The occurrence of ventricular premature depolarizations in survivors of myocardial infarction is a risk factor for subsequent sudden death, but whether antiarrhythmic therapy reduces the risk is not known. The Cardiac Arrhythmia Suppression Trial (CAST) is evaluating the effect of antiarrhythmic therapy (encainide, flecainide, or moricizine) in patients with asymptomatic or mildly symptomatic ventricular arrhythmia (six or more ventricular premature beats per hour) after myocardial infarction. As of March 30, 1989, 2309 patients had been recruited for the initial drug-titration phase of the study: 1727 (75 percent) had initial suppression of their arrhythmia (as assessed by Holter recording) through the use of one of the three study drugs and had been randomly assigned to receive active drug or placebo. During an average of 10 months of follow-up, the patients treated with active drug had a higher rate of death from arrhythmia than the patients assigned to placebo. Encainide and flecainide accounted for the excess of deaths from arrhythmia and nonfatal cardiac arrests (33 of 730 patients taking encainide or flecainide [4.5 percent]; 9 of 725 taking placebo [1.2 percent]; relative risk, 3.6; 95 percent confidence interval, 1.7 to 8.5). They also accounted for the higher total mortality (56 of 730 [7.7 percent] and 22 of 725 [3.0 percent], respectively; relative risk, 2.5; 95 percent confidence interval, 1.6 to 4.5). Because of these results, the part of the trial involving encainide and flecainide has been discontinued. We conclude that neither encainide nor flecainide should be used in the treatment of patients with asymptomatic or minimally symptomatic ventricular arrhythmia after myocardial infarction, even though these drugs may be effective initially in suppressing ventricular arrhythmia. Whether these results apply to other patients who might be candidates for antiarrhythmic therapy is unknown.

The nature of localized atrial activation during atrial fibrillation was characterized in 34 patients following open heart surgery. Bipolar atrial electrograms (AEG) recorded in each patient with atrial fibrillation exhibited a myriad of sizes, shapes, polarities, amplitudes, and beat-to-beat intervals. On the basis of the AEG morphology and the nature of its baseline, we have classified the recordings into four Types. Type I was characterized by discrete AEG complexes separated by an isoelectric baseline free of perturbation, Type II by discrete AEG complexes but with perturbations of the baseline between complexes, Type III by AEGs which failed to demonstrate either discrete complexes or isoelectric intervals, and Type IV in which AEGs of Type III alternated with periods characteristic of Type I and/or Type II. In 22 patients, the AEGs were recorded a second time, and in 11 of these patients the type of atrial fibrillation changed between the first and second recording period. An atrial flutter-fibrillation pattern in the ECG was associated with a relatively ordered atrial activation pattern and a relatively slow atrial rate. Human atrial fibrillation is not an electrophysiologically homogeneous process when compared among different patients or ad seriatim in the same patient.

To examine the question of why the pacing rate and duration of atrial pacing are crucial factors in the successful interruption of atrial flutter, studies were performed on 30 patients in the period following open heart surgery. In each patient the diagnosis of atrial flutter was made using a pair of wire electrodes placed on the right atrial epicardium at the time of operation and brought out through the anterior chest wall. The same electrodes were used for atrial pacing. Pacing faster than the spontaneous rate of the atrial flutter which failed to interrupt the atrial flutter was associated with transient entrainment of the atrial flutter up to the atrial pacing rate. Atrial flutter was interrupted successfully when the atria were paced at a rate which was too fast for the atrial flutter to follow. This was heralded by the conversion of previously negative flutter waves to positive atrial complexes in ECG lead II. When pacing the atria at a constant rate, 2-22 seconds with a mean of 10 seconds were required to interrupt the atrial flutter.

