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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 11 (2000), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Atrial Torsades de Pointes. A patient with long QT syndrome and a history of palpitations underwent electrophysiologic study. Runs of polymorphic self-terminating atrial tachyarrhythmias were easily induced and occurred spontaneously several times. Atrial monophasic action potential (MAP) durations were prolonged at short pacing cycle lengths. Premature high right atrial extrastimuli prolonged MAP duration in the low right atrium, resulting in an inverse electrical restitution curve, and increased dispersion of repolarization. MAP morphology showed gradually increasing early afterdepolarizations. When the arrhythmia was initiated, a new action potential reproducibly emerged from these afterdepolarizations. To the knowledge of the authors, this is the first reported case of “atrial torsades de pointes” in a patient.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 11 (2000), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Arrhythmias in Heart Failure. About one half of deaths in patients with heart failure are sudden, mostly due to ventricular tachycardia (VT) degenerating to ventricular fibrillation or immediate ventricular fibrillation. In severe heart failure, sudden cardiac death also may occur due to bradyarrhythmias. Other dysrhythmias complicating heart failure include atrial and ventricular extrasystoles, atrial fibrillation (AF), and sustained and nonsustained ventricular tachyarrhythmias. The exact mechanism of the increased vulnerability to arrhythmias is not known. Depending on the etiology of heart failure, different preconditions, including ischemia or structural alterations such as fibrosis or myocardial scarring, may he prominent. Reentrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. Furthermore, alterations in potassium currents leading to action potential prolongation and an increase in dispersion of repolarization play a significant role. Treatment of arrhythmias is necessary either because patients are symptomatic or to reduce the risk for sudden cardiac death. The individual history, left ventricular function, electrophysiologic testing, and the signal-averaged ECG give useful information for identifying patients at risk for sudden cardiac death. The implantable cardioverter defibrillator (ICD) has evolved as a promising therapy for life-threatening arrhythmias. A potential role may exist for antiarrhythmic drugs, mainly amiodarone. There is growing evidence that patients with sustained VT or a history of resuscitation have the best outcome with ICD therapy regardless of the degree of heart failure. Many of these patients require additional antiarrhythmic therapy because of AF or nonsustained VTs that may activate the device. Catheter ablation or map-guided endocardial resection are additional options in selected patients but seldom represent the only therapeutic strategy.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 4 (1993), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Late Potentials in CAD. In patients who have survived acute myocardial infarction, thepresence of ventricular late potentials using the high resolution signal-averaged KCG indicatesareas of slow conduction and delayed activation that may potentially serve as a substrate lormalignant ventricular arrhythmias. Although detection of late potentials is technique specific, signal-averaged analysis in the time or frequency domain may he a useful index for riskstratification with regard to ventricular tachycardia or sudden cardiac death. The sensitivityand specificity of late potentials for this purpose may he enhanced by comhination with othervariables, such as left ventricular ejection fraction and presence of complex ventricular ectopy, Therefore, the presence of ventricular late potentials in postmyocardial infarction patients, particularly in those patients with impaired left ventricular function, identifies those patienlswho are at high risk of malignant ventricular tachyarrhythmias, However., (he strategies forprevention of serious arrhythmia complications during follow-up need to be established, Thenegative predictive value of late potentials is very high. Thus, the absence of late potentialsindicates a low propensity to sustained ventricular tachycardia or sudden death, even in thepresence of complex ventricular ectopy. Interventions may therefore not be necessary orshould even he avoided, The incidence of late potentials in patients with spontaneous orinduced ventricular fibrillation is lower and, if present, less pronounced than in those with sustained monomorphic ventricular tachycardia. This presumably is due to a lower degree of conduction delay, which serves as a substrate for reentry. Therefore, the ability of the signal-aver-aged ECG to predict a propensity to ventricular fibrillation is limited, Despite these limitations, the signal-averaged ECG may be used as a risk predictor in evaluation of patients aftermyocardial infarction. Unfortunately, at least as far as time domain analysis is concerned, itcannot be used as an efficacy predictor for response to pbarniacologic interventions, Furtherstudies will determine whether other modes of signal-averaged analysis can predict theresponse to drugs.
    Type of Medium: Electronic Resource
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