Atrioventricular Junctional Reentrant Research Articles

Cardiac memory, a surface electrocardiographic clue in the differential diagnosis of ongoing narrow complex tachycardia

T changes are often encountered when normal QRS complexes resume in patients with an abnormal ventricular activation, such as intermittent left bundle branch block, cardiac pacing, wide complex tachycardia, or Wolff-Parkinson-White syndrome. This phenomenon is called “cardiac memory,” and it may be due to changes in the expression of specific potassium channels (e.g., transient outward current [Ito]) in the subepicardial myocardium. Additional channels are also likely to be involved. Directional discordance of the T wave from the R wave may persist for days, weeks, or months after the restoration of a normal QRS pattern. Cardiac memory should be evident during orthodromic atrioventricular tachycardia (AVT), which is associated with the restoration of normal ventricular activation in a previously excited ventricle. Differentiation of AVT from atrioventricular junctional reentrant tachycardia (AVJRT) during narrow complex tachycardia with a short RP interval is often difficult. The objective of this study was to assess whether the presence or absence of directional RT discordance due to cardiac memory might facilitate the surface electrocardiographic differentiation of ongoing AVT from AVJRT.

Electrophysiological characteristics during slow pathway ablation of posterior atrioventricular junctional reentrant tachycardia.

The purpose of this study was to compare the electrophysiological characteristics of posterior and anterior atrioventricular junctional reentrant tachycardia (AVJRT) during radiofrequency (RF) catheter ablation of a slow pathway. Twenty-four patients with common AVJRT, including 4 posterior (P) and 20 anterior AVJRT (A) were studied. We analyzed the retrograde atrial activation sequence of junctional rhythm and the presence of transient HA block during slow pathway ablation. When HA block developed, the AH interval before ablation and immediately after the end of energy delivery was measured. Successful ablation sites were divided into three groups; high (H), middle (M), and low (L) from the His bundle to the floor of the coronary sinus orifice. The results were: (1) the number of successful ablation sites were H 0, M 1, L 3 in P and H 1, M 8, L 11 in A; (2) the HA interval during AVJRT in P was longer than that in A (109 +/- 48 ms vs 43 +/- 6 ms, P < 0.01); (3) the retrograde atrial activation sequence during junctional rhythm was strictly concordant with that during AVJRT in both groups, but HA block developed during slow pathway ablation more often in P than in A (100% vs 30%, P < 0.01); and (4) The AH interval did not lengthen after HA block developed in P. These data suggest that another pathway does exist from the AV node to the atrium in addition to anterograde fast pathway and slow pathway, and that this pathway is used as the retrograde limb of P.

Analysis of electrophysiological activity in Koch's triangle relevant to ablation of the slow AV nodal pathway.

Atrioventricular junctional reentrant tachycardia (AVJRT) is the most common form of paroxysmal regular supraventricular tachycardia. In patients with disabling, drug refractory AVJRT, catheter ablation has evolved rapidly from a last-resort treatment in the form of interruption of atrioventricular (AV) conduction to selective modification of AV nodal function as an ideal treatment. This article will focus on the frequently unappreciated electrophysiological activities recordable in man in Koch's triangle during ablation of the so-called slow pathway.

Mechanisms of AV node modulation in AV node reentry tachycardia.

Atrioventricular nodal reentrant tachycardia has been recognized for many years as a very common cause of supraventricular tachycardia. First curable by surgery, this tachycardia is now successfully approached by selective radiofrequency current application to the slow pathway of the reentrant circuit. Importantly, these curative treatments brought evidence that the reentrant circuit of this arrhythmia was not confined to the compact atrioventricular (AV) node. These findings stimulate anatomists and basic and clinical electrophysiologists to fundamentally reconsider the atrioventricular junction in order to better understand the mysteries of atrioventricular junctional reentrant tachycardia, as we still do not know exactly what we are doing in AV node region procedures. This article will focus on the different hypotheses regarding the effect of selective slow AV pathway ablation in AV junctional reentrant tachycardia.

