Treatment of recent onset atrial fibrillation with intravenous sotalol and/or flecainide.

AIM: The purpose of our study (conducted between August 1995 and September 1996) was to evaluate prospectively the efficacy of intravenous administration (in 10 min) of sotalol, flecainide or the combination of these drugs to restore sinus rhythm in patients (without cardiac/pulmonary failure) who came to the First Heart Aid of our hospital with atrial fibrillation lasting less than 24 h. METHODS AND RESULTS: Patients in whom the rhythm was not converted to sinus rhythm by intravenous sotalol within 60 min, we started to give flecainide intravenously (2 mg/kg). In patients on oral beta blockade we started flecainide intravenously (2 mg/kg) over 10 min. Of the 92 patients who fulfilled the entry criteria 51 were on oral beta blocking agents for angina, hypertension or to prevent atrial fibrillation. Of these patients, 43 (84%) converted to sinus rhythm with intravenous flecainide. The 41 patients not on a beta blocking agents were treated with 40 mg sotalol intravenously which led to sinus rhythm in 22 patients (54%). Sixteen of the 19 remaining patients (84%) converted to sinus rhythm after subsequent administration of flecainide. Therefore of the whole group of 70 patients treated with flecainide, 59 (84%) were successfully converted. Out of the 92 patients, 11 patients were not converted to sinus rhythm. Six were treated successfully by electrical cardioversion. The others were treated with oral flecainide/sotalol or digoxine with persistence of atrial fibrillation. CONCLUSION: The findings of this study suggest that intravenous sotalol is a good choice for termination of recent onset atrial fibrillation in a patient with a good left ventricular function. If not successful then flecainide had to be added.

A transcardiac lead system for identification and termination of supraventricular and ventricular tachycardia.

The value of a transcardiac lead system (coronary sinus to right ventricular apex) to record atrial and ventricular electrical activity and its pacing capabilities was assessed in 20 patients with a variety of tachycardias (atrial tachycardia in 3 patients, atrial flutter in 4, intranodal tachycardia in 6, circus movement tachycardia using an accessory pathway in 1 patient, and ventricular tachycardia in 9). The transcardiac lead invariably showed both atrial and ventricular electrical activity during sinus rhythm and tachycardias, allowing application of the same criteria as used when analyzing cardiac rhythm on the surface electrocardiogram. Atrial complexes had a mean amplitude of 4.2 mV during sinus rhythm and varied from 3.0 to 4.1 mV during the different types of tachycardia. Ventricular complexes had a mean amplitude of 9.8 mV during sinus rhythm, 13.8 mV during supraventricular tachycardia and 16.1 mV during ventricular tachycardia. The duration of the QRS complex on the transcardiac lead was equal to the duration of the QRS complex on the surface electrocardiogram during tachycardias with a small or wide QRS complex. By varying the intensity of current delivered through the transcardiac lead, only right ventricular pacing (mean current intensity 1.2 +/- 0.4 mA) or simultaneous atrioventricular pacing (mean current intensity 4.7 +/- 3.3 mA) could be achieved. Termination of all episodes of tachycardia was achieved with either ventricular pacing or simultaneous atrioventricular pacing. This transcardiac lead system allows clear identification of atrial and ventricular events, is suitable for tachycardia analysis using simple surface electrocardiographic algorithms and allows pacing termination of a variety of tachycardias.

Lack of clinically significant beta-blocking effect of propafenone.

To study possible beta-blocking effects of propafenone, a class 1c antiarrhythmic agent, electrocardiographic variables were studied at rest and during exercise. Forty-two patients with symptomatic ventricular arrhythmias were included. In 31 patients, exercise electrocardiograms before and after propafenone were available for study. The mean dose of propafenone was 603 mg for all 42 patients, 585 mg for patients undergoing exercise testing (range 450-1200). At rest, the PR interval, duration of P wave and QRS complex changed significantly without any change in the resting heart rate and QTc interval. During exercise there were no changes after propafenone in peak heart rate, PR interval, QTc interval, duration of exercise, or blood pressure. We conclude that, while class I effects are evident both at rest and after exercise, no clinically significant beta-blocking effects of propafenone could be demonstrated either at rest or during exercise.