Uneven vectorial projection is the best explanation for QRS dispersion, not the asynchronic ventricular activation

Abstract

BackgroundIt is believed that QRS dispersion (QRSd) is caused by asynchrony of ventricular activation, but there are no studies that prove it. ObjectivesTo determine the mechanism that best explains QRSd in surface electrocardiogram (ECG). MethodsCross-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. ResultsQRSmax 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). ConclusionWhen 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.