New insights on anatomical location of components of the reentrant circuit and ablation therapy for atrioventricular junctional reentrant tachycardia

The success of radiofrequency catheter ablation in the treatment of atrioventricular junctional, or atrioventricular nodal, reentrant tachycardia has rekindled interest in the electrophysiological and anatomical characteristics of the reentrant circuit. We conclude that there is no evidence that within the atrioventricular nodal area, which contains both the compact node and transitional cells, there are anatomically delineated dual or multiple pathways. Rather, the two main atrial inputs into the atrioventricular nodal area (posterior and anterior) seem to be the anatomically relevant structures for "slow" and "fast" pathways. Two other inputs (sinus septum and left atrial) may be the cause for multiple pathways in some individuals. Nonuniform anisotropic properties of the zone of transitional cells may account for slow or fast conduction in the same area, depending on directional differences of wavefronts. We prefer the term atrioventricular junctional reentrant tachycardia rather than atrioventricular nodal reentrant tachycardia because of mounting evidence that perinodal tissue is involved in the reentrant circuit. Finally, the role and origin of double extracellular electrograms is discussed. Further research is required to establish whether an anatomical or an electrogram-guided approach for catheter ablation is preferred.

Surgical procedure for the cure of atrioventricular junctional (“AV node”) reentrant tachycardia: Anatomic and electrophysiologic effects of dissection of the anterior atrionodal connections in a canine model

Objectives. This study was undertaken to examine the electrophysiologic and anatomic efects of a surgical procedure that cures the anterior (common) type of atrioventricular (AV) junciional reentrant tachycardia.Background. The procedure was designed to interrupt the reentrant circuit at the point of earliest atrial activation during AV junctional reentrant tachycardia, the anterior atrionodal connections.Methods. Atrioventricular node function and the sequence of electrical excitation of Koch's triangle were examined in 18 dogs. Excitation of Koch's triangle was mapped using a 60-channel mapping system. Surgical dissection was performed in 10 dogs and a sham procedure in 8. After 28 to 35 days, AV node function and the atrial excitation pattern were reassessed. The AV junction was examined using light microscopy.Results. Some degree of AV node damage was visible in all dogs in the dissection group, but it was minor in 40% of cases. The anterior part of the AV node was disconnected from the anterior atrionodal connections in all cases. Anterograde AV node function was mildly impaired. The median AH interval was increased (62 vs. 76 ms [interquartile ranges 48 to 72 and 64 to 104, respectively], P = 0.05), and the AV Wenckebach cycle length was increased (210 vs. 245 ms [interquartile ranges 200 to 230 and 210 to 260, respectively], p = 0.02). The degree of impairment of conduction was directly proportional to the length of dissection (p < 0.05) but not to the degree of damage to the AV node. Ventriculoatrial (VA) conduction was destroyed in 50% of dogs undergoing dissection but in none of those with a sham operation (p < 0.04). The AV node remained responsive to autonomic blocking drugs, and atrial mapping during ventricular pacing revealed that the site of exit from the AV node had been altered.Conclusions. The atrionodal connections closest to the His bundle are the preferred route of conduction through the AV node during normal AV or VA conduction. Destruction of these connections modifies AV node conduction. The surgical procedure selectively interrupts these connections, and this interruption is likely to be the mechanism of cure.

