Paradoxical QRST integral changes with ventricular repolarization dispersion.
Body surface QRST integral (QRSTI) maps have been shown theoretically to reflect disparity of intrinsic repolarization properties and have been experimentally linked to increased arrhythmia susceptibility. Paradoxically, a lower magnitude of QRSTI in patients with heart disease and at risk for arrhythmias has been reported. We hypothesized that this paradoxical reduction in QRST magnitude is a consequence of increased heterogeneity of repolarization gradients in normal hearts. We generated QRSTI using a previously published heart model to compare QRSTI for aligned and random repolarization gradients. The heart model consisted of 50,000 cubic units in an anatomically correct arrangement that included parameters to simulate anisotropic conduction and inhomogeneous distribution of refractoriness. Body surface potential maps (BSPMs) were generated on a torso surface assuming a homogeneous torso and using the boundary element method for normal alignment of repolarization gradients and spatially reassigned repolarization values that randomized repolarization directions. QT duration was measured by the subtraction of Q onset time from T offset time on the BSPM. T offset was defined as the last potential to be detected at intervals of 3 ms that was above the threshold of 0.1 mV during recovery. The time of T offset showed a consistent tendency to shift to the left posterior and to split. When slow conduction velocities were assigned, BSPMs showed delayed propagation and multiple extrema. QRSTI showed systematic magnitude decrease with increasing randomness of repolarization gradient direction. Ventricular fibrillation (VF) could be induced by successive extrastimuli under the conditions of over 70% deviation and slow conduction of 0.5 m/s for the longitudinal direction. In conclusion, a possible explanation for the paradoxical reduction in QRSTI in the presence of constant repolarization disparity is the change in alignment of repolarization gradients.
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Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City 84112-5000, USA.
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D018780:Body Surface Potential Mapping / Q000295:instrumentation*; D003198:Computer Simulation; D004562:Electrocardiography / Q000295:instrumentation*; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans; D007091:Image Processing, Computer-Assisted / Q000295:instrumentation*; D008133:Long QT Syndrome / Q000175:diagnosis / Q000503:physiopathology; D008955:Models, Cardiovascular; D012815:Signal Processing, Computer-Assisted / Q000295:instrumentation*; D014693:Ventricular Fibrillation / Q000175:diagnosis* / Q000503:physiopathology