Junctional Reentrant Tachycardia Research Articles

Overdrive atrial stimulation during transesophageal electrophysiological study: usefulness of post-pacing VA interval analysis in differentiating supraventricular tachycardias with 1:1 atrio-ventricular relationship

We evaluated the feasibility and usefulness of overdrive atrial pacing to identify the relationship between atrial and ventricular activation in supraventricular tachycardias with a stable 1:1 atrio-ventricular (AV) conduction ratio during a transesophageal electrophysiological investigation. Overdrive atrial stimulation was performed in 42 consecutive patients (11 males and 31 females; mean age 49±17 years) during AV junctional reentrant tachycardia, orthodromic AV reentrant tachycardia and ectopic atrial tachycardia (22, 13 and seven subjects, respectively). Trains of 12 stimuli at a constant rate were introduced starting at a cycle length 10 ms shorter than the tachycardia cycle length; stimulation was repeated with a 10-ms decrement in pacing cycle length at each step until tachycardia terminated and/or second-degree AV block occurred. The difference between the VA interval duration at baseline and in the first post-pacing tachycardia beat was measured at each step and provided identification of the AV relationship. At least one post-pacing VA interval was evaluable in 90% of the cases and measured 2±4 and 1±3 ms in AV junctional and AV reentrant tachycardia groups, respectively, and 83±42 ms in the ectopic atrial tachycardia group ( P<0.0000001 ectopic atrial tachycardia group vs. others). When three or more post-pacing VA intervals were obtained during the same tachycardia, a curve was constructed by plotting their values against the corresponding pacing cycle lengths. A curve could be constructed in 36% of the cases and was flat in all patients with AV junctional and AV reentry, while it was completely irregular in the ectopic atrial tachycardia group ( P<0.003). The analysis of post-pacing VA interval behaviour in response to overdrive atrial stimulation provides a rapid and reliable differentiation between supraventricular tachycardias with 1:1 AV conduction ratio during a transesophageal electrophysiological study.

Catheter ablation in competitive athletes: indication.

Some supraventricular tachyarrhythmias (SVT), particularly if paroxysmal and/or related to Wolff-Parkinson-White syndrome (WPW), may in some cases endanger an athlete's professional career due to hemodynamic consequences during athletic activity, which in some instances may be life-threatening. One must also take into account that in Italy the law makes antiarrhythmic drug treatment (AAD) incompatible with sport eligibility. For these reasons, the utilization of radiofrequency ablation (RFA) in athletes has different indications as opposed to the normal population, since the primary goal is "the eligibility of the athlete." In our study, we discuss the criteria for indication of RFA in athletes with SVT on the basis of the data obtained from our population of athletes, studied over a 20-year period, from 1974 to the 31st of December 1993. These athletes were evaluated for arrhythmic events, utilizing a standardized cardioarrhythmological protocol: 1,325 athletes (1,125 men, 200 women, mean age 20.7 years). One subgroup included 380 athletes with WPW (28.7%), 22 athletes with aborted sudden death (1.6%), 6 of whom had WPW, 13 athletes with sudden death (0.98%), and 2 of whom had WPW. Another subgroup was formed by 116 top level elite professional athletes (TLA) (mean age 22.9 years), of which 10 of 116 (8.6%) had WPW and 12 of 116 (10.3%) had paroxysmal SVT. The most important indications for RFA in athletes are represented by: WPW asymptomatic at risk, symptomatic during athletic activity, and/or requiring AAD treatment: paroxysmal junctional reentrant tachycardia: when this condition is disabling and related to exercise and therefore compromising an athlete's performance and sports career. Paroxysmal junctional reentrant tachycardia is easily reproduced via transesophageal atrial pacing (TAP) during exercise (bicycle ergometer), common in athletes but normally the recurrences are concentrated only during the period in which the athlete is engaged in sport. Rare indications for RFA are focal or reentry, permanent SVT, and particularly junctional reentrant tachycardia. For each individual athlete, we have to consider the possible side-effects of RFA, the possible recurrences with psychobiological traumatic consequences, the effective recovery period, and the natural history of the tachyarrhythmias, which frequently disappear after interruption of the sports career.

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.

Origin and significance of double potentials near the atrioventricular node. Correlation of extracellular potentials, intracellular potentials, and histology.

