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We evaluated two patients without previous episodes of syncope who showed characteristic ECG changes similar to Brugada syndrome following administration of Class IC drugs, flecainide and pilsicainide, but not following Class IA drugs. Patient 1 had frequent episodes of paroxysmal atrial fibrillation resistant to Class IA drugs. After treatment with flecainide, the ECG showed a marked ST elevation in leads V2 and V3, and the coved-type configuration of ST segment in lead V2. A signal-averaged ECG showed late potentials that became more prominent after flecainide. Pilsicainide, a Class IC drug, induced the same ST segment elevation as flecainide, but procainamide did not. Patient 2 also had frequent episodes of paroxysmal atrial fibrillation. Pilsicainide changed atrial fibrillation to atrial flutter with 2:1 ventricular response, and the ECG showed right bundle branch block and a marked coved-type ST elevation in leads V1 and V2. After termination of atrial flutter, ST segment elevation in leads V1 and V2 continued. In this patient, procainamide and quinidine did not induce this type of ECG change. In conclusion, strong Na channel blocking drugs induce ST segment elevation similar to Brugada syndrome even in patients without any history of syncope or ventricular fibrillation.

A prospective study correlated the effect of quinidine or procainamide versus no antiarrhythmic drug on sudden cardiac death, total cardiac death and total death in 406 elderly patients with heart disease and asymptomatic complex ventricular arrhythmias detected by 24-hour ambulatory electrocardiograms. Of 397 patients treated with quinidine, 184 (46%) developed adverse effects during the first 2 weeks of therapy and were given no further antiarrhythmic therapy. Of 9 patients treated with procainamide, 2 (22%) developed adverse effects during the first 2 weeks of therapy and were given no further antiarrhythmic therapy. Adverse effects developed during long-term therapy in 6 patients (2%) receiving quinidine and in 3 patients (33%) receiving procainamide. Mean follow-up was 24 +/- 15 months in both groups. Sudden cardiac death, total cardiac death and total death occurred in 21, 43 and 65% of patients receiving quinidine or procainamide, respectively, and in 23, 44 and 63% of patients receiving no antiarrhythmic drug, respectively (difference not significant). Survival by Kaplan-Meier analysis showed no significant difference between the 2 groups for sudden cardiac death, total cardiac death or total death through 4 years. Patients with abnormal left ventricular ejection fraction had a 3.4 times higher incidence of sudden cardiac death, a 2.4 times higher incidence of total cardiac death and a 1.4 times higher incidence of total death than patients with normal left ventricular ejection fraction. These data showed no significant difference in sudden cardiac death, total cardiac death or total death between patients treated with quinidine or procainamide or with no antiarrhythmic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Unlabelled: Three patients with paroxysmal supraventricular tachycardia underwent electrophysiologic studies that included His bundle recordings, incremental atrial and ventricular pacing and extrastimulation before and after intravenous infusion of 500 mg of procainamide. In all three patients the tachycardia was induced during atrial pacing or premature atrial stimulation, or both. Two of the three patients had discontinuous atrioventricular (A-V) nodal curves with induction of a slow-fast tachycardia during failure in anterograde fast pathway conduction and one patient had a smooth A-V nodal curve with induction of a slow-fast tachycardia at critical A-H interval delays. After procainamide: (1) in all three patients atrial pacing induced A-V nodal Wenckebach periodicity (cycle length 300 to 400 ms) resulting in simultaneous anterograde fast and slow pathway conduction (one atrial beat resulting in two QRS complexes) and retrograde fast pathway conduction initiating an echo response or a slow-fast tachycardia, or both; (2) in all three patients there was enhanced conduction and shortening of refractoriness of the anteriograde fast pathway and depressed conduction and lengthening of refractoriness of the retrograde fast pathway; and (3) in two patients there was inability to sustain tachycardia because of selective block within the retrograde fast pathway., In Conclusion: (1) procainamide altered conduction and refractoriness of the anterograde fast and slow pathways so that simultaneous conduction could occur during atrial pacing, resulting in a double ventricular response and a slow-fast echo or tachycardia, or both; and (2) the differential effects of procainamide on anterograde fast and retrograde fast pathways suggests two functional A-V nodal fast pathways, oine for anterograde and the other for retrograde conduction.

Six patients with idiopathic paroxysmal ventricular tachycardia were investigated by external electrocardiography, intracardiac electrography and pacing, exercise testing, cardiac catheterization and coronary angiography. All had normal hemodynamics and coronary arteries. His bundle electrography proved ventricular origin in five; one had no paroxysmal ventricular tachycardia during His bundle electrography. Treatment with diphenylhydantoin, 4.2 to 8.0 mg/kg/day, and propranolol, 0.8 to 2.7 mg/kg/day, appeared effective, well tolerated therapy in three, and procainamide and propranolol in one requiring medical treatment. Abstinence from tobacco and coffee abolished paroxysmal ventricular tachycardia in one of two who required no medication. The other has no recurrence of paroxysmal ventricular tachycardia since study.

