The American journal of cardiology
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We report our experience with flecainide and propafenone therapy for inducible supraventricular tachycardias and paroxysmal supraventricular tachycardias due to atrioventricular (AV) nodal reentry or the Wolff-Parkinson-White syndrome. We performed an electropharmacologic test (ET) that consisted of first inducing a clinical arrhythmia by transesophageal atrial pacing (TAP) protocol. This was followed by intravenous drug administration and TAP reevaluation, either after acute intravenous administration or in oral steady-state. ⋯ In 15 patients, both flecainide and propafenone were tested, 8 receiving flecainide after a negative ET with propafenone, and 7 receiving propafenone after a negative ET with flecainide. In the first group, the ET was positive in 7 (87.5%), and in the second group, it was positive in 3 (42.9%). In a follow-up of 40.1 +/- 11 months, 38 (65.5%) patients had positive outcomes, 5 (8.6%) had to stop receiving the drugs because of side effects, 3 (5.2%) stopped because of inefficacy, and 12 (20.7%) dropped out.(ABSTRACT TRUNCATED AT 250 WORDS)
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Meta Analysis
Short- and long-term efficacy and safety of flecainide acetate for supraventricular arrhythmias.
This report summarizes efficacy and safety data on the use of flecainide acetate for supraventricular arrhythmias. For this purpose, 60 original articles were identified by a literature search representing data from 1,835 treatment courses. In 18 trials, flecainide was administered intravenously; in 19, orally; and in 23, both forms of therapy were applied. ⋯ Ectopic atrial tachycardia responded in 86% and 95% of patients treated with flecainide acutely or chronically. Data concerning drug-related side effects were available for 1,794 of 1,835 treatment courses (98%). Overall, 352 of 1,794 patients (20%) reported at least one non-cardiac or cardiac adverse experience.(ABSTRACT TRUNCATED AT 250 WORDS)
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Review Comparative Study
Flecainide in the Wolff-Parkinson-White syndrome.
The effects of flecainide on electrophysiologic parameters and arrhythmias in the Wolff-Parkinson-White syndrome were reviewed. Acute administration of flecainide blocks conduction across the accessory pathway in the anterograde direction in 40% and in the retrograde direction in 50% of cases and markedly prolongs refractoriness in the remaining cases. Flecainide has a lesser effect on refractoriness of the His-Purkinje system, atrium, ventricle, and atrioventricular node. ⋯ Administered during preexcited atrial fibrillation, flecainide consistently slows the ventricular response and converts the majority of cases to sinus rhythm. Serious ventricular proarrhythmia is seen almost exclusively in patients with structural cardiac disease. Flecainide is a useful drug for the acute and chronic control of tachycardia in Wolff-Parkinson-White syndrome.
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Multicenter Study Clinical Trial
Long-term safety and efficacy of flecainide in the treatment of supraventricular tachyarrhythmias: the United States experience. The Flecainide Supraventricular Tachyarrhythmia Investigators.
Information about long-term safety and effectiveness is important for appropriate use of antiarrhythmic drug therapy. We report the results of an open-label, long-term (mean, 15 months) therapy extension for 66 patients with paroxysmal supraventricular tachycardia (PSVT) or atrial fibrillation (PAF) in whom short-term therapy in 2 controlled studies was deemed beneficial by both patient and investigator. Follow-up was accomplished by clinic visits and telephone calls. ⋯ No clinically significant laboratory, electrocardiographic, or physical abnormalities were ascribed to flecainide. Thus, the long-term safety and efficacy profile of the drug for treatment of PSVT and PAF is encouraging. This promising clinical experience is relatively small and so should be reinforced by larger patient trials in the future.
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Comparative Study
Comparison of heart rate variability in survivors and nonsurvivors of sudden cardiac arrest.
Imbalances in autonomic nervous system function have been posed as a possible mechanism that produces ventricular fibrillation and sudden cardiac arrest in patients with cardiovascular disease. Heart rate (HR) variability is described in survivors and nonsurvivors of sudden cardiac arrest within 48 hours after resuscitation using time and frequency domain analytic approaches. HR data were collected using 24-hour ambulatory electro-cardiograms in 16 survivors and 5 nonsurvivors of sudden cardiac arrest, and 5 control subjects. ⋯ Analysis of 24-hour electrocardiograms demonstrated that control subjects had the highest HR variability (standard deviation of all RR intervals = 155.2 +/- 54 ms), with nonsurvivors demonstrating the lowest HR variability (standard deviation of all RR intervals = 52.3 +/- 6.1 ms) and survivors of sudden cardiac arrest falling between the other 2 groups (standard deviation of all RR intervals = 78 +/- 25.5 ms, p less than or equal to 0.0000). Two other indexes of HR variability (mean number of beat to beat differences in RR intervals greater than 50 ms/hour and root-mean-square of successive differences in RR intervals) did not demonstrate the expected pattern in this sample, indicating that perhaps patterns of HR variability differ between groups of patients with cardiovascular disorders. Spectral analytic methods demonstrated that survivors of sudden cardiac arrest had reduced low- and high-frequency spectral power, whereas nonsurvivors demonstrated a loss of both low- and high-frequency spectral power.(ABSTRACT TRUNCATED AT 250 WORDS)