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  • The lead ECG and dimensional geometrical maps for corrected

    2019-05-15

    The 12-lead ECG and 2-dimensional geometrical maps for corrected RT interval difference and corrected Tp–e interval difference obtained by using 187-ch RIDM-ECG before and during the intravenous amiodarone infusion for representative cases are shown in Figs. 1 and 2 respectively. The mean value of QTc measured by using the 12-lead ECG increased during the intravenous administration of amiodarone. By contrast, the maximum value of the QT interval among the 12 leads decreased, and its minimum value increased during the intravenous administration of amiodarone. Although the mean value of the Tp–e interval measured by using the 12-lead ECG was not affected during the intravenous administration of amiodarone, the maximum value of the Tp–e interval among the 12 leads decreased, and its minimum value increased during the intravenous administration of amiodarone. Additionally, QT dispersion and Tp–e dispersion significantly decreased during the intravenous amiodarone administration. The maximum inter-lead difference between the corrected Tp–e intervals, but not the corrected RT intervals, as measured by using 187-ch RIDM-ECG, significantly decreased during the intravenous infusion of amiodarone (Table 2). These effects of intravenous amiodarone on ECG parameters were similar between the patients who received and those who did not receive prior oral amiodarone treatment (Table 2).
    Discussion The mean value of the inter-lead difference between corrected RT intervals determined by using 187-ch RIDM-ECG decreased during the intravenous administration of amiodarone, but this abnormal lipid metabolism difference was not statistically significant. In contrast, QT dispersion on the 12-lead ECG significantly decreased. The RT interval was defined as the time difference between the R-wave peak and the T-wave peak of the relative electrical current density of the variable-moment dipole current, which was calculated from the 187-channel electrical potentials on the basis of the Coulomb Law [11,12]. Therefore, the R-wave and T-wave peaks on the 187-ch RIDM-ECG images were not identical to those on the 12-lead ECG image. The inter-lead difference between the corrected RT intervals obtained from the 187-ch RIDM-ECG image may be less likely to be modified by the effect of amiodarone on depolarization and repolarization of the ventricle. The acute effects of amiodarone are the blockade of the L-type calcium inward current; the sodium inward current (INa), with a high affinity for its inactivated state; and the rapid and slow components of the delayed rectifier potassium current (IKr and IKs). In contrast, its chronic effect is mediated by prolonging the action potential duration (APD) through a decrease in the potassium channel density, especially IKs and transient outward current [13]. A single intravenous bolus of amiodarone does not prolong the QRS duration or QTc in humans, as observed on ECG [14,15]. In an experimental study, amiodarone produced little change in the APD of epicardial and endocardial tissues, but it shortened the APD of the M-region tissue via the blockade of late INa, leading to a decrease in the transmural dispersion of repolarization in the canine ventricle [16]. The results of another experimental study revealed that amiodarone suppressed inducible arrhythmia, with a decrease in the Tp–e and the transmural dispersion of APD secondary to the inhibition of both the IKr and the late INa at high concentrations of the drug (1–10µM) in rabbit heart in which the late INa was augmented in the presence of sea anemone toxin [17]. Although the mechanisms are not well understood, the acute effect of amiodarone in inhibiting the late INa and counterbalancing APD prolongation through the inhibition of IKr may play a role in the beneficial effect of repolarization on LV spatial and transmural dispersion in patients with heart failure. A recurrence of ventricular arrhythmia requiring ICD therapy was observed in 2 patients during the early period of intravenous amiodarone therapy. This recurrence may be due to the slow uptake of amiodarone into heart tissue because of its pharmacokinetic characteristics, which also accounts for its delayed antiarrhythmic effects [14]. In this study, we observed the pharmacological effect of amiodarone on the parameters of dispersion of ventricular repolarization, but it was unclear whether these effects were closely related to the therapeutic value of amiodarone for suppression of ventricular arrhythmias, such as electrical storm. To clarify this issue, further clinical investigation is necessary.