What does the T(peak)-T(end) interval reflect? An experimental and model study.

BACKGROUND: It is unclear whether the Tpeak-Tend interval is an index of the transmural or the total dispersion of repolarization. METHODS: We examined the Tpeak-Tend interval using a computer model of the rabbit heart ventricles based on experimentally measured transmural, apicobasal, and interventricular gradients of action potential duration. RESULTS: Experimentally measured activation-recovery intervals increased from apex to base, from the left ventricle to the right ventricle, and in the apical portion of the left ventricle from epicardium to endocardium and from the right side of septum to the left side. The simulated Tpeak corresponded to the earliest end of repolarization, whereas the Tend corresponded to the latest end of repolarization. The different components of the global repolarization dispersion were discerned by simulation. CONCLUSIONS: The Tpeak-Tend interval corresponds to the global dispersion of repolarization with distinct contributions of the apicobasal and transmural action potential duration gradients and apicobasal difference in activation times.

Load-induced changes in ventricular repolarization: evidence of autonomic modulation.

Augmented hemodynamic load increases the risk of arrhythmogenesis by modulating cardiac repolarization duration. We hypothesized that the intervention on the autonomic tone may affect the load-dependent changes in ventricular repolarization. Activation-recovery intervals were measured in unipolar electrograms simultaneously recorded from 64 ventricular epicardial leads, in a total of 26 chinchilla rabbits in resting conditions, and after 1 and 10 min of aortic stenosis. Eleven animals were given atropine and propranolol before the loading. The short-term stenosis decreased the activation-recovery intervals in the right ventricle, whereas the prolonged overload increased the repolarization duration in both ventricles. The treatment with the ß-adrenergic and M-cholinergic blockers prolonged the activation-recovery intervals, especially at the left ventricle, attenuating the apicobasal and interventricular gradients of repolarization duration seen in the baseline state. Further ventricular loading shortened the repolarization duration in both ventricles in animals with autonomic blockade. Thus, the autonomic tone was shown to be essential for the development of repolarization heterogeneity across the ventricles. The autonomic blockade transformed the biphasic changes of activation-recovery intervals into their monophasic shortening at aortic stenosis.