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Arrhythmia Induction (arrhythmia + induction)
Selected AbstractsSupraventricular Arrhythmia Induction by an Implantable Cardioverter Defibrillator in a Patient with Hypertrophic CardiomyopathyPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2010FARIBORZ AKBARZADEH M.D. A 23-year-old woman with obstructive hypertrophic cardiomyopathy and history of frequent unexplained syncope had undergone implantable cardioverter defibrillator implantation. She had experienced frequent inappropriate shocks since implantation due to T-wave oversensing. After one of the syncopal attacks, she was found to have an atrioventricular (AV)-reentrant tachycardia, induced by a high-voltage shock, with rapid degeneration to atrial fibrillation and then ventricular fibrillation. The AV-reentrant tachycardia was believed to be the cause of both syncopal attacks and inappropriate shocks. The patient has been asymptomatic after ablation of the accessory pathway. To the best of our knowledge, this is the first report of induction of an AV-reentrant tachycardia by a high-voltage implantable cardioverter defibrillator shock. (PACE 2010; 33:372,376) [source] Are Routine Arrhythmia Inductions Necessary in Patients with Pectoral Implantable Cardioverter Defibrillators?JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2000MICHAEL GLIKSON M.D. Routine Arrhythmia Inductions in Patients with ICDs. Introduction: The value of ventricular arrhythmia inductions as part of routine implantable cardioverter defibrillator (ICD) follow-up in new-generation pectoral ICDs is unknown Methods and Results: We performed a retrospective analysis of a prospectively collected database analyzing data from 153 patients with pectoral ICDs who had routine arrhythmia inductions at predismissal, and 3 months and 1 year after implantation. Routine predismissal ventricular fibrillation (VF) induction yielded important findings in 8.8% of patients, all in patients with implantation defibrillation threshold (DFT) , 15 J or with concomitant pacemaker systems. At 3 months and 1 year, routine VF induction yielded important findings in 5.9% and 3.8% of tested patients, respectively, all in patients who had high DFT on prior testing. Ventricular tachycardia (VT) induction at predismissal, and 3 months and 1 year after implantation resulted in programming change in 37.4%, 28.1%, and 13.8% of tested patients, almost all in patients with inducible VT on baseline electrophysiologic study and clinical episodes since implantation. Conclusion: Although helpful in identifying potentially important ICD malfunctions, routine arrhythmia inductions during the first year after ICD implantation may not be necessary in all cases. VF inductions have a low yield in patients with previously low DFTs who lack concomitant pacemakers. VT inductions have a low yield in patients without baseline Inducible VT and in the absence of clinical events. Definite recommendations regarding patient selection must await larger prospective studies as well as consensus in the medical community about what comprises an acceptable risk justifying avoidance of the costs and inconveniences of routine arrhythmia inductions. [source] Impaired Detection of Ventricular Tachyarrhythmias by a Rate-Smoothing Algorithm in Dual-Chamber Implantable Defibrillators: Intradevice InteractionsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2002MICHAEL GLIKSON M.D. Rate-Smoothing Algorithm in ICD.Introduction: Rate smoothing is an algorithm initially designed to prevent rapid changes in pacemaker rates. In this study, we sought to determine the potential of the rate-smoothing mechanism in preventing detection of ventricular tachyarrhythmias. Methods and Results: Clinical testing of rate smoothing was performed at the time of defibrillator arrhythmia induction in 16 patients with implantable defibrillators during 65 episodes of ventricular tachyarrhythmias. We also performed simulator-based testing to assess detection of ventricular tachycardia between 170 and 220 beats/min with systematic sequential change of rate-smoothing percent, AV delay, and maximal rate. During clinical testing of 54 ventricular fibrillation/polymorphic ventricular tachyarrhythmia episodes, there were no cases of nondetection and 3 episodes (5%) of minimally delayed detection. Of 10 monomorphic ventricular tachyarrhythmias, 6 had either delayed (2 cases) or absent (4 cases) detection. During simulator testing, complex interrelationships were demonstrated in AV delay, upper rate, and rate-smoothing percent in determining the severity of the effect on detection. Generally, long AV delay, higher upper rate, and smaller (more aggressive) rate smoothing were associated with increased risk of ventricular tachyarrhythmia underdetection. Importantly, use of parameters that impaired detection was always accompanied by a programmer warning message. Conclusion: Rate smoothing may result in delay or failure of ventricular tachycardia detection. It is important to consider warning messages when programming rate smoothing and to test for appropriate detection when rate smoothing is used despite warning messages. [source] Maturational Atrioventricular Nodal Physiology in the MouseJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2000COLIN T. MAGUIRE B.S. Mouse AV Nodal Maturation. Introduction: Dual AV nodal physiology is characterized by discontinuous conduction from the atrium to His bundle during programmed atrial extrastimulus testing (A2V2 conduction curves), AV nodal echo beats, and induction of AV nodal reentry tachycardia (AVNRT). The purpose of this study was to characterize in vivo murine maturational AV nodal conduction properties and determine the frequency of dual AV nodal physiology and inducible AVNRT. Methods and Results: A complete transvenous in vivo electrophysiologic study was performed on 30 immature and 19 mature mice. Assessment of AV nodal conduction included (1) surface ECG and intracardiac atrial and ventricular electrograms; (2) decremental atrial pacing to the point of Wenckebach block and 2:1 conduction; and (3) programmed