Postmyocardial Infarction Patients Susceptible to Ventricular Tachycardia Show Increased T Wave Dispersion Independent of Delayed Ventricular Conduction

Arrhythmia Markers After Myocardial Infarction. Introduction: Experimentally, both delayed ventricular conduction and nonhomogeneous ventricular repolarization contribute to reentrant arrhythmias. We tested the hypothesis that increased T wave dispersion is independent of delayed ventricular conduction associated with arrhythmia vulnerability in postmyocardial infarction (post-MI) patients.
Methods and Results: We studied 32 post-MI patients with clinical or inducible monomorphic ventricular tachycardia (VT group), 28 post-MI patients without arrhythmias (MI group), and 13 healthy controls, using magnetocardiographic (MCG) mapping with signal averaging. Twelve-lead ECG was the reference. Filtered QRS duration (fQRS) and T wave peak to T wave end interval (TPE) were used as measures of ventricular conduction and nonhomogeneity in ventricular repolarization, respectively. In MCG, the VT group showed the longest fQRS (  135 ± 34  msec vs  114 ± 22  msec in the MI group;  P = 0.012  ). Mean 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 fQRS in the VT group (  r = 0.063; P = NS  ) but did correlate in the MI group (  r = 0.396; P = 0.037  ). For identification of post-MI patients prone to VT, selection of cutoff values for fQRS > 140 msec and mean TPE > 81 msec gave sensitivity and specificity of 41% and 89%, and 31% and 96%, respectively. Their combination increased sensitivity to 63% while maintaining 89% specificity.
Conclusion: Post-MI patients susceptible to VT show increased T wave dispersion independent of delayed ventricular conduction.