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We describe a patient with torsades de pointes (TdP) who was implanted with cardiac resynchronization therapy defibrillator (CRT-D). At the time of CRT-D implantation, left ventricular (LV) epicardial pacing exacerbated TdPs and developed into electrical storm, which was triggered even by biventricular pacing. We needed to inactivate the LV lead fo...
Context in source publication
Context 1
... the LV lead was smoothly placed to the posterolateral branch of the coronary sinus (CS). However, activation of the LV lead remarkably exacerbated the QT interval and dispersion, and several paced events resulted in incessant TdP ( Figure 2). Notably, TdP occurred in response to either LV pacing alone or biventricular pacing, but not to isolated RV pacing from the defibrillator lead. ...
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We report the case of a man in his 60s who had dilated cardiomyopathy with severe functional mitral regurgitation. Four years after a cardiac resynchronization therapy (CRT) device with an implantable cardioverter defibrillator was implanted, this device was replaced with an adaptive CRT device because of battery consumption. Seven months after rep...
Citations
... Proarrhythmic events after CRT have been reported in 5–10% of CRT recipients1234. Gasparini et al. investigated the incidence of electrical storm in patients with heart failure treated with CRT and reported an increased incidence in patients with nonischemic cardiomyopathy in whom a CRT-D was implanted for secondary prevention [5]. In most cases, the arrhythmia can be managed by administration of an antiarrhythmic agent and/or discontinuation of LV pacing within 1 month after implantation of the CRT system. ...
We describe treatment of atrial flutter and electrical storm presenting as incessant ventricular tachycardia (VT) after implantation of a cardiac resynchronization therapy defibrillator (CRT-D) in a patient with dilated cardiomyopathy. No prior arrhythmic event had occurred. Our treatment strategy, including amiodarone administration, was guided in part by signal-averaged vector-projected 187-channel electrocardiogram (SAVP-ECG)-based risk stratification for ventricular arrhythmia. Corrected recovery time (RTc) dispersion and Tpeak-end dispersion were used to evaluate transmural dispersion of repolarization. RTc and Tpeak-end dispersion increased during the period of electrical storm. Values were improved 2 years after CRT-D implantation, and the amiodarone was discontinued. The VT has not recurred despite discontinuation of the antiarrhythmic agent. SAVP-ECG-based risk stratification for ventricular arrhythmia proved useful for the management of antiarrhythmic therapy.
Introduction and objectives:
Implantable cardioverter-defibrillators reduce mortality in some patients with heart disease. Battery replacement is a frequent occurrence in clinical practice and is required in up to 30% of implants. The benefit/risk ratio of defibrillators varies over time and should be reevaluated at the time of replacement. The aim of this study was to determine the clinical characteristics and incidence of defibrillator therapies in patients who underwent generator replacement.
Methods:
This multicenter retrospective study involved patients from the UMBRELLA national registry who underwent replacement due to defibrillator battery depletion. The incidence of ventricular arrhythmias was determined via remote monitoring. Risk factors for sustained ventricular arrhythmia after replacement were analyzed.
Results:
A total of 354 patients were included (mean age [standard deviation], 61.8 [14.5] years; men, 80%; secondary prevention, 42%; ventricular arrhythmias in the explanted generator, 62%). After a 25-month follow-up, 70 patients (20%) received appropriate therapies and 8 (2.3%) received inappropriate discharges. Male sex, structural heart disease, heart failure, and the absence of resynchronization were independent predictors of ventricular arrhythmia occurrence.
Conclusions:
One-fifth of patients had appropriate defibrillator therapies in the first 2 years after generator replacement. Determination of the factors associated with arrhythmia occurrence after replacement may be useful to optimize implantable cardioverter-defibrillator treatment.
Introduction and objectives
Implantable cardioverter-defibrillators reduce mortality in some patients with heart disease. Battery replacement is a frequent occurrence in clinical practice and is required in up to 30% of implants. The benefit/risk ratio of defibrillators varies over time and should be reevaluated at the time of replacement. The aim of this study was to determine the clinical characteristics and incidence of defibrillator therapies in patients who underwent generator replacement.
Methods
This multicenter retrospective study involved patients from the UMBRELLA national registry who underwent replacement due to defibrillator battery depletion. The incidence of ventricular arrhythmias was determined via remote monitoring. Risk factors for sustained ventricular arrhythmia after replacement were analyzed.
Results
A total of 354 patients were included (mean age [standard deviation], 61.8 [14.5] years; men, 80%; secondary prevention, 42%; ventricular arrhythmias in the explanted generator, 62%). After a 25-month follow-up, 70 patients (20%) received appropriate therapies and 8 (2.3%) received inappropriate discharges. Male sex, structural heart disease, heart failure, and the absence of resynchronization were independent predictors of ventricular arrhythmia occurrence.
Conclusions
One-fifth of patients had appropriate defibrillator therapies in the first 2 years after generator replacement. Determination of the factors associated with arrhythmia occurrence after replacement may be useful to optimize implantable cardioverter-defibrillator treatment.
Full English text available from:www.revespcardiol.org/en
Various clinical data demonstrate that cardiac resynchronization therapy (CRT) provides a favorable structural as well as electrical remodeling. The CArdiac Resynchronization-Heart Failure study, which tested the pure effect of CRT (using CRT devices without the capability of defibrillation) clearly showed a significant reduction in the total mortality by partly preventing sudden cardiac death. The antiarrhythmic effects of CRT are explained, at least in part, by ionic and genetic modulation of ventricular myocytes. It has been revealed in animal experiments to mimic disorganized ventricular contraction that CRT reverses down-regulation of certain K(+) channels and abnormal Ca(2+) homeostasis in the failing heart. However, CRT can be proarrhythmic in some particular cases especially in the early phase of this therapy. According to our study, proarrhythmic effects after CRT can be observed in approximately 10% of patients. The relatively high incidence of the proarrhythmic effects of CRT may promote a trend toward selecting CRT-D rather than CRT-P.
