Background: Ventricular repolarization (VR) is strongly influenced by heart rate (HR) and autonomic nervous activity, both of which also are important for arrhythmogenesis. Their relative influence on VR is difficult to separate, but might be crucial for understanding while some but not other individuals are at risk for life-threatening arrhythmias at a certain HR. This study was therefore designed to assess the "pure" effect of HR increase by atrial pacing on the ventricular gradient (VG) and other vectorcardiographically (VCG) derived VR parameters during an otherwise unchanged condition.Methods: In 19 patients with structurally normal hearts, a protocol with stepwise increased atrial pacing was performed after successful arrhythmia ablation. Conduction intervals were measured on averaged three-dimensional (3D) QRST complexes. In addition, various VCG parameters were measured from the QRS and T vectors as well as from the T loop. All measurements were performed after at least 3 minutes of rate adaptation of VR.Results: VR changes at HR from 80 to 120 bpm were assessed. The QRS and QT intervals, VG, QRSarea, Tarea, and Tamplitude were markedly rate dependent. In contrast, the Tp-e/QT ratio was rate independent as well as the T-loop morphology parameters Tavplan and Teigenvalue describing the bulginess and circularity of the loop.Conclusions: In healthy individuals, the response to increased HR within the specified range suggests a decreased heterogeneity of depolarization instants, action potential morphology, and consequently of the global VR.Ann Noninvasive Electrocardiol 2011;16(3):287-294 repolarization; heart rate; vectorcardiography; T-wave vector

Autonomic nervous system activity is essential for regulation of ventricular repolarization (VR) and plays an important role in several arrhythmogenic conditions. This study in 31 healthy adult subjects (16 men, 15 women) evaluated the VR response to pharmacologically modulated autonomic nervous system activity applying vectorcardiography (VCG) analysis. During continuous VCG recording, 0.01-0.1 μg·kg(-1)·min(-1) isoprenaline (Iso) was infused at an increasing flow rate until three targeted heart rates (HR) were reached. After Iso washout, one intravenous bolus of 0.04 mg/kg atropine was given followed by an intravenous bolus of 0.2 mg/kg propranolol. A 5-min steady-state VCG recording was analyzed for each of the seven phases (including baseline 1 and 2). Furthermore, during the first 4 min following atropine, six periods of 10-s VCG were selected for subanalysis to evaluate the time course of change. The analysis included QRS, QT, and T-peak to T-end intervals, measures of the QRS and T vectors and their relation, as well as T-loop morphology parameters. By increasing HR, Iso infusion decreased HR dependent parameters reflecting total heterogeneity of VR (T area) and action potential morphology (ventricular gradient). In contrast, Iso prolonged QT HR corrected according to Bazett and increased the T-peak to T-end-to-QT ratio to levels observed in arrhythmogenic conditions. HR acceleration after atropine was accompanied by a transient paradoxical QT prolongation and delayed HR adaptation of T area and ventricular gradient. In addition to the expected HR adaptation, the VR response to β-adrenoceptor stimulation with Iso and to muscarinic receptor blockade with atropine thus included alterations previously observed in congenital and acquired long QT syndromes, demonstrating substantial overlap between physiological and pathophysiological electrophysiology.

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Adequate adaptation of ventricular repolarization (VR) duration to changes in heart rate (HR) is important for cardiac electromechanical function and electrical stability. We studied the QT and QTpeak adaptation in response to abrupt start and stop of atrial and ventricular pacing on two occasions with at least one month's interval in 25 study subjects with permanent pacemakers. Frank vectorcardiography was used for data collection. Atrial or ventricular pacing was performed for 8 minutes aiming at a cycle length (CL) of 500 ms. We measured the immediate response (IR), the time constant (τ) of the exponential phase, and T90 End, the time to reach 90% change of QT and QTpeak from baseline to steady-state during and after pacing. During atrial pacing the CL decreased on average 45% from mean (SD) 944 (120) to 518 (46) ms and QT on average 18% from 388 (20) to 318 (17) ms. For QT, T90 End was 103 (24) and 126 (15) s after start versus stop of atrial pacing, a difference of 24 (27) s (p=0.006). The response pattern was similar for τ but IR did not differ significantly between pacing start and stop. The response pattern was similar for QTpeak and also for QT and QTpeak following ventricular pacing start and stop. The coefficients of variation for repeated measures were 7-21% for T90 End and τ. In conclusion, the adaptation of VR duration was significantly more rapid following increasing than decreasing HR and intra-individually a relatively reproducible process.