Postmyocardial infarction patients susceptible to ventricular tachycardia show increased T wave dispersion independent of delayed ventricular conduction

Arrhythmia Markers After Myocardial Infarction. Introduction: Experimentall y, both delayed ventricular conduction and nonhomogeneous ventricular repol arization contribute to reentrant arrhythmias. We tested the hypothesis tha t increased T wave dispersion is independent of delayed ventricular conduct ion associated with arrhythmia vulnerability in postmyocardial infarction ( post-MI) patients. Methods and Results: We studied 32 post-MI patients with clinical or induci ble monomorphic ventricular tachycardia (VT group), 28 post-MI patients wit hout arrhythmias (MI group), and 13 healthy controls, using magnetocardiogr aphic (MCG) mapping with signal averaging. Twelve-lead ECG was the referenc e. Filtered QRS duration (fQRS) and T wave peak to T wave end interval (TPE ) were used as measures of ventricular conduction and nonhomogeneity in ven tricular repolarization, respectively. In MCG, the VT group showed the long est QRS (135 +/- 34 msec vs 114 +/- 22 msec in the MI group; P = 0.012). Me an TPE and maximum TPE in VT versus MI groups were 78 +/-9 msec versus 70 /-6 msec (P < 0.001) and 117 +/- 23 msec versus 104 +/- 19 msec (P = 0.020) , respectively. Maximum TPE did not correlate with QRS in the VT group (r = 0.063; P = NS) but did correlate in the MI group (r = 0.396; P = 0.037). F or identification of post-MI patients prone to VT, selection of cutoff valu es for QRS > 140 msec and mean TPE > 81 msec gave sensitivity and specifici ty of 41% and 89%, and 31% and 96%, respectively. Their combination increas ed sensitivity to 63% while maintaining 89% specificity. Conclusion: Post-MI patients susceptible to VT show increased T wave disper sion independent of delayed ventricular conduction.