Fernando Rodríguez-González, Elizabeth Lorenzo-Martínez, Marianela Ballesteros-Hernández, Elibet Chávez-González, Juan Miguel Cruz-Elizundia, Armando E Hernández-Castellón, Raimundo Carmona-Puerta
The spatial hypothesis can satisfactorily explain QT dispersion.
BACKGROUND: The origin of QT interval dispersion has remained elusive for decades. Both the regional hypothesis and the spatial hypothesis continue to be opposed, with no consensus on which better explains the phenomenon.
OBJECTIVES: To determine the impact of digital signal magnification and spatial lead orientation on QT dispersion.
METHODS: A cross-sectional study was conducted in 122 adult patients diagnosed with atrioventricular nodal reentrant tachycardia (AVNRT) or orthodromic atrioventricular reentrant tachycardia (OAVRT), without structural heart disease. Radial plots were constructed for spatial analysis in the frontal plane. The QT interval was manually measured using a digital caliper, first with a calibration of 20 mm/mV, sweep speed of 50 mm/s, and 10× enhancement, and subsequently at 20 mm/mV, 150 mm/s, with enhancement at 80× and 160 × .
RESULTS: Radial plots showed that in most patients the maximum QT interval was located in leads arranged parallel to the mean frontal T-wave axis, while the minimum QT interval was found in leads perpendicular to it. The odds of these coincidences were high regardless of age, sex, or arrhythmic substrate type. QT dispersion measured across the 12 leads progressively decreased with magnification, from a baseline value of 41.0 ms [32.5-48.0 ms] to 22 ms [18.0-30.0 ms] and 13.5 ms [10.0-18.0 ms] at 80× and 160×, respectively. This indicates that interlead differences tend to disappear as electrocardiographic magnification increases.
CONCLUSIONS: The spatial hypothesis can satisfactorily explain QT dispersion.