Atrioventricular junctional (AV nodal) reentrant tachycardia can be cured by catheter ablation of the slow pathway, which is part of the reentrant circuit. Previous work has suggested that extracellular double potentials may help identify the site of the slow pathway, but the origin and significance of these potentials are controversial. The aim of this study was to identify the source of these potentials. Studies were performed in isolated, blood-perfused porcine (n = 8) and canine (n = 4) hearts. Several methods were used to identify the origin of potentials: microelectrode recording, extracellular mapping, pacing from multiple sites, and light microscopy. Two types of double potentials, similar to those found in humans, were found in all hearts. LH potentials consisted of a low-frequency deflection followed by a high-frequency deflection during sinus rhythm or anterior septal pacing. HL potentials consisted of a high-frequency deflection followed by a low-frequency deflection. LH potentials were found close to the coronary sinus orifice. They were caused by asynchronous activation of the sinus septum and the region between the coronary sinus orifice and tricuspid annulus. HL double potentials were found along the tricuspid annulus. They were caused by asynchronous activation of two cell layers. The high-frequency component was caused by depolarization of atrial-type cells in the deep subendocardial layer. The low-frequency component was caused by depolarization of cells with nodal characteristics close to the endocardium. These cells were present around the entire tricuspid annulus, were not part of the compact AV node, and could be dissociated from the bulk of the atria by rapid atrial pacing. LH potentials are caused by asynchronous activation of muscle bundles above and below the coronary sinus orifice. Their proximity to the site of the slow pathway is probably serendipity. HL double potentials are caused by asynchronous activation of atrial cells and a band of nodal-type cells close to the tricuspid annulus. The band of nodal-type cells is not part of the compact AV node and may represent the substrate of the slow AV nodal pathway.

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.

Electrophysiologic and histologic effects of dissection of the connections between the atrium and posterior part of the atrioventricular node

Objectives. This study was designed to examine the effects of destroying the posterior approaches to the atrioventricular (AV) node.Background. Surgical and catheter ablation procedures have been developed for the cure of AV junctional reentrant tachycardia. Some of these destroy the posterior approaches to the AV node.Methods. Atrioventricular node function and electrical excitation of Koch's triangle and the proximal coronary sinus were examined in 18 dogs. Dissection of the posterior atrionodal connections was performed in 10 dogs and a sham procedure in 8. After 28 to 35 days, repeat electrophysiologic and mapping studies were performed to assess changes in AV node function and the routes of AV and ventriculoatrial (VA) conduction. The AV junction was then examined with light microscopy.Results. The compact AV node was undamaged in eight cases (80%). In two cases minor fibrosis occurred at the posterior limit of the compact node. The right-sided posterior atrionodal connections lying between the coronary sinus orifice and the tricuspid annulus were replaced by scar tissue in all cases, but the left-sided posterior connections and the anterior connections remained intact. Atrioventricular and VA conduction intervals and refractory periods were not altered. Atrioventricular junctional echoes were present in 10 dogs before and in 7 dogs after dissection (p = 0.06). Posterior (slow pathway) retrograde exits from the AV node were present in seven dogs before and in seven dogs after dissection. However, retrograde atrial excitation was altered in four of these seven dogs, so that the site of exit from the AV node was more leftward than it had been preoperatively. The node remained responsive to autonomic blocking drugs postoperatively. Double atrial electrograms similar to slow pathway potentials were found in all dogs.Conclusions. This procedure ablates the posterior atrionodal connections but rarely damages the compact AV node. Atrioventricular node function is not impaired and the node is not denervated. The mechanism of cure of AV junctional reentrant tachycardia is probably damage to the perinodal atrium. This suggests that part of the slow AV node pathway may lie outside the compact AV node. Dual AV node exits and double atrial electrograms are present in the normal canine heart.

Atypical AV junctional reentrant tachycardia following AV nodal modification

The authors present a patient who initially underwent anterior approach atrioventricular (AV) nodal modification for treatment of typical AV junctional reentrant tachycardia (AVJRT) and subsequently developed clinical episodes of a previously undocumented type of supraventricular tachycardia. Findings during electrophysiologic studies suggest that this tachycardia is due to both anterograde and retrograde conduction in a slow AV nodal pathway. A “slow pathway” potential was identified and dissociated from the local atrial and ventricular depolarizations. Posterior approach AV nodal modification was successfully used to ablate this tachycardia. These findings suggest that atypical AVJRT occurring after AV nodal modification may be “slow-slow” AVJRT.

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.

Radiofrequency catheter ablation for paroxysmal supraventricular tachycardia: a report of 135 procedures.

