Demonstration of two anomalous bypasses in concealed Wolff-Parkinson-White syndrome

Two patients with a history of paroxysmal supraventricular tachycardia but no evidence of the Wolff-Parkinson-White syndrome in the conventional electrocardiograms were studied utilizing atrial and ventricular extrastimuli. The evidence obtained in these patients was consistent with a concealed Wolff-Parkinson-White syndrome. In one patient, ventricular extrastimuli revealed three different responses in the curve of ventriculoatrial conduction, depending upon the interval of stimulus. In the other patient, intracardiac recordings, including the left atrial potential, showed that paroxysmal supraventricular tachycardia was induced by an impulse via an anomalous bypass which diverged from the main bypass or stemmed independently from the left ventricle and was maintained by impulses via the main bypass which lay between the left ventricle and the left atrium. The mechanisms for initiation of the paroxysmal supraventricular tachycardia were discussed.     

Atrial and accessory pathway activation direction in patients with orthodromic supraventricular tachycardia: insights from vector mapping

OBJECTIVES: The purpose of this study was to utilize vector mapping to investigate atrial and accessory pathway activation direction during orthodromic supraventricular tachycardia. BACKGROUND: Although advances have been made in the electrophysiologic evaluation and management of accessory pathways, our understanding of accessory pathway anatomy and physiology remains incomplete. Vector mapping has been validated as a method of studying local myocardial activation. METHODS: In 28 patients with a left-sided or posteroseptal accessory atrioventricular (AV) pathway referred for ablation, atrial and accessory AV pathway activation direction was determined during ventricular pacing or orthodromic supraventricular tachycardia, or both, by summing three orthogonally oriented bipolar electrograms recorded from the coronary sinus to create three-dimensional vector loops. Atrial and accessory AV pathway activation direction was determined in all patients from the maximal amplitude vectors of the vector loops. Because of beat to beat variability in the directions of the vector loops, data from 8 of 28 patients could not be analyzed. RESULTS: At 81 of 83 sites, atrial activation direction along the long axis of the coronary sinus corresponded with the direction suggested by activation time mapping. Activation direction along the anteroposterior and inferosuperior axes was variable, potentially due to variations in the level of the atrial insertion of the accessory AV pathway and in the depth or angling of pathway fibers in the AV fat pad. In eight patients, at least one recording was obtained at the site of an accessory AV pathway potential. Accessory AV pathway activation proceeded superiorly and to the right in seven of eight patients; in one patient with a posteroseptal pathway, accessory AV pathway activation proceeded superiorly and to the left. CONCLUSIONS: 1) Vector mapping is a useful technique for localizing accessory AV pathways; 2) left-sided accessory AV pathways angle from left to right as they traverse the AV groove; and 3) variable activation directions of the atrial myocardium adjacent to the coronary sinus suggest that accessory AV pathway insertion into the atrium differs from patient to patient.     

Narrow complex tachycardia with VA block: diagnostic and therapeutic implications

To review our experience with cases of narrow complex tachycardia with VA block, highlighting the difficulties in the differential diagnosis, and the therapeutic implications. Prior reports of patients with narrow complex tachycardia with VA block consist of isolated case reports. The differential diagnosis of this disorder includes: automatic junctional tachycardia, AV nodal reentry with final upper common pathway block, concealed nodofascicular (ventricular) pathway, and intra-Hissian reentry. Between June 1994 and January 1996, six patients with narrow complex tachycardia with episodes of ventriculoatrial block were referred for evaluation. All six patients underwent attempted radiofrequency ablation of the putative arrhythmic site. Three of six patients had evidence suggestive of a nodofascicular tract. Intermittent antegrade conduction over a left-sided nodofascicular tract was present in two patients and the diagnosis of a concealed nodofascicular was made in the third patient after ruling out other tachycardia mechanisms. Two patients had automatic junctional tachycardia, and one patient had atrioventricular nodal reentry with proximal common pathway block. Attempted ablation in the posterior and mid-septum was unsuccessful in patients with nodofascicular tachycardia. In contrast, those with atrioventricular nodal reentry and automatic junctional tachycardia readily responded to ablation. The presence of a nodofascicular tachycardia should be suspected if: (1) intermittent antegrade preexcitation is recorded, (2) the tachycardia can be initiated with a single atrial premature producing two ventricular complexes, and (3) a single ventricular extrastimulus initiates SVT without a retrograde His deflection. The presence of a nodofascicular pathway is common in patients with narrow complex tachycardia and VA block. Unlike AV nodal reentry and automatic junctional tachycardia, the response to ablation is poor.     

