Atrial conduction explains the occurrence of the P‐wave dispersion phenomenon, but weakly

Abstract Background P‐wave dispersion (PWD) is believed to be caused by inhomogeneous atrial conduction. This statement, however, is based on limited little solid evidence. The aim of this study was to determine the relationship between atrial conduction and PWD by means of invasive electrophysiological studies. Methods Cross‐sectional study in 153 patients with accessory pathways and atrioventricular node reentry tachycardia (AVNRT) undergoing an electrophysiological study. Different atrial conduction times were measured and correlated with PWD. Results Only the interatrial (P‐DCS) and left intra‐atrial conduction times (ΔDCS‐PCS) showed a significant correlation with PWD, but this correlation was weak. Multivariate linear regression analysis determined that both P‐DCS (β = 0.242; P = .008) and ΔDCS‐PCS (β = 0.295; P < .001) are independent predictors of PWD. Performing the multivariate analysis for arrhythmic substrates, it is observed that only ΔDCS‐PCS continued to be an independent predictor of PWD. Analysis of the receiver operating characteristic curves showed that regardless of the types of arrhythmic substrates, PWD discriminates significantly, but moderately, to patients with P‐DCS and ΔDCS‐PCS ≥75 percentile. Conclusions Interatrial and intraleft atrial conduction times were directly and significantly correlated with PWD, but only weakly, and were independent predictors of PWD. In general, PWD correctly discriminates patients with high values in interatrial and intraleft atrial conduction times, but moderately. This is maintained in cases with accessory pathways; however, in patients with AVNRT it only does so for intraleft atrial conduction times. Interatrial and intraleft atrial conduction times weakly explains PWD.


| INTRODUC TI ON
In 1998 Dilaveris et al 1 proposed the use of P-wave dispersion (PWD) as a predictor of atrial fibrillation. Two main theories have been proposed to explain the origin of PWD. The local theory and the global theory. 2 The local theory is the most widely disseminated theory. It argues that atrial zones with different conduction velocities give rise to P waves of different durations throughout the 12 leads of the electrocardiogram. 3 Most connoisseurs of this topic accept that PWD reflects prolonged, inhomogeneous, and anisotropic distribution of connections between myocardial fibers resulting in discontinuous anisotropic propagation of sinus impulses, as well as, inhomogeneous and discontinuous atrial conduction. 4 However, there are no studies specially designed to test this theory and those that approach the subject study atrial conduction through noninvasive methods. Therefore, we set out to determine the relationship between atrial conduction and PWD through invasive electrophysiological studies.

| ME THODS
A cross-sectional study was carried out in 153 patients (mean age 39.53 ± 14.36; range 18-70 years). The cases were randomly selected from a study population of 286 patients with a clinical history of palpitations and a confirmed diagnosis of atrioventricular node reentry tachycardia (AVNRT) or accessory pathways, who underwent electrophysiological study and endocardial ablation at the service of Cardiac Electrophysiology of the Cardiovascular Hospital "Ernesto Guevara" from Santa Clara city, Cuba, between June 2017 and February 2020.
The electrophysiological study was performed after at least 6-8 hours fasting and without antiarrhythmic medication, at least for 5 or more half-lives of the drug. All subjects were assessed by transthoracic echocardiography for exclusion of cardiac anomaly. Exclusion criteria were: (a) Had >2 electrocardiographic leads that did not allow measurement of the P wave and/or any channel of the atrial intracavity records with poor signal quality. (b) Permanent ventricular preexcitation (excluded because of the difficulty of measuring the P-wave offset).