Posterior (“atypical”) atrioventricular junctional reentrant tachycardia

The aim of this study was to characterize a relatively rare type of atrioventricular (AV) junctional reentrant tachycardia (AVJRT). Posterior AVJRT is a type of AV nodal tachycardia in which the site of earliest atrial activation is posterior to the AV node near the coronary sinus orifice. The mechanism of this tachycardia is not well understood. The characteristics of posterior AVJRT (n = 15) were compared with those of anterior (“common”) AVJRT (n =146) and supraventricular tachycardia using single posterior septal accessory pathways (n = 13). During posterior AVJRT, the AH interval was longer than the, retrograde conduction time (His to earliest atrial activity) in 11 cases (73%), indicating that these tachycardias were not fast-slow types of AVJRT. The mean ventriculoatrial (VA) interval in posterior AVJRT (93 ± 41 ms) was longer than in anterior AVJRT (11 ± 20 ms; p <0.005), but was similar to that in tachycardias using accessory pathways (106 ± 16 ms; p = NS). The site of earliest atrial activation during posterior AVJRT was similar to that in tachycardias using accessory pathways. In all cases of accessory pathway-friediated tachycardia, atrial activation could be advanced by ventricular extrastimuli delivered coincident with the His deflection, but atrial activation was not advanced in any case of posterior AVJRT unless the extrastimulus was delivered >80 ms before the His deflection. Anterograde conduction was similar in the posted or and anterior AVJRT groups. During ventricular pacing, the VA interval was longer in patients with posterior AVJRT (287 ± 113 ms) than in those with anterior AVJRT (199 ± 48 ms; p <0.005) or accessory pathways (133 ± 43 ms; p <0.005), and closely coupled ventricular extrastimuli caused greater increases in the VA interval (172 ± 114 vs 102 ± 31 and 60 ± 60 ms, respectively; both p <0.01). In 73% of cases, posterior AVJRT used a slow pathway for anterograde conduction and a different “slow” pathway for retrograde conduction, and thus was not an antidromic form of “common” AV nodal reentry. The retrograde limb of the circuit did not have the characteristics of an accessory pathway.

High resolution mapping of Koch's triangle using sixty electrodes in humans with atrioventricular junctional (AV nodal) reentrant tachycardia.

Recent evidence suggests that atrioventricular junctional reentrant tachycardia (AVJRT) uses a reentrant circuit that involves the atrioventricular (AV) node, the atrionodal connections, and perinodal atrial tissue. Electrogram morphology has been used to target the delivery of radiofrequency energy to the site of the "slow pathway," a component of this reentrant circuit. The aim of this study was to localize precisely the sites of atrionodal connections involved in AVJRT and to examine atrial electrogram morphologies and their spatial distribution over Koch's triangle. Electrical activation of Koch's triangle and the proximal coronary sinus was examined in 13 patients using a 60-point plaque electrode and computerized mapping system. Recordings were made during sinus rhythm (n = 12), left atrial pacing (n = 8), ventricular pacing (n = 12), and AVJRT (n = 12). During sinus rhythm electrical activation approached Koch's triangle and the AV node from the direction of the anterior limbus, activating the anterior part of the triangle before the posterior part. A zone of slow conduction during sinus rhythm was found within Koch's triangle in 64% of patients. The pattern of atrial activation in Koch's triangle during anterograde fast pathway conduction was similar to that seen during anterograde slow pathway conduction. Retrograde fast pathway conduction during ventricular pacing and during anterior (typical) AVJRT caused earliest atrial activation at the apex of Koch's triangle near the AV node-His bundle junction. In individual patients the site of earliest atrial activation was similar for both anterior AVJRT and retrograde fast pathway conduction during ventricular pacing. Retrograde slow pathway conduction during ventricular pacing and during posterior (uncommon or atypical) AVJRT caused earliest atrial activation posterior to the AV node near the orifice of the coronary sinus. This posterior or "slow pathway" exit site was 15 +/- 4 mm from the His bundle. In individual patients the site of earliest atrial activation was similar for both posterior AVJRT and retrograde slow pathway conduction during ventricular pacing. In one patient anterograde and retrograde conduction occurred via separate slow pathways during AVJRT: Complex atrial electrograms with two or more components were observed near the coronary sinus orifice and in the posterior part of Koch's triangle in all cases. These were categorized as either low or high frequency potentials according to the rapidity of the second component of the electrogram. Low frequency potentials were present at the site of earliest atrial excitation during retrograde slow pathway conduction in 5 of 5 cases (100%) and high frequency potentials in 4 of 5 cases (80%). However, both slow and high frequency potentials could be found at sites up to 16 mm from the site of earliest atrial excitation. At least two distinct groups of atrionodal connections exist. The site of earliest atrial activation during anterior AVJRT is similar to that of fast pathway conduction during ventricular pacing. This site is close to the His bundle-AV node junction. The site of earliest atrial activation during posterior AVJRT is similar to that of slow pathway conduction during ventricular pacing. This site is near the coronary sinus orifice, approximately 15 mm from the His bundle. The anterograde slow pathway appears to be different from the retrograde slow pathway in some patients. Double atrial electrograms are an imprecise guide to the site of earliest atrial excitation during retrograde slow pathway conduction.