Radiofrequency catheter ablation of concealed atrioventricular accessory pathways using a "simultaneous pacing method"

The retrograde atrial potential at a successful ablation site is usually obscured by the wide and large ventricular potential during atrioventricular reentrant tachycardia or ventricular pacing, which makes it difficult to determine the appropriate ablation site for a concealed accessory pathway. A pacing maneuver named the "simultaneous pacing method" is proposed herein to differentiate the retrograde atrial potential from the ventricular potential for a successful ablation of the concealed accessory pathway. Catheter ablation was performed in 12 patients with a single left free-wall concealed accessory pathway. The atrial insertion site was determined by the simultaneous pacing method in six patients (group I) and by ventricular pacing in six patients (group II). In the simultaneous pacing method, electrograms recorded during ventricular pacing in the earliest retrograde atrial activation site are a fusion of the ventricular potential and the following retrograde atrial potential. When atrial and ventricular pacings are performed simultaneously (simultaneous pacing), the end portion of the electrograms recorded at the same site is solely the ventricular component, because atrial is activated earlier. The atrial potential can be confirmed during ventricular pacing in comparison with the electrograms during the "simultaneous pacing." Radiofrequency catheter ablation was successful in eliminating conduction through the accessory pathway in all 12 patients. The radiofrequency applications in group I were significantly fewer than those in group II (1.7 +/- 1.0 in group I, 5.3 +/- 3.2 in group II, P < 0.05). The total procedure time in group I was significantly shorter than in group II (57.8 +/- 15.7 vs 106.7 +/- 41.6 mins in group II, respectively, P < 0.05). The fluoroscopy time in group I was significantly shorter than in group II (54.0 +/- 7.9 vs 81.3 +/- 26.3 mins, respectively, P < 0.05). We were able to determine the atrial insertion site of accessory pathways by the simultaneous pacing method. The simultaneous pacing method was useful in eliminating concealed left free-wall accessory pathways.     

Adenosine-sensitive atrial reentrant tachycardia originating from the atrioventricular nodal transitional area

INTRODUCTION: Atrial tachycardia shows wide variations in its electrophysiologic properties and sites of origin. We report an atrial tachycardia with ECG manifestations and electrophysiologic characteristics similar to an atypical form of AV nodal reentrant tachycardia (AVNRT). METHODS AND RESULTS: This supraventricular tachycardia was observed in 11 patients. It was initiated by atrial extrastimulation with an inverse relationship between the coupling interval of an extrastimulus and the postextrastimulus interval. Its induction was not related to a jump in the AH interval, and its perpetuation was independent of conduction block in AV node. Ventricular pacing during tachycardia demonstrated AV dissociation without affecting the atrial cycle length. A very small dose of adenosine triphosphate (mean 3.9 +/- 1.2 mg) could terminate the tachycardia. The earliest atrial activation during tachycardia was recorded at the low anteroseptal right atrium with a different intra-atrial activation sequence from that recorded during ventricular pacing, where the tachycardia was successfully ablated in 9 of 10 attempted patients. Bidirectional AV nodal conduction remained unaffected after successful ablation. CONCLUSION: There may be an entity of adenosine-sensitive atrial tachycardia probably due to focal reentry within the AV node or its transitional tissues without involvement of the AV nodal pathways. This tachycardia can be ablated without disturbing AV nodal conduction from the right atrial septum.     