| Study variables
The following general variables were taken into account: age, sex, comorbidities, body weight, and occurrence of atrial fibrillation during the electrophysiological study. Atrial fibrillation was considered to be present if paroxysms lasting >10 seconds were documented.
The electrocardiographic parameters studied included: Heart rate: measured from R-R interval, at time of the P wave and electrophysiological measurements.
Maximum P-wave duration (PMax): P wave of greater duration in any of the 12 leads of the electrocardiogram.
Minimum P-wave duration: P wave of shortest duration in any of the 12 leads of the electrocardiogram. P-wave dispersion (PWD): determined by subtracting the minimum P-wave duration from the maximum P-wave duration in any of the 12 standard leads of the electrocardiogram ( Figure 1A).
Up to three consecutive P waves were measured in each of 12 leads and averaged. Electrocardiographic records were obtained at a calibration of 20 mm/mV and a sweep speed of 50 mm/s. The onset of the P wave is defined as the point of first detectable upward or downward slope from the isoelectric line for positive or negative waveforms, respectively. Return to the isoelectric line is considered as the end of the P wave. If the start or end of the P wave was not clearly defined, that lead was excluded. All electrocardiographic measurements were expressed in milliseconds.
The electrophysiological parameters studied included: P-high right atrium (HRA) interval: Measured from the onset of the P wave to the onset of the earliest reproducible rapid deflection of the atrial electrogram in the high right atrium, recorded with the distal pair of a BIOTRONIK quadripolar catheter (interelectrode distance of the same pair, 5 mm; distance between pairs, 10 mm). This parameter was accepted as a measure of the intraright atrial conduction time from the sinus node to the respective recording area ( Figure 1B Method used for the measurement of atrial conduction times (P-A intervals). DCS, distal coronary sinus; HIS, atrial electrogram in the His bundle recording; HRA, high right atrium; P, earliest onset of the P wave; PCS, proximal coronary sinus; Pmax, maximum P-wave duration; Pmin, minimum P-wave duration; PWD, P-wave dispersion Echocardiography and the European Association of Cardiovascular Imaging. 5 The echocardiographic study was performed prior to the electrophysiological study according to the protocol established in the institution.

| Ethical aspects
All patients included in the study gave their informed consent to carry out the electrophysiological study and radiofrequency endocavity ablation. The local ethics committee approved this study.

| RE SULTS
General data shows that patients with AVNRT were older than those with accessory pathways. The prevalence of male sex and atrial fibrillation was higher in cases with accessory pathways. High blood pressure was more prevalent in the AVNRT group. No significant differences were found in diabetes mellitus, heart rate, body weight or echocardiographic parameters ( Table 1).
The Pmax and PWD showed average values that are higher than the normal cutoff points for these variables but with no significant differences between patients with AVNRT and accessory pathways (  In the multivariable linear regression analysis, ΔDCS-PCS and P-DCS were independent predictors of PWD controlling for Values are presented as mean ± standard deviation.

| D ISCUSS I ON
The mean values of PWD and Pmax are increased in our series with respect to the reported upper cutoff points for these parameters. PWD is considered by many to be an electrocardiographic parameter originating from regional differences in atrial conduction, but the evidence supporting such an assertion derives primarily from echocardiographic techniques (tissue doppler, strain rate) that are approximations of true electrophysiological measurements, although such techniques have been validated. [9][10][11] Demir et al 12  and intraleft (r = .722) atrial conduction times. 13 Ermis et al 14 also found that PWD was significantly correlated with intra-atrial and interatrial conduction times in prehypertensive patients, also using the same measurement method. In a case-control study conducted in healthy nonsmokers and smokers, significant correlations were obtained between PWD and interatrial electromechanical delay (r = .653; P = .001), 15 a finding that has also been documented in hypertensive patients (r = .72; P < .001). 16 Even in pregnant women with The regression analysis did not include P-DCS and ΔDCS-PCS together because it weakened and lost statistical significance.
preeclampsia, PWD and interatrial (r = .46; P < .001) and intra-atrial (r = .39; P < .001) electromechanical delay have been shown to correlate directly and significantly. 17 There is a significant correlation between PWD and the interatrial electromechanical delay interval (r = .54; P < .01) in patients with polycystic ovary syndrome. 18 Badran et al 19 using 2D-strain rate in patients with idiopathic dilated cardiomyopathy found that PWD is directly correlated in these patients (r = .45, P < .00001) with the quantification of the electromechanical delay of the left atrium, but this finding was not found in the control group. In addition, higher values of PWD and of the interatrial, right atrial and left atrial electromechanical delay times measured by 2D strain rate have been found in nondipper hypertensive patients compared to dipper. 20 The previous studies show that there is a relationship between PWD and atrial conduction, which coincides with our results that also demonstrate this relationship, which occurs mainly with electrophysiological parameters that involve the left atrium.
Although we analyzed 16 variables that evaluate atrial conduction, only P-DCS and ΔDCS-PCS are related to PWD, and predict it.
These data suggest that PWD may be preferentially explained by changes in left atrial conduction and/or interatrial conduction. PWD was better related to ΔDCS-PCS than P-DCS, a parameter that constitutes a measure of left intraatrial conduction time. No conduction parameters confined to the right atrium had any effect on PWD.
Previous research has found moderate to strong relationships between atrial conduction and PWD. 12,13,[15][16][17][18][19] However, in our study they were weak as observed in the correlation coefficients obtained.
Furthermore, in the multivariate analysis we also obtained lower beta coefficients than in the study by Djikic et al, 13