SUMMARYElectrophysiologic characteristics of five patients with Ebstein's anomaly of the tricuspid valve were defined with studies using luminal intracardiac electrode catheters. The diagnosis was made in each case from clinical data and confirmed at.cardiac catheterization by the presence of an atrialized right ventricular chamber with atrial mechanical activity and ventricular electrical activity. In three cases intra-right atrial conduction was prolonged (P-A intervals of 50, 50,

SUMMARYStudies have shown that in patients with paroxysmal supraventricular tachycardia (SVT), spontaneous or stimulated atrial premature depolarizations (APD) falling within a specific portion of the relative refractory period of the atrioventricular (A-V) conduction system initiate SVT. The present study was designed to determine whether the A-V nodal conduction delay these APDs exhibit, or their coupling interval, is essential for the initiation of SVT. Multiple episodes of SVT were initiated and terminated by single APDs in four patients with a history of paroxysmal SVT. The atria were then paced at numerous fixed rates in excess of the spontaneous sinus rate. In each patient, at atrial rates where progressive A-V nodal conduction delay occurred from beat to beat (Wenckebach cycles), a specific degree of A-V nodal conduction delay always resulted in atrial reentry or SVT. Although the atrial coupling interval was considerably longer during Wenckebach cycles initiating SVT than for single APDs resulting in the arrhythmia, the prolongation of A-V nodal conduction was identical. Independent of atrial coupling interval, a requisite degree of A-V nodal conduction delay always resulted in atrial echoes or SVT. This supports the conclusion that SVT results from atrial reentry via the A-V node. Circulation, Volume XLIII, May 1971 the Wolff-Parkinson-White syndrome, SVT was demonstrated to result from spontaneous or stimulated atrial premature depolarizations (APD) which occur during a specific portion of the atrial cycle-the "echo" zone.'3 Atrial reentry via the A-V node was demonstrated to be the mechanism initiating and sustaining SVT in these patients.'4The present study was undertaken to determine the essential condition by which any atrial beat results in atrial reentry or SVT. The prolonged A-V nodal conduction of atrial depolarizations resulting in atrial reentry and SVT, could be analyzed apart from their coupling interval by atrial pacing at rates sufficient to produce A-V nodal Wenckebach cycles. In our patients, sufficient prolongation of A-V nodal conduction resulted in SVT independent of the atrial coupling interval.

The circulatory effects of supraventricular tachycardia (SVT) were studied in eight patients who reported disabling symptoms during paroxysms of the arrhythmia. Supraventricular tachycardia was induced in each patient by rapid atrial pacing or with atrial premature stimuli. Hemodynamic parameters in sinus rhythm and following the initiation of SVT were recorded and compared. The following mean values were observed in sinus rhythm (SR) and SVT. Heart rate (beats/min): SR 79, SVT 183; P-R interval (msec): during SR, 154; during SVT, 256; ratio of mean P-R intervals to mean R-R cycl lengths: SR 20%, SVT 76%; brachial artery pressures (mmHg): SR 141, SVT 99; cardiac index (L/min/m2): SR 3.6, SVT 2.2; pulmonary artery pressures (mmHg): SR 18/7, SVT 26/15; peak right atrial pressures (mm Hg): SR 4, SVT 17. Large waves appeared in the right atrium during SVT due to atrial contraction against closed tricuspid valves. Pulsus alternans were observed in each case during SVT. Despite the presence of chest pain during SVT, the coronary arteries were normally patent in four patients who underwent coronary arteriography.

In six successive patients, none of whom had the Wolf-Parkinson-White syndrome, recurrent episodes of paroxysmal supraventricular tachycardia (SVT) were analyzed to determine the mechanism by which this arrhythmia is initiated and sustained. In each patient, simultaneous intracavitary atrial electrograms and surface electrocardiograms were recorded during the onset of numerous spontaneous episodes of SVT. Atrial premature depolarizations (APD) produced by programmed stimulation sequences were used to measure atrioventricular refractory periods and to produce atrial echoes and episodes of SVT. Stimulated APDs introduced during sustained episodes of SVT either altered its behavior or terminated it. The electrophysiologic behavior of SVT in these patients strongly suggests that the mechanism responsible for paroxysmal supraventricular tachycardia is atrial reentry utilizing the A-V conducting system.

