. The wavelength is calculated by multiplying the refractory period by conduction velocity, and it is considered as the distance traveled by the depolarization wave during the duration of refractoriness. If the atrial wavelength is long, reentry may not be maintained and the episode of PAF may terminate spontaneously. On the other hand, if the atrial wavelength is relatively short because of either a short refractory period, depressed conduction, or both, then a greater number of wave fronts can circulate through the atrium and atrial fibrillation may be sustained. Therefore, prolonged atrial conduction delay and/or shortened ERP could be expected to increase the propensity to develop episodes of PAF [12][13][14]. The atrial vulnerability of the atrial myocardium in patients with PAF can be easily exposed in the electrophysiology laboratory. Abnormal responses of the atrial muscle can be elicited by programmed atrial stimulation during the electrophysiological study [15][16][17][18]. Certain parameters of atrial vulnerability, namely, repetitive atrial firing, fragmented atrial activity, and intraatrial conduction delay (IACD) can be induced by atrial stimulation. These electrophysiological parameters of atrial vulnerability are more frequently induced in patients with PAF than in those patients without it [1-5].Shorter atrial ERP has been also shown to be of electrophysiological significance in the genesis of PAF. On the other hand, the slowing in conduction of the atrial impulses may set the background for reentry to occur [1][2][3][4][5]. Although an increase of 20 ms or more in the atrial conduction time in response to early extra-stimuli appears to be a physiological response of the normal atrium, patients with PAF show longer IACD zones and maximum IACDs than control subjects without atrial arrhythmias [15][16][17][18]. Thus, the IACD zone and maximum IACD are believed to be good indices of a tendency to develop AF. We have previously shown that these indices of atrial vulnerability were greater in patients with hyperthyroidism and PAF than in control subjects [19,20]. The greater atrial IACD and shorter atrial ERP resulted in shortening of the atrial wavelength, which predisposed to development of PAF [19][20][21][22]. The mean atrial ERP in patients with hyperthyroidism (187±7 ms) was significantly shorter than that of controls (215±29 ms, p<0.01). The mean IACD zone in patients with hyperthyroidism (63±57ms) was significantly greater than that of controls (34±22ms) (p<0.01) [19]. The mean maximum IACD in patients with hyperthyroidism (64±37 msec) was also significantly greater than that of controls (43±20 msec) (p<0.01) [19]. Therefore, the increase of atr...