Atrioventricular junctional and orthodromic atrioventricular reentrant tachycardia in Wolff-Parkinson-White syndrome

The existence of two or more types of reentrant tachycardias in the same patient with Wolff-Parkinson-White syndrome has been emphasized, and the occurrence of orthodromic atrioventricular (AV) reentrant tachycardia and AV junctional reentrant tachycardia have been well documented. This report describes a patient with Wolff-Parkinson-White syndrome in whom the phenomena of spontaneous transition from AV reentry to AV junctional reentry and adenosine-induced conversion from AV junctional reentry to AV reentry were observed.

Physiology of "atypical" atrioventricular junctional reentrant tachycardia occurring following radiofrequency catheter modification of the atrioventricular node.

The physiology of atypical atrioventricular junctional reentrant tachycardia (AVJRT) occurring following catheter modification of the AV node is poorly defined. Six patients undergoing radiofrequency current catheter modification of the AV node had inducible atypical AVJRT before or after AV nodal modification. Typical AVJRT was differentiated from atypical AVJRT by a ventriculoatrial (VA) time < 60 msec in the His-bundle electrogram recording. Five of six patients had typical AVJRT and two had atypical AVJRT prior to AV nodal modification. Following anterior approach AV nodal modification, previously undetected atypical AVJRT was induced in four patients. Earliest retrograde atrial activation in the posterior septum was documented in all patients with atypical AVJRT prior to modification and in three of four patients with atypical AVJRT following modification. The AH intervals during tachycardia were 320 +/- 52 msec in typical AVJRT, 88 +/- 33 msec in the premodification atypical AVJRTs, and 172 +/- 12 msec in the postmodification atypical AVJRTs (P = 0.0001). The AH/HA ratios were 4.1 +/- 0.9 in typical AVJRT, 0.5 +/- 0.2 in the premodification atypical AVJRTs, and 0.9 +/- 0.2 in the postmodification atypical AVJRTs (P = 0.0001). Two patients with postmodification atypical AVJRT underwent further posterior approach AV node modification that resulted in VA block. One patient with postmodification atypical AVJRT had further anterior approach AV nodal modification that resulted in heart block. The retrograde limb of the atypical AVJRT seen following anterior approach AV nodal modification is a posterior, slow pathway.

Clinical experience with surgery for paroxysmal supraventricular tachycardia: a report of 103 cases

One-hundred-and-three patients underwent surgery for paroxysmal supraventricular tachycardia (PSVT). In eighty-three patients (81%), PSVT was due to an accessory atrioventricular pathway (Group I) and in 20 (19%) to Atrioventricular Junctional (AV nodal) Reentrant Tachycardia (AVJRT:Group II). Initial surgery successfully divided 77 of 83 accessory pathways, including 58 of 60 left free wall pathways, 12 of 15 posteroseptal pathways, six of seven right free wall pathways and one anteroseptal pathway. Twenty patients had successful surgery for AVJRT. Surgery was performed with low morbidity and no early or late mortality in either group. One patient in each group required permanent pacemaker implantation. Immediate (within one week) postoperative electrophysiological study using epicardial wires was performed in 96% of patients and repeat electrophysiological study six months later was possible in 65/103 (63%) patients. Patients with surgery for accessory pathways were followed-up for a mean 34 +/- 23 months, while those with surgery for AVJRT for a mean of 13 +/- seven months. No patient with successful surgery has had a clinical recurrence of PSVT. Thus the results indicate that surgery is a safe and curative therapy for patients with PSVT.

