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It is believed that QRS dispersion (QRSd) is caused by asynchrony of ventricular activation, but there are no studies that prove it. To determine the mechanism that best explains QRSd in surface electrocardiogram (ECG). Cross-sectional study in 95 consecutive patients (median age: 31.0 years [25–52], female sex: 66.3%) with atrioventricular nodal reentrant tachycardia. All 12 ECG leads were recorded at once, simultaneously with the intracardiac recordings. QRSd was quantified as the difference between maximum (QRSmax) and minimum QRS duration (QRSmin). QRS was measured firstly at a calibration of 20 mm/mV and a sweep speed of 50 mm/s, enhancement 10× (basic measurement [BM]), and after at sweep speed of 150 mm/s, enhancement 80 - 160×. The interventricular dyssynchrony (IVD) was also quantified. QRSmax increased from BM (98 ms [91–103]) to 80× (102 ms [99–108]; p = 0.029) and 160× (104 ms [101.5–110]; p = 0.027). QRSmin, almost equaled the duration of QRSmax at 160× (103 ms [100–108]). With BM, QRSd was 26 ms [22–35] and was reduced 26-fold (p < 0.001) by magnifying the QRS at 160× (1 ms [0–3]). IVD was weakly correlated with QRSd (r = 0.234, p = 0.023), but strongly with the total QRS at 160× (r = 0.676, p < 0.001). When QRS complex is narrow, the best explanation for the origin of QRSd on the surface ECG is the unequal projection of the ventricular depolarization vector in the different axis of the leads. • After QRS amplification, interlead differences tend to disappear. • QRS dispersion is explained by unequal vectorial projection. • Interventricular dyssynchrony is better related to the total duration of the QRS. [ABSTRACT FROM AUTHOR]

Background: Local theory and the vectorial theory are used to explain the origin of P-wave dispersion (PWD). There are no previous studies that analyze both at the same time.Objectives: We set out to determine the implication of local and vectorial theories in the origin of PWD.Methods: Cross-sectional study in 153 randomly selected patients aged 18-70 years, undergoing electrophysiological study. Inhomogeneous atrial conduction was evaluated by atrial electrogram dispersion in terms of duration (EGMdurdis) and morphology (EGMmorph dis). P-distal coronary sinus interval (P-DCS) was also measured. P-wave was measured twice, firstly at a calibration of 20 mm/mV and a sweep speed of 50 mm/s, enhancement 10× (basic measurement [BM]), and second time at sweep speed of 150 mm/s, enhancement 80-160× (high precision measurement [HPM]).Results: PWD with BM was 48 ms [36-54 ms] while with HPM it was 4 ms [0-10 ms], p < 0.001. With BM, maximum and minimum P- wave duration presented a moderate correlation (r = 0.342; p < 0.001), using HPM it becomes strong (r = 0.750; p < 0.001). In cases with P-DCS < 80 ms (r = 0.965; p < 0.001), but not with P-DCS ≥ 80 ms (r = 0.649; p < 0.001), the previous correlation became almost perfect with HPM. EGMdurdis and EGMmorphdis were weak but significantly correlated with PWD. This correlation became moderate in patients with P-DCS ≥ 80 ms and disappeared in those with P-DCS, using BM and HPM.Conclusion: Vectorial theory explains almost entirely the PWD phenomenon. Inhomogeneous conduction could be an additional mechanism to explain PWD, but its contribution is small. [ABSTRACT FROM AUTHOR]