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  • 1
    Electronic Resource
    Electronic Resource
    Divergent Effect of Acute Ventricular Dilatation on the Electrophysiologic Characteristics of d,I-Sotalol and Flecainide in the Isolated Rebbit heart (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 9 (1998), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Ventricular Dilatation and d,l-Sotalol/Flecainide in Isolated Rabbit Heart. Introduction: The interaction between acute ventricular dilatation (AVD) as one aspect of ventricular dysfunction and Class I and III antiarrhythmic drugs is uncertain. We therefore investigated the effects of AVD on the electrophysiologic properties of d,l-sotalol and flecainide. Methods and Results: The isolated rabbit heart was used as a model of AVD. The ventricular size and, therefore, the diastolic pressure were modified by sudden volume changes of a fluid-filled balloon placed in the left ventricle. Pacing was performed alternately using epi- and endocardial monophasic action potential (MAP)-pacing catheters at cycle lengths from 1,000 to 300 msec. d,l-Sotalol (10 μM) resulted in a significant (P 〈 0.05) lengthening of refractoriness (+13.5%± 3.1%), MAP duration (+14.9%± 3.2%), and QT interval (+15.5%± 4.1%) (mean ± SEM at 1,000 msec). These effects had a reverse rate-dependence. AVD to a diastolic pressure of 30 mmHg reduced refractoriness and left ventricular MAP duration. In comparison with the control group with the same extent of WD, d,l-sotalol still led to a significant prolongation of repolarization for all cycle lengths except 300 msec, so that its effects were not absolutely but relatively preserved. In contrast, flecainide (2μM) had no significant effects on refractoriness or MAP duration. It led to a significant, rate-dependent increase of pacing thresholds (+47.6%± 8.2%), prolongation of QRS (+48.8%± 5.6%), and conduction time (+78.6%± 8.6%) (mean ± SEM at 300 msec). In the flecainide group, AVD significantly increased the normal rate-dependent prolongation of QRS (+16.7%± 5.5%) and conduction time (+17.1%± 4.3%). Conclusion: Our data demonstrate that, during AVD, the Class III effect of d,l-sotalol is preserved, whereas flecainide's effect of slowing conduction is exaggerated. This may contribute to flecainide-related proarrhythmia in certain clinical situations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1998.tb00925.x
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  • 2
    Electronic Resource
    Electronic Resource
    A Patient with “Atrial Torsades de Pointes” (2000)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 11 (2000), S. 0 
    Details
    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
    URL: http://dx.doi.org/10.1111/j.1540-8167.2000.tb00052.x
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  • 3
    Electronic Resource
    Electronic Resource
    Transient Local Changes in Right Ventricular Monophasic Action Potentials Due to Ajmaline in a Patient with Brugada Syndrome (1999)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 10 (1999), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Monophasic Action Potential Recording in Brugada Syndrome. A 48-year-old patient with recurrent episodes of palpitations and syncope presented with transient ST segment elevation in the right precordial ECG leads. Structural heart disease was excluded. No arrhythmias were inducible by programmed ventricular stimulation. Parallel to ST elevation after intravenous ajmaline, a gradual and reversible delay in the upstroke of right ventricular (RV) monophasic action potentials (MAPs) occurred that was most marked in the RV outflow tract and nearly absent at right free-wall recordings. Ajmaline led to a cycle length-dependent increase in RV dispersion of repolarization. Thus, right endocardial MAPs may demonstrate regionally different action potential changes that may contribute to the ECG changes in Brugada syndrome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1999.tb01272.x
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  • 4
    Electronic Resource
    Electronic Resource
    Reproducible Conversion from Wide to Narrow Complex Tachycardia: (2000)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 11 (2000), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.2000.tb00078.x
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  • 5
    Electronic Resource
    Electronic Resource
    Brugada Syndrome and Supraventricular Tachyarrhythmias: A Novel Association? (2001)
    Oxford, UK : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 12 (2001), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Brugada Syndrome and Supraventricular Tachyarrhythmias. Introduction: The Brugada syndrome is a distinct form of idiopathic ventricular fibrillation characterized by a unique ECG pattern consisting of a right bundle branch block-like aspect and ST segment elevation in leads V1 to V3. As a high induction rate of ventricular tachyarrhythmias has been reported in Brugada syndrome, we hypothesized that this also may be true for supraventricular tachycardias in these patients. Methods and Results: Between January 1995 and December 2000, we identified 35 consecutive patients with Brugada syndrome; 26 had a history of cardiac arrest or syncope and 9 were asymptomatic. All patients underwent electrophysiologic study, including an atrial and ventricular stimulation protocol. Ten patients (29%) were found to have supraventricular tachyarrhythmias (SVT) in addition to the Brugada syndrome. These 10 patients presented with aborted sudden cardiac death (n = 3) and/or a family history of sudden cardiac death (n = 4), syncope (n = 4), or primarily with a Brugada typical ECG, a positive family history, and palpitations (n = 2). Eight of them underwent genetic testing, but only 1 had a mutation in the SCN5A gene. In 6 patients, an AV nodal reentrant tachycardia was easily and reproducibly inducible. Two patients had clinical documented and inducible episodes of an atrial tachycardia (1 in addition to an AV nodal reentrant tachycardia). One patient had paroxysmal atrial fibrillation alternating with sinus rhythm, and 2 patients with accessory pathways were identified. Conclusion: This is the first description of an association of the Brugada syndrome with SVT. Thus, the arrhythmogenic substrate in Brugada syndrome may not be restricted to the ventricular level. Palpitations in this syndrome should raise the possibility of SVT. Conversely, in patients with SVT and aborted sudden cardiac death or syncope not related to SVT, the Brugada syndrome should be considered a possible additional electrophysiologic abnormality.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1540-8167.2001.00680.x
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  • 6
    Electronic Resource
    Electronic Resource
    Arrhythmias in Heart Failure: (2000)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 11 (2000), S. 0 
    Details
    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
    URL: http://dx.doi.org/10.1111/j.1540-8167.2000.tb00746.x
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  • 7
    Electronic Resource
    Electronic Resource
    Wolff-Parkinson-White Syndrome Associated with Brugada Syndrome (2001)
    Oxford, UK : Blackwell Futura Publishing, Inc.
    Pacing and clinical electrophysiology 24 (2001), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9592.2001.01423.x
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