Persistent inappropriate sinus tachycardia after radiofrequency current catheter modification of the atrioventricular node

Atrioventricular (AV) junctional reentrant tachycardia (JRT) is the most frequent cause of paroxysmal supraventricular tachycardia. 1 Recently, radiofrequency current delivered through a transvenous catheter was used to modify AV nodal properties so that AVJRT is no longer inducible while preserving normal AV nodal conduction. 2–4 This technique has produced high success rates with relatively few complications. In this report, we present a previously unreported complication observed in 3 patients undergoing AV node modification using radiofrequency current: persistent, inappropriate and symptomatic sinus tachycardia.

Patients with two types of atrioventricular junctional (AV nodal) reentrant tachycardia. Evidence that a common pathway of nodal tissue is not present above the reentrant circuit.

The site of the reentrant circuit in atrioventricular (AV) junctional reentrant tachycardia has not been defined; in particular, the existence of a common pathway of AV nodal tissue above the reentrant circuit is controversial. Two types of AV junctional reentrant tachycardia were induced in each of three patients at electrophysiological study. In one type of tachycardia (anterior), the onset of atrial activity occurred from 0 to 12 msec before the onset of ventricular activation, and earliest atrial activity was recorded near the His bundle. In the second type of tachycardia (posterior), the ventriculoatrial intervals were longer (76-168 msec), and earliest atrial activity was recorded near the mouth of the coronary sinus. In individual patients, the two types of tachycardia had different cycle lengths. Posterior AV junctional reentrant tachycardia was not a fast-slow form of AV junctional reentry in at least two of the three patients. Surgical cure was attempted in two patients. In one patient, anterior AV junctional reentrant tachycardia was abolished by dissection of the anterior perinodal atrium, but posterior AV junctional reentrant tachycardia could still be induced. At reoperation 4 months later, dissection of the posterior perinodal atrium abolished posterior AV junctional reentrant tachycardia while preserving AV conduction. Differences in ventriculoatrial intervals and cycle lengths and the results of selective surgery suggest that the two types of AV junctional reentrant tachycardia used different reentrant circuits. These observations imply that a common pathway of AV nodal tissue is not present above the reentrant circuit and suggest that perinodal atrium is part of these circuits.

What is the best method for assessing the long-term outcome of surgery for accessory pathways and atrioventricular junctional reentrant tachycardias?

The success of surgery for supraventricular tachycardia (SVT) is evaluated by a variety of methods in different hospitals. Unfortunately, the predictive values of these methods are not known. We therefore compared the various methods in 261 patients undergoing surgery for SVT at Westmead Hospital since 1981. Surgical outcome was assessed by early tests during the first week after surgery (serial 12-lead electrocardiograms, telemetric monitoring of the electrocardiogram, and electrophysiological study performed using epicardial wires); later tests at 6 months after surgery (12-lead electrocardiograms and electrophysiological study); and symptomatic review done by telephone interview at a median of 34 months after surgery. Early tests were obtained in 97%, later tests were obtained in 76%, and symptomatic review was obtained in 98% of patients. All of the examined tests were inaccurate methods of surgical assessment compared with the late electrophysiological study. A large proportion of the patients proven to be surgical failures at the late electrophysiological study were not detected by early tests (83%), by later electrocardiograms (66%), or by symptomatic assessment (41%). Accurate assessment of surgical outcome requires a late electrophysiological study to permit comparison of surgical techniques. Late electrophysiological study also provides accurate information on the current risks and benefits of proposed surgery for communication to patients to enable them to make an informed decision on future treatment. Most patients are willing to have a late electrophysiological study and usually benefit from clarification of their true surgical outcome.