SUMMARY We studied transient entrainment and interruption of atrioventricular (AV) bypass pathway-type paroxysmal atrial tachycardia in 15 patients during overdrive pacing from selected atrial sites. Overdrive atrial pacing at less than a critically rapid rate for interruption transiently entrained the tachycardia. Transient entrainment was due to repeated early entrance of the wave front from the pacing impulse into the reentry loop in both antidromic and orthodromic directions. The antidromic wave front of each pacing impulse was repeatedly blocked as it collided with the orthodromic wave front of the previous beat, in effect extinguishing the tachycardia. However, the early entrance of the orthodromic wave front of each pacing impulse repeatedly reset the tachycardia. The result was that during transient entrainment, the tachycardia rate increased to the pacing rate. Interruption of the tachycardia occurred when overdrive pacing produced block within the reentry loop of both the antidromic and orthodromic wave fronts of the same pacing impulse, the block occurring either at separate sites within the reentry loop or at the same site. Atrial fusion beats were demonstrated during transient entrainment in nine patients and resulted from intraatrial collision of the antidromic wave front from the pacing impulse with the orthodromic wave front of the previous beat. The presence offusion beats depended critically on the relationship of the pacing site to the reentry loop and the duration of conduction around the reentry loop, particularly through the area of slow conduction.The data from this study suggest that (1) if one can demonstrate constant fusion beats during transient entrainment of a tachyarrhythmia except for the last transiently entrained beat; or (2) if during transient entrainment of a tachyarrhythmia at two or more different pacing rates, one can demonstrate constant fusion at each of the different pacing rates, but different degrees of fusion at the different rates; or (3) if interruption of a tachyarrhythmia by overdrive pacing is associated with localized conduction block to a site followed by activation of that site by the next pacing impulse from a different direction and with a shorter conduction time, then the underlying mechanism of the arrhythmia can be best explained by reentry.PAROXYSMAL atrial tachycardia that involves antegrade conduction from the atria through the atrioventricular (AV) node-His-Purkinje system to the ventricles with retrograde conduction from the ventricles via an AV bypass pathway back to the atria is the best understood example of putative reentrant rhythms.1AThis arrhythmia is often found in patients with the Wolff-Parkinson-White syndrome and in patients with a so-called concealed AV bypass pathway, i.e., one that conducts only in the retrograde direction. The many types of treatment for this arrhythmia include its interruption by overdrive cardiac pacing.' We have found that overdrive pacing used to interrupt paroxysmal atrial tachycardia of this variety has much in ...

SUMMARY Studies were performed using bipolar atrial wire electrodes to record atrial electrograms and to pace the atria in 27 patients who developed atrial flutter after open heart surgery. Two types of atrial flutter, classic or type I atrial flutter, and type II atrial flutter, were identified. Both types of atrial flutter were characterized by uniformity of the beat-to-beat atrial cycle length, morphology, polarity, and amplitude of the recorded bipolar atrial electrogram. Both types sometimes manifested a beat-to-beat electrical alternans, which in turn was sometimes associated with an alternans in beat-to-beat cycle length. ATRIAL FLUTTER is a supraventricular arrhythmia which has long been recognized in man,' although its underlying mechanism has not been explained. Based on the ECG, it has been characterized as a regular, rapid atrial rhythm, most often with an atrial rate close to 300 beats/min, with the upper and lower limits of its range uncertain and variously stated.2-8 At our institution, at the time of open heart surgery, bipolar wire electrodes are routinely placed on the right atrial epicardium for possible diagnostic or therapeutic use in the immediate postoperative period.9-12 Since many patients develop atrial flutter spontaneously during this latter period, this was an opportunity to use these electrodes to characterize and define this rhythm better while providing patient care. Methods Twenty-seven patients who developed atrial flutter in the immediate period after open heart surgery were studied. The atrial flutter was identified initially from a standard or monitored ECG, or from bipolar atrial electrograms recorded from a pair of atrial wire electrodes placed routinely 0.5-1.0 cm apart on the epicardial surface of the superior portion of the right atrium.9 12 The atrial electrograms were used to distinguish atrial flutter from atrial fibrillation when this differentiation was not clear from the ECG recording alone.'2 After identifying atrial flutter, bipolar atrial electrograms were recorded simultaneously with ECG leads II and IIII for as long as 15 minutes with an Electronics for Medicine Model DR-12 switched beam oscilloscopic recorder. In one patient, the recordings were made using a Medical Systems Corporation Model DU-35 three-channel ECG machine and in two patients using a Hewlett-Packard Model 1151B ECG machine. Then, the atria were paced rapidly at rates up to 600 beats/min in an attempt to interrupt the atrial flutter.10 11 All data were recorded on magnetic FM tape (Honeywell Model 5600) for later playback and analysis, except in three patients. In the 24 patients in whom recordings were made using the Electronics for Medicine DR-12 machine, allECGs and atrial electrograms were recorded between a bandpass of 0