“…PD is a noninvasive indicator of intra-atrial conduction heterogeneity producing substrate for reentry, which is a pathophysiological mechanism of atrial fibrillation [16,17]. PD has been studied in some other conditions such as hypertension [18], obesity [19], diabetes mellitus [20], metabolic syndrome [21], dilated cardiomyopathy [22], myocardial infarction [23], atrial septal defect [24], hypertrophic cardiomyopathy [25], obstructive sleep apnea [26] and Wilson's disease [27]. The exact mechanism of PD prolongation in these clinical conditions is not well known, but it is thought that structural and electrophysiological changes in the atrial myocardium caused by elevated plasma volume [28], ventricular diastolic dysfunction [29] and enhanced neurohormonal activation [30], that accompany these diseases, may contribute to left atrial enlargement and electrical instability.…”