Transvenous Ablation with High Frequency Energy for Atrioventricular Junctional (AV Nodal) Reentrant Tachycardia

We performed transcatheter AV junction ablation with high frequency energy in four patients with AV nodal reentrant tachycardia where extensive trials of several antiarrhythmic drugs failed to prevent further recurrences of tachycardia. Initially high frequency catheter ablation induced complete AV block in all patients. A recuperation of AV 1:1 conduction followed some time later, persisting in follow-up. No complications have been encountered in either the acute phase or the follow-up (from 6 to 8 months; mean +/- SD: 8.7 +/- 2.5 months). The electrophysiological study was carried out 6 weeks following ablation, and all patients showed AV 1:1 conduction. No dual nodal pathway was encountered and no tachycardia could be triggered. With refinement of the method, the potential application of high frequency energy to interrupt intranodal or perinodal connections responsible for reentrant supraventricular tachycardia or to retard AV nodal conduction appears promising.

Modulation of conduction and refractoriness in atrioventricular junctional reentrant circuit. Effect on reentry initiated by atrial extrastimulus.

The importance of activation sequence of an atrioventricular junctional reentrant (AVJRe) circuit, before delivery of an extrastimulus, has received little attention in studies concerned with clinical tachycardias. In this study a change in activation sequence was accomplished using bidirectional activation (V-A sequential pacing) during the basic drive (V1A1-V1A1). It was noted that, compared with an atrial extrastimulus (A2) after an atrial drive (A1-A1), earlier activation (by V1 impulse of the V1A1-V1A1 drive) consistently improved conduction, or decreased refractoriness, or both, in the anterograde as well as the retrograde pathway of the AVJRe circuit. In all patients, five with AV nodal reentry and six with Wolff-Parkinson-White syndrome, reentrant tachycardia could be prevented during V-A sequential pacing. In four of eleven patients, reentry was prevented despite achieving the so-called critical atrioventricular nodal delays that had previously caused reentry during control study. This finding suggested that conduction delay necessary for reentry was related to the site of block, which in turn was affected by V-A sequential pacing. We concluded that changing the activation sequence during basic drive modulates conduction and refractoriness in AVJRe circuits, and allows the study of a wide range of electrophysical factors that prevent or permit reentry.

Surgical therapy for supraventricular tachycardia, a potentially curable disorder

One hundred fifty-six patients underwent investigation and operation for supraventricular tachycardia: 145 had attempts at curative operations and 11 had His bundle section. Operative mortality was 0.68% and there were no late deaths among patients having curative operations. One patient died suddenly 1 year after His bundle section. All patients underwent electrophysiologic study before discharge and 6 months postoperatively. A satisfactory result, without supraventricular tachycardia and without medication, was achieved in 96.5% of all patients. Ninety-three percent have no supraventricular tachycardia and no demonstrable reentrant pathway at electrophysiologic study. All free wall accessory atrioventricular connections were divided and 97.7% of the patients were cured. Ninety percent of patients with posterior septal accessory atrioventricular connections had a satisfactory result, with cure demonstrated at late electrophysiologic study in 84%. Fifteen patients with atrioventricular junctional reentrant tachycardia were all cured, with preservation of normal atrioventricular conduction. Eight (88%) of nine patients with right atrial tachycardia were cured, and two patients with nodoventricular fibers and one patient with incessant atrioventricular junctional tachycardia had satisfactory results. Supraventricular tachycardia is now a potentially curable disorder when managed by low risk surgical procedures that offer a high cure rate.

