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Abstract. Nowinski K, Jensen S, Lundahl G, Bergfeldt L (Karolinska Hospital, Stockholm, Norrlands University Hospital, Umea Ê and Ortivus AB, Ta Èby, Sweden). Changes in ventricular repolarization during percutaneous transluminal coronary angioplasty in humans assessed by QT interval, QT dispersion and T vector loop morphology. J Intern Med 2000; 248: 126±136.Objectives. Based on clinical, epidemiological, and experimental data, transient cardiac ischaemia is one of the major triggering factors of malignant ventricular arrhythmia. According to animal studies, increased dispersion of repolarization is of pathophysiological relevance in this context. Therefore we explored the impact of myocardial ischaemia during single vessel coronary angioplasty on the change in ventricular repolarization, measured by QT and JT intervals and their dispersion in the 12-lead electrocardiogram. We also assessed a novel method, the 3-dimensional T vector loop, to find out whether it was sensitive to changes in ventricular repolarization during ischaemia, and whether there was any correlation with changes in the dispersion of the QT and/or JT intervals. Design. This study was prospective with consecutive patients. Only patients in sinus rhythm and without bundle branch block were included. Setting. All coronary angioplasties were performed at Norrlands University Hospital, Umea Ê. The analysis of the material was performed at the Karolinska Hospital, Stockholm. Subjects. Twenty-nine consecutive patients went through 30 elective one-vessel percutaneous transluminal coronary angioplasty (PTCA) procedures. PTCA was performed in 10 stenoses of the left anterior descending, 10 of the left circumflex, and 10 of the right coronary artery. Interventions. A 12-lead electrocardiogram was recorded continuously as part of routine monitoring of the patient during PTCA and the T vector loop was calculated from the simultaneously recorded. X, Y, Z leads. Main outcome measures. Repolarization was assessed by the QRS, QT and JT intervals as well as by the T vector loop parameters (Tarea, Tavplan, and Teigenv) before and at the end of the first occlusion during PTCA. Results. PTCA, with an average occlusion time of 171 6 60 s (mean 6 SD), induced ischaemia on the 12-lead electrocardiogram in 73% of cases. The overall response for the 30 procedures was a significantly increased dispersion of ventricular repolarization, both corrected and uncorrected for heart rate. QT dispersion increased by, on average, 19% from 74 6 35 to 88 6 36 ms, QT c dispersion by 27% from 71 6 39 to 90 6 42 ms, and JTc dispersion by 19% from 78 6 32 to 94 6 43 ms (P , 0.05). The T vector loop became more circular and bulgy during occlusion (all three parameters changed by between 33% and 59%). There was a significant correlation between changes in one of the T vector loop parameters (Teigenv), and changes in JT and QT dispersion in the left anterior descending group. Conclusions. Transient ischaemia during PTCA induced significant changes in ventricular repolarization, especial...

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This study was designed to prospectively assess ventricular de- and repolarization by the QRS, QT, and JT intervals, and their dispersion in the 12-lead ECG during right ventricular pacing at 60, 70, and 80 beats/min during the first month after AV junctional RF ablation. Previous reports have found early polymorphic ventricular arrhythmia after RF AV junctional ablation. Our hypothesis was that there is a proarrhythmic state following this procedure, which depends on the paced rate and time after ablation. The analysis of the immediate changes was based on 17 patients (10 men) with a mean age of 64 years (SD 14) (range 38-82 years). A 12-lead ECG was recorded during right ventricular pacing at 60, 70, and 80 beats/min within 24 hours (day 1), between 24 and 48 hours (day 2), and 1 week after ablation (day 7). For analysis of changes beyond 1 week, 13 additional patients with a mean age of 73 years (SD 8) (range 62-90 years) were analyzed on days 1, 7, and 30. All intervals were measured with a digitizing table. The mean QRS duration shortened by 2.4% at 60 beats/min (P <0.01), and the mean QT and JT intervals shortened by 5-7% between days 1 and 7 (P < 0.001). The mean QT was 9% shorter and the mean JT interval was 13% shorter at 80 compared to 60 beats/min on day 1 (P < 0.001). QT dispersion was reduced by 13% when the stimulation rate was increasedfrom 60 to 80 beats/min on day 1 (P < 0.05). There were no significant changes beyond the first week. The study results point to the induction of a proarrhythmic state immediately after AV junctional RF ablation resolving during the first week. Repolarization shortened gradually between 80 and 60 beats/min to an extent that is suggestive of a clinically important antiarrhythmic effect at the higher rate, which was supported also by clinical experience.

Measurement of the QT dispersion (the maximal interlead difference) on the surface electrocardiogram has been suggested for assessing the risk for ventricular arrhythmias and for examining drug effects and their proarrhythmic potential. The acute response of QT dispersion was assessed in 10 healthy subjects receiving disopyramide, which is known to delay repolarization and to prolong global measures thereof. The QRS, JT, and QT intervals and their dispersion were assessed at spontaneous rhythm and at atrial pacing at baseline and after an intravenous injection of disopyramide 2 mg/kg over 5 minutes. The short-term (within 30 minutes) and long-term (> or = 2 weeks) variabilities of the QT interval and the QT dispersion, expressed as the coefficient of variation, were also analyzed. At spontaneous rhythm the group average QT interval was between 369 and 375 msec, and the QT dispersion was between 33 and 37 msec; both were relatively stable over time. All subjects responded homogeneously to disopyramide with a significant QT prolongation (p < 0.001), but no consistent response of the QT dispersion was observed. This discrepancy reflects the significant difference in time-dependent variability with a coefficient of variation of spontaneous, paced, and heart rate-corrected QT dispersion between 25% and 42%, 8-42 times greater than the corresponding values of 1-4% for the QT intervals. The individual response of the QT dispersion to drug challenge should therefore be interpreted with caution. Furthermore and as a consequence, QT dispersion is less sensitive for assessing drug effects on ventricular depolarization and repolarization than the QT interval.

Importantly, the development of cardiac memory-induced different repolarization responses depending on baseline structure and electrophysiology. In HOCM patients repolarization was shorter during right ventricular apical pacing than during normal activation despite prolonged activation time.