Seven children with idiopathic PVT ranging in age from one day to 18 yr, have been observed during the past three years. The presenting complaints and frequency of paroxysms varied greatly. Three patients presented with syncope; four were asymptomatic. Lidocaine was effective in terminating acute symptomatic attacks; procaine amide and propranolol were effective in long-term control of the arrhythmia. Monitoring of the dynamic ECG was invaluable in establishing the diagnosis, characterizing the arrhythmia, and evaluating the effects of activity and therapy.

A double-blind cross-over study has been performed in 10 patients with an established diagnosis of paroxysmal suptraventricular tachycardia to compare the effectiveness of three active agents with placebo. The drugs were administered in random sequence for two-week periods with three-day washout intervals and in standard dose regimes as recommended for prophylaxis by authoritative works on the subject. The results suggest that digoxin is ineffective at the recommended dosage. Procaineamide was effective in controlling some arrhythmias, but disopyramide was the most effective agent studied. All these patients showed a mixture of arrhythmias, and also had a lot of ectopic activity. Arrhythmic activity is erratic and unpredictable, and a larger number of patients would need to be studied for long periods of time to obtain enough data for valid statistical assessment.

A critically ill infant with paroxysmal supraventricular tachycardia and hydrops fetalis responded well to aggressive management. Care must be taken to avoid digitalis toxicity. Procaine amide or quinidine are effective alternate therapies.

Patient-controlled rapid atrial pacing was used to manage 12 cases of recurrent supraventricular tachycardia refractory to drug therapy. The pacing system consists of an implanted receiver-lead system and an external patient-activated transmitter. In each case, brief periods (5 to 20 seconds) of rapid atrial pacing were effective in terminating the supraventricular tachycardia and resulted in a return to normal sinus rhythm. In three patients, occasional transient episodes of atrial flutter or atrial fibrillation preceded a spontaneous return to normal sinus rhythm. The pacing system was removed in one patient 13 months postoperatively because of persistent pericarditis; one patient died of an unrelated cerebral hemorrhage 13 months postoperatively. Successful management of supraventricular tachycardia has been maintained in the 10 remaining patients for 15 to 36 months (average 26.4). In more than 6,000 patient applications of rapid atrial pacing, there has been only one failure to convert the tachycardia. Successful application of permanent rapid atrial pacing requires (1) prescreening of patients with temporary external rapid atrial pacing to verify susceptibility to conversion of supraventricular tachycardia and absence of anomalous conduction pathways that may permit conduction of rapid pacing rates to the ventricles, and (2) assessment of the patient's ability to use the transmitter properly.

A comparison of the effects of several antiarrhythmic agents was made in a study of 70 patients - 15 with manifest Wolff-Parkinson-White (WPW) syndrome, 17 with concealed WPW syndrome, 18 with AV nodal re-entrant tachycardia, 14 with paroxysmal atrial fibrillation and 6 with paroxysmal atrial flutter - employing intracardiac stimulation and esophageal pacing. For the termination of paroxysmal supraventricular tachycardia, intravenous administration of verapamil or aprindine was more effective than that of disopyramide or procainamide. In AV nodal re-entrant tachycardia, verapamil was the most effective for termination. In the manifest WPW syndrome, disopyramide or aprindine was indicated especially for patients with the accessory pathways of the short antegrade refractory period, because these drugs lengthened the refractory period of the accessory pathways. For the purpose of converting atrial fibrillation or flutter to the sinus rhythm, type IA drugs such as disopyramide were indicated. However, verapamil was effective for slowing down the ventricular rate in atrial fibrillation or flutter except in cases of manifest WPW syndrome. A 6-month follow-up study showed that oral administration of verapamil was also useful for putting a stop to the attacks in 24 out of 32 patients with paroxysmal supraventricular tachycardia, while oral disopyramide prevented the recurrence of atrial fibrillation in only 4 of 10 patients.

A patient who had disabling supraventricular tachycardia showed electrophysiologic evidence of coexistent right and left Kent bundles. The supraventricular tachycardia was accelerated by sequential antegrade and retrograde conduction over the right and left Kent bundles, respectively. Spontaneous blocking of the conduction through the right Kent bundle was associated with a slowing of the tachycardia and with the appearance of right bundle branch block (RBBB). Antegrade conduction was through the left bundle branch and was followed by an early retrograde atrial activation through the left Kent bundle, with consequent shortening of the ventriculoatrial (VA) interval. Thus, the coexistence of bilateral Kent bundles can be suspected whenever shortening of the VA interval in external electrocardiographic recordings occurs in the presence of a tachycardia with a RBBB pattern in a patient with right-sided preexcitation. Our data also showed that bilateral accessory pathways may have different electrophysiologic properties and that unequal response to antiarrhythmic drugs may be expected.