Journal of cardiovascular electrophysiology
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J. Cardiovasc. Electrophysiol. · Apr 1996
ReviewPropafenone: an effective agent for the management of supraventricular arrhythmias.
Propafenone is a sodium channel blocking antiarrhythmic drug. It also has beta-adrenergic, potassium channel, and weak calcium channel blocking activity. The drug is metabolized in the liver with rates dependent on the debrisoquin phenotype. ⋯ The drug may produce SA block in patients with underlying sinus node dysfunction. Propafenone has comparatively few noncardiac side effects. It is a useful primary drug or an alternative to more commonly used drugs used for the treatment of supraventricular arrhythmias.
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J. Cardiovasc. Electrophysiol. · Mar 1996
Management of ventricular fibrillation with transvenous defibrillators without baseline electrophysiologic testing or antiarrhythmic drugs.
Baseline electrophysiologic study (EPS) is routinely performed in patients resuscitated from ventricular fibrillation (VF) to risk stratify and select patients for chronic antiarrhythmic drug therapy. The role of EP testing prior to insertion of a multiprogrammable implantable cardioverter defibrillator (ICD), however, is unclear. ⋯ After a cardiac arrest due to primary VF, select patients treated with multiprogrammable ICDs can be managed successfully without baseline EPS or antiarrhythmic drug therapy.
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J. Cardiovasc. Electrophysiol. · Nov 1995
Case ReportsRadiofrequency catheter ablation of multiple morphologies of ventricular tachycardia by targeting a single region of the left ventricle.
As treatment options for ventricular tachycardia (VT) continue to evolve, the use of radiofrequency catheter ablation is rapidly expanding. However, in the presence of multiple morphologies of VT, achieving successful results may seem less likely. We report two patients with multiple morphologies of VT who underwent successful radiofrequency ablation by application of radiofrequency energy to a single region in the left ventricle. ⋯ VTs with distinctly different morphologies can occur in patients with no detectable structural heart disease. These VT circuits may share a common pathway and, therefore, may readily be amenable to therapy with radiofrequency catheter ablation.
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J. Cardiovasc. Electrophysiol. · Oct 1995
Comparative StudyContemporary clinical trials in ventricular tachycardia and fibrillation: implications of ESVEM, CASCADE, and CASH for clinical management.
Recent clinical trials in patients with ventricular tachycardia (VT) or fibrillation (VF) have occurred in the setting of the disappointing results of postinfarction secondary prevention studies using Class I antiarrhythmics (e.g., CAST). ESVEM addressed in a randomized trial whether electrophysiologic study (EPS) or Holter monitoring (HM) is a more accurate predictor of long-term antiarrhythmic drug efficacy in VT/VF patients (N=486) and what the relative efficacy of various antiarrhythmic agents is for VT/VF. Surprisingly, arrhythmia recurrence rates were not significantly different by the method of determining an efficacy prediction. ⋯ The primary endpoint of cardiac death, resuscitated VF, or syncopal shock (in ICD patients) was reduced by amiodarone compared with conventional therapy (9% vs 23% at 1 year). An interim report of the ongoing CASH study suggested in 230 survivors of cardiac arrest that propafenone (Class IC) provided less effective prophylaxis (approximately 20% 1-year mortality) compared with randomly assigned therapies with amiodarone, metoprolol, or an ICD (approximately 14% mortality rates) and was excluded from further study. These studies have led to a paradigm shift in the approach to antiarrhythmic therapy of VT/VF: drugs with antisympathetic plus Class III (refractoriness prolonging) action (i.e., sotalol, amiodarone) are superior to traditional drugs with Class I( conduction slowing) effects, even when guided by EPS or HM.
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J. Cardiovasc. Electrophysiol. · May 1994
Differences in corrected QT intervals at minimal and maximal heart rate may identify patients at risk for torsades de pointes during treatment with antiarrhythmic drugs.
The mechanism of torsades de pointes as a proarrhythmic response to antiarrhythmic drugs is not clear. We hypothesized that the difference in the corrected QT interval (QTc, Bazett's formula) with varying autonomic tone and heart rate during 24-hour ambulatory ECG would help identify patients at risk. Ten patients with antiarrhythmic drug-induced torsades de pointes were compared with 28 controls. ⋯ Using an arbitrary QTc difference cutoff of 0.075 seconds, this approach identified patients at risk for antiarrhythmic drug-induced torsades de pointes with a sensitivity of 70% (7 of 10) and a specificity of 89% (P < or = 0.003 by Chi-square analysis with Yates' correction). In conclusion, patients with antiarrhythmic drug-induced torsades de pointes had a greater rise in QTc from minimal to maximal heart rate during ambulatory ECG than controls. Further larger prospective trials will be required to establish the value of this approach to identify patients at risk for this type of proarrhythmia.