premature atrial extrastimuli to determine AV effective refractory periods (AVERP), construct A2V2 conduction curves, and attempt arrhythmia induction. The mean Wenckebach block interval was 73 ± 12 msec, 2:1 block pacing cycle length was 61 ± 11 msec, and mean AVERP100 was 54 ± 11 msec. The frequency of dual AV nodal physiology increased with chronologic age, with discontinuous A2V2, conduction curves or AV nodal echo heats in 27% of young mice < 8 weeks and 58% in adult mice (P = 0.03). Conclusion: These data suggest that mice, similar to humans, have maturation of AV nodal physiology, hut they do not have inducible AVNRT. Characterization of murine electrophysiology may be of value in studying genetically modified animals with AV conduction abnormalities. Furthermore, extrapolation to humans may help explain the relative rarity of AVNRT in the younger pediatric population. [source] Cardiac cell therapy: overexpression of connexin43 in skeletal myoblasts and prevention of ventricular arrhythmiasJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 9b 2009Sarah Fernandes Abstract Cell-based therapies have great potential for the treatment of cardiovascular diseases. Recently, using a transgenic mouse model Roell et al. reported that cardiac engraftment of connexin43 (Cx43)-overexpressing myoblasts in vivo prevents post-infarct arrhythmia, a common cause of death in patients following heart attack. We carried out a similar study but in a clinically relevant context via transplantation of autologous connexin43-overexpressing myoblasts in infarcted rats. Seven days after coronary ligation, rats were randomized into three groups: a control group injected with myoblasts, a null group injected with myoblasts transduced with an empty lentivirus vector (null) and a Cx43 group injected with myoblasts transduced with a lentivirus vector encoding connexin43. In contrast to Roell's report, arrhythmia occurrence was not statistically different between groups (58%, 64% and 48% for the control (n= 12), null (n= 14) and Cx43 (n= 23) groups, respectively, P= 0.92). Using ex vivo intramural monophasic action potential recordings synchronous electrical activity was observed between connexin43-overexpressing myoblasts and host cardiomyocytes, whereas such synchrony did not occur in the null-transduced group. This suggests that ex vivo connexin43 gene transfer and expression in myoblasts improved intercellular electrical coupling between myoblasts and cardiomyocytes. However, in our model such electrical coupling was not sufficient to decrease arrhythmia induction. Therefore, we would suggest a note of caution on the use of combined Cx43 gene and cell therapy to prevent post-infarct arrhythmias in heart failure patients. [source] More types than one: multiple muscarinic receptor coupled K+ currents undergo remodelling in an experimental model of atrial fibrillationBRITISH JOURNAL OF PHARMACOLOGY, Issue 7 2007A F James The common cardiac arrhythmia atrial fibrillation (AF) tends to show progression in its severity, which is associated with ,remodelling': structural and electrophysiological changes that facilitate arrhythmia induction and maintenance. In this issue of the BJP, Yeh and colleagues demonstrate for the first time, down-regulation of three types of muscarinic cholinergic receptor (mAChR) coupled K+ currents (IKM2, IKM3 and IKM4) and of M2, M3 and M4 mAChR subtype proteins, in a canine model of atrial tachycardia (AT) induced remodelling. The IKMs and their extent of AT-induced remodelling were similar in left-atrial and pulmonary vein (PV) myocytes, so remodelling of M2,M4 receptor-linked currents appears not to underlie the unique contribution of PVs to AF. Parasympathetic stimulation can increase susceptibility to AF; thus remodelling of M2,M4 receptors and K+ currents could be adaptive in AT. Further work is warranted to determine whether or not remodelling of multiple mAChRs and currents also contributes to human AF. British Journal of Pharmacology (2007) 152, 981,983; doi:10.1038/sj.bjp.0707437; published online 10 September 2007 [source] Are Routine Arrhythmia Inductions Necessary in Patients with Pectoral Implantable Cardioverter Defibrillators?JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2000MICHAEL GLIKSON M.D. Routine Arrhythmia Inductions in Patients with ICDs. Introduction: The value of ventricular arrhythmia inductions as part of routine implantable cardioverter defibrillator (ICD) follow-up in new-generation pectoral ICDs is unknown Methods and Results: We performed a retrospective analysis of a prospectively collected database analyzing data from 153 patients with pectoral ICDs who had routine arrhythmia inductions at predismissal, and 3 months and 1 year after implantation. Routine predismissal ventricular fibrillation (VF) induction yielded important findings in 8.8% of patients, all in patients with implantation defibrillation threshold (DFT) , 15 J or with concomitant pacemaker systems. At 3 months and 1 year, routine VF induction yielded important findings in 5.9% and 3.8% of tested patients, respectively, all in patients who had high DFT on prior testing. Ventricular tachycardia (VT) induction at predismissal, and 3 months and 1 year after implantation resulted in programming change in 37.4%, 28.1%, and 13.8% of tested patients, almost all in patients with inducible VT on baseline electrophysiologic study and clinical episodes since implantation. Conclusion: Although helpful in identifying potentially important ICD malfunctions, routine arrhythmia inductions during the first year after ICD implantation may not be necessary in all cases. VF inductions have a low yield in patients with previously low DFTs who lack concomitant pacemakers. VT inductions have a low yield in patients without baseline Inducible VT and in the absence of clinical events. Definite recommendations regarding patient selection must await larger prospective studies as well as consensus in the medical community about what comprises an acceptable risk justifying avoidance of the costs and inconveniences of routine arrhythmia inductions. [source] | ||||||||||