Experimental verification of the value of the T_peak–T_end interval in ventricular arrhythmia inducibility in an early repolarization syndrome model

Abstract

Introduction In patients with early repolarization patterns on ECG, many researchers have studied to find predictors of fatal arrhythmia. However, there are no satisfying clinical predictors. We evaluated the value of the Tpeak–Tend interval on pseudo‐ECG in canine myocardial wedge preparation models of early repolarization syndrome. Methods and Results Transmural pseudo‐ECG and endocardial/epicardial action potentials were recorded from coronary‐perfused canine left ventricular wedge preparations (n = 34). The Ito agonist NS5806 (8‐10 µM), the calcium channel blocker verapamil (3 µM) and acetylcholine (2‐3 µM) were used to mimic the disease model. A ventricular arrhythmia induction test was performed. QTpeak, QTend, Tpeak–Tend, and Tpeak–Tend/QTend were measured at 15 to 20 minutes after the provocative agent infusion. Polymorphic ventricular tachycardias (pVT) developed in 23 of the 34 preparations (67%). The maximal values of Tpeak–Tend and Tpeak–Tend/QTend were recorded just before pVT induction. At baseline, without the provocative agents, Tpeak–Tend and Tpeak–Tend/QTend were not different between pVT‐induced and pVT‐noninduced preparations. The Tpeak–Tend of the pVT‐induced preparations was longer than that of non‐induced preparations (58 ± 26.8 msec vs 33 ± 6.8 msec, P < .001). The Tpeak–Tend/QTend of pVT‐ induced preparations was larger than that of noninduced preparations (0.220 ± 0.1017 vs 0.128 ± 0.0312, P < .001). The transmural and epicardial dispersion of repolarization of pVT‐induced preparations were larger than those of pVT‐noninduced preparations. The transmural dispersion of repolarization showed a positive correlation with Tpeak–Tend. Conclusion Tpeak–Tend predicted malignant ventricular arrhythmias in early repolarization syndrome models. Tpeak–Tend reflects the repolarization heterogeneity of ventricular myocardium.

Transmural conduction time in an early repolarization syndrome model

“…Koncz et al ( 9 ) reported the heterogeneous shortening of APD 90 in the same model. According to our previous study, the QT interval was only prolonged by 13 msec, and the value did not contribute to the occurrence of ventricular arrhythmia ( 28 ). Moreover, the results of the present study indicated that there was no significant difference in the QT interval when compared to the baseline state.…”

Exercise-Induced Electrocardiographic Changes in Healthy Young Males with Early Repolarization Pattern

“…The repolarization phase of the ventricular myocardium is well characterized by the QT interval and the T-peak-T-end interval. A prolonged QT interval increases the risk of malignant ventricular arrhythmias [16,25], and prolongation of the T-peak-T-end interval has been associated with arrhythmogenesis in J-wave syndromes [28,29]. Our results showed a shorter resting QT time in the ERP+ group, a difference that can be explained by the higher resting heart rate, as it disappeared when comparing the baseline corrected QT interval (QTc) and during exercise, when the heart rate of both groups reached similar values.…”

Tpeak‐tend interval as a marker of arrhythmic risk in early repolarization syndrome

“…The paper by Yoon et al adds to the growing body of evidence in support of a prognostic role of Tpeak‐Tend in predicting the development of malignant ventricular arrhythmias, in this case, in the setting of ERS. The study also elegantly provides a mechanistic understanding of the cellular basis for arrhythmogenicity encountered under these conditions.…”

“…In this issue of Journal of Cardiovascular Electrophysiology , Yoon et al explored the cellular basis for augmentation of Tpeak‐Tend in an experimental model of ERS as well as the mechanism underlying the development of pVT. Using coronary‐perfused canine left ventricular wedge preparations, the authors recapitulated the ECG and arrhythmic manifestations of ERS by pharmacologically mimicking the genetic defects and neurohormonal factors known to be associated with ERS, using a combination of the I to agonist NS5806, calcium channel blocker verapamil, and acetylcholine.…”