Surgical treatment of ventricular tachycardia after surgical repair of tetralogy of Fallot. Relation between intraoperative mapping and histological findings

BACKGROUND: The mechanism of ventricular tachycardia (VT) after correction of tetralogy of Fallot (TF) is poorly understood. The purpose of this study was to examine the histopathology of the arrhythmogenic area detected by intraoperative mapping. METHODS AND RESULTS: The patients were three men who underwent radical surgery for TF at age 3, 3, or 5 years, respectively. VT developed at 8, 9, or 11 years, respectively, after surgery, and shock developed during VT in every case. The ECG revealed monomorphic VT in two cases and polymorphic VT in one case. Induction of VT resulted in a wide left-axis deviation-pattern QRS with cycle lengths varying between 260 and 330 milliseconds. The VT origin was identified at the right ventricular outflow tract (RVOT). A radical operation was performed with the patient under cardiopulmonary bypass. On epicardial mapping, delayed activation of the RVOT was recorded during sinus rhythm, and clockwise circus movement of the macroreentry current during VT on the right ventricular free wall was documented in each case. The VTs were treated successfully by surgical resection and cryoablation of the myocardium. In every patient, histology of the myocardial specimens showed degeneration, adiposis, fibrosis, inflammatory cell infiltration, and scattered myocyte islets. These lesions corresponded anatomically to the area of myocardium in which delayed activation was evident during epicardial mapping. CONCLUSIONS: The results of this study indicate that patients with VT after radical correction of the TF have abnormal histopathological findings at the site of the prior right ventriculotomy scar. These lesions were noted within the region of delayed activation found during epicardial mapping and were found to be a part of the reentrant circuit.     

Atrial septal pacing: a method for pacing both atria simultaneously

By pacing both atria simultaneously, one could reliably predict and optimize left-sided AV timing without concern for IACT. With synchronous depolarization of the atria, reentrant arrhythmias might be suppressed. We studied four male patients (73 +/- 3 years) with paroxysmal atrial fibrillation and symptomatic bradyarrhythmias using TEE and fluoroscopy as guides; a standard active fixation screw-in lead (Medtronic model #4058) was attached to the interatrial septum and a standard tined lead was placed in the ventricle. The generators were Medtronic model 7960. The baseline ECG was compared to the paced ECG and the conduction time were measured to the high right atrium, distal coronary sinus and atrial septum in normal sinus rhythm, atrial septal pacing, and AAT pacing. On the surface ECG, no acceleration or delay in AV conduction was noted during AAI pacing from the interatrial septum as compared with normal sinus rhythm. The mean interatrial conduction time for all 4 patients was 106 +/- 2 ms; the interatrial conduction time measured during AAT pacing utilizing the atrial septal pacing lead was 97 +/- 4 ms (P = NS). During atrial septal pacing, the mean conduction time to the high right atrium was 53 +/- 2 ms. The mean conduction time to the lateral left atrium during atrial septal pacing, was likewise 53 +/- 2 ms. We conclude that it is possible to pace both atria simultaneously from a single site using a standard active fixation lead guided by TEE and fluoroscopy. Such a pacing system allows accurate timing of the left-sided AV delay.     

Transesophageal pacing and recording

Identification of P wave is essential for the diagnosis of various arrhythmias. The transesophageal ECG is useful for obtaining the relationship of atrial-ventricular activation when P wave is difficult to recognize on the surface ECG. Transesophageal pacing is also helpful to evaluate the function of the conduction system and to clarify the mechanism of arrhythmias. Thus, transesophageal pacing and recording can be used as beside electrophysiologic studies in patients with sick sinus syndrome, atrial-ventricular block, atrial flutter, and paroxysmal supraventricular tachycardia.     