Curative surgery for atrioventricular junctional (“AV Nodal”) reentrant tachycardia

A new surgical approach was studied prospectively in 10 consecutive patients with atrioventricular (AV) junctional reentrant tachycardia. The aim was to abolish tachycardia yet preserve normal AV conduction. On the basis of electrophysiologic study before operation, patients were classified as type A (ventriculoatrial [VA] intervals during tachycardia less than or equal to 40 ms) (seven patients) or type B (VA intervals greater than 40 ms) (three patients). Dual AV junctional pathways were demonstrable with single extrastimulus testing in seven patients before operation. Endocardial mapping during tachycardia at surgery revealed earliest atrial activation anteromedial to the AV node in type A patients and posterior to the node in the type B patients. The perinodal atrium in the region of earliest atrial activation during tachycardia was carefully disconnected from the AV node. After operation, AV junctional reentrant tachycardia was not inducible at comprehensive electrophysiologic study in any patient, and no clinical recurrences have occurred during a follow-up period of 2 to 14 months (mean 8 +/- 4). Normal AV conduction was preserved in all cases. Anterograde slow AV junctional pathway conduction was abolished in five of seven cases. Retrograde His to atrium conduction time was prolonged in type A patients but the capacity for retrograde VA conduction remained excellent. Retrograde His to atrium conduction was interrupted or severely compromised in the type B patients. These data show that there are at least two types of AV junctional reentry. Perinodal atrium appears to be part of the reentrant circuit in human AV junctional reentry. Although the most consistent effect of surgery was on the retrograde limb of the circuit, anterograde slow pathway conduction was also modified. AV junctional reentry is surgically curable with a high success rate.

Antegrade and retrograde conduction characteristics in three patterns of paroxysmal atrioventricular junctional reentrant tachycardia

In 20 patients with PSVT without ventricular pre-excitation, the site of reentry and functional characteristics of Ant. and Ret. pathways were studied. Three distinct patterns of PSVT were observed. In 13 patients (group I) in whom A-V node was the site of reentry, the interval between the Ant. H bundle deflection and the following atrial echo response (H-Ae) measured 30 to 85 msec. and the Ae was partially or completely obscured by ventricular electrogram. The ratio between the H-Ae and the subsequent Ae-H interval ranged 1:3.1–17.3. In a majority of Group I patients (eight out of 13) the Ret. conduction was better than Ant. conduction, as the VACS sustained a 1:1 response at faster paced rates than AVCS. The FRP of the AVCS in Group I was determined by the A-V node in all patients and significantly exceeded the FRP of the VACS; the latter was determined by the HPS in 12 out of 13 patients. In four patients (Group II) a V-A AP silent antegradely was operative during PSVT. The H-Ae in Group II valued 145 to 200 msec. and the Ae clearly followed the ventricular electrogram, the H-Ae: Ae-H being 1:0.5–1.7. The V-A conduction in all Group II patients was better than the A-V conduction. A-V node determined the FRP of the AVCS, whereas AP determined the FRP of the VACS in Group II patients, and the former significantly exceeded the latter. Good correlation existed between PSVT, Ant. and Ret. conduction patterns in Group I and Group II patients. In three patients (Group III) the H-Ae measured 270 to 470 msec. with an H-Ae:Ae-H of 1:0.2–0.4, a relationship quite the opposite of Group I patients. No definite relationship existed between PSVT, Ant. and Ret. conduction patterns in Group III patients. The data in Group III patients were compatible with (1) A-V nodal reentry with reversal of conduction balance compared to Group I, (2) intra-atrial reentry, and (3) enhanced atrail automaticity. It is concluded (1) the site of reentry in patients with PSVT is variable, (2) a fair estimation of reentry site can be made from H-Ae and Ae-H relationship, (3) all patients with PSVT have intact V-A conduction and in most the V-A conduction is better than A-V conduction, and (4) in the majority of patients with PSVT refractoriness of the AVCS exceeds that of the VACS.