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An in vitro preparation of rabbit right atrium, including the A-V node (AVN) and bundle of His, was utilized to evaluate the mechanism of paroxysmal supraventricular tachycardia (SVT). Microelectrode recordings from atrium and AVN were obtained. During sinus rhythm the atrial cycle was explored with atrial premature depolarizations (APD). Fifty episodes of an arrhythmia with characteristics identical to SVT in man were produced in six of 40 rabbits. In vitro, SVT: (1) was initiated by a single APD showing prolonged conduction in the AVN; (2) had initial cycles similar to atrial echoes; (3) in most instances showed 1:1 A-V conduction; (4) lasted 20 to 500 cycles; and (5) could be ended by a single APD which penetrated the AVN. Reentry in the upper AVN was established by the recording of action potentials from nodal cells which showed marked electrotonic "humps" during repolarization. SVT and atrial echoes could not be produced after damaging or sectioning the upper AVN. An in vitro model of SVT supports the hypothesis that this arrhythmia results from reentry within the AVN.

His bundle recordings during spontaneous and induced episodes of paroxysmal supraventricular tachycardia (SVT) demonstrated that the site of reentry responsible for this arrhythmia was in the A-V node. In five patients studied, A-V conduction time and refractory periods were normal, but atrial premature depolarizations (APD) within a portion of the relative refractory period of the A-V node consistently produced atrial reentry-echoes or sustained SVT. In two patients, APDs falling within the A-V effective refractory period failed to excite the His bundle but still reentered within the A-V node and began SVT. It was noted that the various relationships between atrial and ventricular depolarizations on the surface ECG did not reflect different mechanisms for SVT, but only variations in A-V nodal conduction time.Additional Indexing Words: Paroxysmal atrial tachycardia His bundle depolarization Reciprocal tachycardia A-V refractory period A-V nodal tachycardia Atrial reentry Atrial echoes A-V conduction T HERE IS A long-standing controversy as to whether the mechanism of paroxysmal supraventricular tachycardia (SVT) in man is caused by an ectopic pacemaker or by reentry. Recent studies strongly suggest that the mechanism for this arrhythmia is most often reentry.l However, the site of reentry has not been demonstrated. Intraatrial reentry was postulated as early From the

Transvenous electrodes were placed in the right atrium and ventricle of 50 patients with heart disease and arrhythmias. The ventricles were paced at several rates, each in excess of the sino-atrial rate. An atrial electrogram and surface electrocardiogram were recorded simultaneously in each patient; utilizing strict criteria, the incidence with which 1:1 ventriculo-atrial conduction (VAC) could be elicited in these patients was assessed. These patients were divided into two groups-26 patients with normal A-V conduction comprised group 1, and 24 patients with prolonged A-V conduction, group 2. VAC was demonstrated in 89% of group 1 patients but in only 8% of the group 2 patients. The difference in the incidence of 1:1 VAC between the two groups was statistically significant (P < 0.01). The presence or absence of 1:1 VAC could not be related to type of heart disease, medication, presence of acute myocardial infarction, or presence of intraventricular conduction defect.Altering the paced ventricular rate or introducing stimulated ventricular premature depolarization in group 1 patients could produce any degree of VAC impairment. During such maneuvers, ventricular reciprocal beats (ventricular echoes) and ventricular reciprocal rhythms were observed. Additional Indexing A-V block Ventricular echoesWords:Cardiac electrograms Ventricular pacing Complete heart block Reciprocal rhythm T HE bidirectional conduction capacity of the A-V conduction system has been demonstrated in many classes of animals.1-5 Using specialized technics for P-wave recognition, V-A conduction has occasionally been demonstrated in patients with spontaneous ventricular premature contractions,6 spon-taneous7 and catheter-induced ventricular tachycardia,8'9 complete A-V block during ventricular pacing,'0-12 normal A-V conduction, and severe sinus bradycardia, when ventricular pacing was employed.13