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  • Introduction Cardiac resynchronization therapy CRT reduces

    2019-06-11

    Introduction Cardiac resynchronization therapy (CRT) reduces mortality and morbidity in selected heart failure patients with impaired left ventricular (LV) function and cardiac dyssynchrony [1]. Most patients receive CRT with a defibrillator (CRT-D) because the indications for an implantable cardioverter-defibrillator (ICD) overlap with those for CRT. Electrical storm, which is commonly defined as the occurrence of 3 or more separate episodes of ventricular tachyarrhythmia requiring ICD therapies within 24h [2], is associated with worse heart failure-related morbidity and survival among patients who receive CRT-D [3,4]. CRT may increase LV transmural dispersion of repolarization, leading to ventricular tachyarrhythmia and electrical storm induced by epicardial LV pacing [4–6]. Moreover, some reports have demonstrated that ICD shocks alone can cause an increase in QT dispersion, which may contribute to the proarrhythmic effects of ICD shocks such as electrical storm [7,8]. Myocardial ischemia increases the dispersion of repolarization and may result in shock-induced arrhythmia [9,10]. Intravenous amiodarone is widely used in the treatment of electrical storm [2]. However, few clinical studies have evaluated the effect of intravenous amiodarone on the spatial and transmural dispersion of ventricular repolarization in patients treated with CRT.
    Methods We studied 14 patients treated with CRT-D who were admitted to our hospital because of electrical storm (Table 1). Patients who were in atrial fibrillation were excluded. Amiodarone diluted with 5% AMG 925 was administered as a loading dose of 2.0mg/kg for 10min and was subsequently infused continuously as a maintenance dose of 0.5mg/kg/h. Twelve-lead electrocardiography (ECG) was performed by using a standard digital recorder (CardiofaxV, Nihon Kohden Co., Tokyo, Japan) at a gain of 20mm/mV and a speed of 50mm/s; a 187-channel repolarization interval-difference mapping electrocardiograph (187-ch RIDM-ECG, Fukuda Denshi Co. Ltd., Tokyo, Japan) was also used. The data from both procedures were recorded before and during the intravenous infusion of amiodarone. Additionally, blood samples were drawn to assess the concentration of amiodarone in the patients׳ plasma. This study was approved by the institutional review board of the Tokyo Women׳s Medical University (approval no. 2036), and all patients provided written informed consent. The QT intervals and T-peak to T-end (Tp–e) intervals were measured by using leads II and V2 of the 12-lead ECG. The QT interval was obtained from the onset of the QRS complex to the end of the T wave. The corrected QT interval (QTc) was calculated using the Bazett formula. QT dispersion was defined as the difference between the maximum and minimum QT intervals of the 12 ECG leads. The Tp–e interval was obtained from the peak of the T wave to the end of the T wave, which corresponded to the bottom of the T wave in cases of negative or biphasic T waves. The Tp–e dispersion was obtained by assessing the difference between the maximum and minimum Tp–e intervals of the 12 ECG leads (Fig. 1). Measurements of the recovery time (RT) and Tp–e AMG 925 intervals according to the results of the 187-ch RIDM-ECG were previously described in detail [7], and the corrected RT and corrected Tp–e intervals were calculated by using the Bazett formula. The maximum inter-lead differences between corrected RT intervals and between corrected Tp–e intervals were automatically calculated based on the difference between the maximum and minimum values in this system. The corrected RT and Tp–e interval difference maps were displayed as a color-coordinated map according to time differences. The data are presented as the mean±SD. The parameters were compared before and during the intravenous amiodarone infusion by using the Mann–Whitney U test, and a P-value <0.05 was considered significant.
    Results Among the 14 patients who received intravenous amiodarone for the treatment of electrical storm, 1 patient received an inotropic agent (intravenous dopamine) and 2 patients received a sedative agent concomitant with the administration of intravenous amiodarone. The other patients continued to receive the same dose of beta-blockers and other cardiovascular drugs during the intravenous amiodarone treatment as they did prior to treatment. Ventricular tachyarrhythmia that required ICD shock recurred in 2 patients after the initiation of amiodarone infusion but it was not observed after the initial 16h of continuous infusion. No recurrence of ventricular tachyarrhythmia that required ICD therapy occurred in the other patients during the intravenous amiodarone infusion. The mean treatment period of intravenous amiodarone was 105±98h. The results of the 12-lead ECG and the 187-ch RIDM-ECG recorded during the intravenous amiodarone infusion were obtained 26±19h after the start of therapy.