Paroxysmal Supraventricular Tachycardia (PSVT) is a common condition which until recently has been treated with anti-arrhythmic drugs or surgery. Radiofrequency (RF) catheter ablation is a new mode of treatment which provides a cure of this condition. To present our early experience of RF catheter ablation for PSVT. One hundred and thirty-five procedures were performed in 117 patients. The diagnostic study and therapeutic catheter ablation were performed as a combined electrophysiological procedure in 74 patients (63%). In 58 patients (50%), PSVT was due to Atrio-ventricular junctional (nodal) re-entrant tachycardia (AVJRT). Twenty-five of the 58 patients underwent a fast pathway ablation while 33 had ablation of their slow pathway. The mean number of radiofrequency pulses delivered was ten for a mean duration of 25 seconds. Radiofrequency ablation of accessory pathways was attempted in 58 patients; pathways were left-sided in 29 patients, postero-septal in 21, midseptal in five, Mahaim connection in two, antero-septal in one and right free wall in one patient. One patient with incessant automatic atrial tachycardia also underwent a successful RF ablation. Using RF ablation cure of PSVT was achieved in 90% of patients. Cure of AVJRT was achieved in 95% (55/58) of patients using either fast or slow pathway ablation. Only one patient required permanent pacemaker implantation for Mobitz type I AV block following fast pathway ablation. The overall success rate for ablation of accessory pathways was 85%. There is an operator learning curve for this procedure suggested by the fact that the success rate for accessory pathway ablation at first attempt was 63% in the first 29 patients and 93% in the remaining 29. There was no significant morbidity or mortality during or after the procedure. In a mean follow-up of nine months in the patients with successful ablation only two patients with AVJRT had a recurrence of documented PSVT. Both these patients had successful repeat RF ablation. Catheter ablation using radiofrequency energy is an effective and safe therapeutic option for patients with symptomatic PSVT.

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.

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.

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.

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.

The Electrocardiographic Manifestation of Combined AV Nodal Wenckebach Periodicity and Reentry

Presented are three patients with Wenckebach type second degree AV block that was complicated with AV nodal reentry producing different arrhythmias. The common presentation of manifest AV nodal reentry is an incomplete Wenckebach periodicity, whereby the retrograde impulse interrupts the Wenckebach cycle; rarely, the retrograde impulse initiates an AV junctional reentrant tachycardia. The documentation of concealed AV nodal reentry is more difficult and should be considered if there is a sudden increase of the PR interval in the Wenckebach cycle.

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.

Value and limitations of adenosine in the diagnosis and treatment of narrow and broad complex tachycardias.

The diagnostic and therapeutic potential of intravenous adenosine was studied in 64 patients during 92 episodes of regular sustained tachycardia. In 40 patients who had narrow complex tachycardias (QRS less than 0.12 s) adenosine (2.5-25 mg) restored sinus rhythm in 25 with junctional tachycardias (46 of 48 episodes) and produced atrioventricular block to reveal atrial or sinus tachycardia in 15. In 24 patients with broad complex tachycardias (QRS greater than or equal to 0.12 s) adenosine terminated the tachycardias in six patients and revealed atrial or sinus arrhythmias in four. The tachycardias persisted in 14 patients despite doses up to 20 mg, but adenosine allowed the diagnosis of ventricular tachycardia with retrograde atrial activation in two patients by producing transient ventriculoatrial dissociation. Diagnosis based on adenosine induced atrioventricular nodal block was correct in all patients with narrow complex tachycardias and in 92% of those with broad complex tachycardias, compared with correct electrocardiographic diagnoses in 90% and 75% respectively. Adenosine gave diagnostic information additional to the electrocardiogram in 25%. The response to adenosine in broad complex tachycardias identified those of supraventricular origin with 90% sensitivity, 93% specificity, and 92% predictive accuracy. Adenosine restored sinus rhythm in all patients with junctional reentrant tachycardias, but in 10 (35%) the arrhythmias recurred within two minutes. Symptomatic side effects (dyspnoea, chest pain, flushing, headache) were reported by 40 (63%) patients and, although transient, were severe in 23 (36%). There were ventricular pauses of over 2 s in 16% of patients, the longest pause being 6.1 s. Adenosine is of value in the diagnosis and treatment of narrow and broad complex tachycardias, but its use is limited by symptomatic side effects, a tenfold range in minimal effective dosage, occasional action at sites other than the atrioventricular node, and early recurrence or arrhythmia.