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In the treatment of chronic ectopic atrial tachycardia, standard antiarrhythmic therapy has been shown to be ineffective in the majority of patients. The intravenous and oral effects of two class IC antiarrhythmic drugs, encainide and flecainide, in five patients with chronic ectopic atrial tachycardia were studied using exercise testing, 24 hour long-term electrocardiography and programmed electrical stimulation. All patients had been treated unsuccessfully with at least four antiarrhythmic drugs. In two patients tachycardia was persistent, and in three patients tachycardia occurred intermittently for more than 12 hours/day. Intravenous encainide and flecainide at doses ranging from 0.3 to 2.0 mg/kg and from 0.5 to 1.5 mg/kg body weight, respectively, terminated atrial ectopic tachycardia in all patients. Oral encainide, 150 to 225 mg/day, completely suppressed ectopic atrial activity in four patients during a mean follow-up period of 8 +/- 3 months. In the remaining patient encainide markedly reduced the number of episodes of tachycardia. In three patients encainide had to be withdrawn because of intolerable side effects. These patients were well controlled with oral flecainide, 200 to 300 mg/day, without side effects. On the basis of these results, the efficacy of encainide and flecainide in the treatment of chronic ectopic atrial tachycardia appears to be not drug-specific but rather a general class IC property.

To assess the influence of time on the inducibility by programmed electrical stimulation of ventricular arrhythmias after acute myocardial infarction, 18 patients were studied on day 5 and day 24 after infarction with a stimulation protocol employing a maximum of three right ventricular extrastimuli during sinus rhythm and at three paced cycle lengths. All patients were without documented sustained ventricular arrhythmia (sustained ventricular tachycardia or ventricular fibrillation) before the investigation. Sustained ventricular arrhythmia was induced in two patients on day 5, but in nine on day 24 after infarction. This difference in incidence was statistically significant (p less than 0.05), as was the change in the distribution ratio of induced sustained ventricular arrhythmia from day 5 to day 24 (p less than 0.05). The types of arrhythmia induced on day 24 were sustained ventricular tachycardia with a mean cycle length of 207 ms in six cases (five monomorphic, one polymorphic), and ventricular fibrillation in three cases. These nine patients did not differ from the remaining nine patients in maximal serum creatine kinase, infarct site, number of stenosed coronary arteries, global left ventricular ejection fraction (47 +/- 7% versus 46 +/- 10%) and results of 24 hour ambulatory electrocardiographic (Holter) monitoring, but they had a significantly shorter right ventricular effective refractory period (223 +/- 10 ms versus 259 +/- 28 ms; p less than 0.05). During the follow-up period of 24 +/-5 months no patient died, had syncopal attacks or developed spontaneous episodes of sustained ventricular arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

In 12 patients with accessory pathway-mediated supraventricular tachycardia, programmed electrical stimulation with a rapid train of 10 stimuli was assessed for prevention of tachycardia induction. Tachycardia was induced with one or two extrastimuli from both the right and the left atrium (by way of the coronary sinus). Preventive train stimulation, with the train delivered after the tachycardia-initiating stimulus, was attempted at the site of tachycardia induction as well as at the opposite site. Prevention at the site of tachycardia induction was successful in all patients when the length of the train (90 ms) exceeded the effective refractory period of the tachycardia-initiating stimulus to achieve single atrial capture within the "preventive zone." However, in patients with a left-sided accessory pathway, preventive stimulation at the right atrium failed when tachycardia was induced from the coronary sinus because of interatrial conduction delay. It is concluded that train stimulation is an effective mode for supraventricular tachycardia prevention, yet the site of preventive stimulation should lie as close as possible to the anatomic site of the reentrant circuit to reduce interatrial conduction delay.

The formation of a right atrial mass was detected in a patient by two-dimensional echocardiography 3 weeks after successful transvenous electrical ablation of the atrioventricular node had been performed. The mass was attached to the atrial septum at the site where the electrode catheter used for the ablation had supposedly been located and it exhibited no mobility. It was interpreted as a right atrial thrombus induced by the ablation procedure. Although no pulmonary embolic events have been observed during a 7 month follow-up period, right atrial thromboembolism must be considered a potentially dangerous complication of transvenous catheter ablation to control cardiac arrhythmias.