Atypical atrioventricular nodal reentry tachycardia with atrioventricular block mimicking atrial tachycardia: electrophysiologic properties and radiofrequency ablation therapy

INTRODUCTION: Fast-intermediate form AV nodal reentry tachycardia (AVNRT) sometimes may mimic atrial tachycardia or atrial flutter and render the diagnosis difficult when the tachycardia rate is fast and AV block occurs during tachycardia. METHODS AND RESULTS: A 45-year-old woman with paroxysmal supraventricular tachycardia was referred to this institution. Initially, the tachycardia was thought to be an atrial tachycardia because of: (1) a short cycle length of the tachycardia with 2:1 and Wenckebach AV block; (2) a difference in the atrial activation sequence during tachycardia and during ventricular pacing; and (3) failure of burst ventricular pacing to affect the atrial rate and the atrial activation sequence during tachycardia. An accurate diagnosis of fast-intermediate form AVNRT was subsequently made based on the finding that the tachycardia was induced following delivery of a third ventricular extrastimulus, which showed a sequence of V-A-H and a change on atrial activation sequence of the induced beat. Successful radiofrequency ablation was achieved only after accurate diagnosis of the tachycardia was made. CONCLUSION: Fast-intermediate form AVNRT sometimes may masquerade as atrial tachycardia. Accurate diagnosis is mandatory for successful ablation therapy.     

Cryosurgical ablation of accessory atrioventricular connections: a method for correction of the pre-excitation syndrome

Cryothermia, a new technique for definitive treatment of the pre-excitation syndrome, is described in two patients. The first patient presented with a normal P-R interval with a delta wave and reciprocating tachycardia. Preoperative electrophysiologic study suggested a free-wall atrioventricular connection on the left posterior atrioventricular (A-V) groove. At surgery, epicardial mapping confirmed the site of pre-excitation on the posterior left ventricular (LV) wall. An electrogram arising from the accessory pathway (AP) was recorded at the site of earliest ventricular activation. Interatrial delay combined with an apparently long accessory pathway to the ventricle caused the P-R interval to appear normal. Local pressure abolished pre-excitation. The site of early ventricular activation was cooled to -60 degrees C with a specially designed cryoprobe. All evidence of pre-excitation and arrhythmias disappeared. The second patient presented with a refractory reciprocating tachycardia and was found to have an AP in the septum capable of only retrograde conduction. Retrograde conduction was abolished by applying a temperature of 0 degrees C to the anulus at this site during tachycardia. Conduction over the AP and reciprocating tachycardia returned with rewarming. Ablation of the AP was obtained by applying a temperature of -60 degrees C for 90 seconds on two occasions to the same area. The His bundle was not injured.     

Different modes of cell death induced by 5-fluoro-2''-deoxyuridine in two clones of the mouse mammary tumor FM3A cell line

OBJECTIVES: To clarify the prevalence and mechanism of supraventricular tachycardia in patients with right atrial isomerism. BACKGROUND: Paired SA and dual atrioventricular (AV) nodes have been described in patients with right atrial isomerism. However, the clinical significance remains unclear. METHODS: From 1987 to 1996, a total of 101 patients (61 male, 40 female) and four fetuses were identified with right atrial isomerism. The diagnosis of supraventricular tachycardia exclude the tachycardia with prolonged QRS duration or AV dissociation, and primary atrial tachycardia. RESULTS: The median follow-up duration was 38 months (range 0.2-270 months). Supraventricular tachycardia was documented in 25 patients (24.8%) and one fetus (25%) (onset age ranged from prenatal to 14 years old; median 4 years old). Actuarial Kaplan-Meier analysis revealed that the probability of being free from tachycardia was 67% and 50% at 6 and 10 years of age, respectively. These tachycardias could be converted by vagal maneuvers in one, verapamil in seven, propranolol in four, digoxin in two, procainamide in one, and rapid pacing in five. Spontaneous conversion was noted in six (including the fetus). Seven cases had received electrophysiological studies. Reciprocating AV tachycardia could be induced in five and echo beats in one. The tachycardia in three patients was documented as incorporating a posterior AV node (antegrade) and an anterior or a lateral AV node (retrograde). Two of them received radiofrequency ablation. Successful ablation in both was obtained by delivering energy during tachycardia, aimed at the earliest retrograde atrial activity and accompanied by junctional ectopic rhythm. The patient with echo beats developed tachycardia soon after operation. CONCLUSIONS: Supraventricular tachycardia is common in patients with right atrial isomerism and can occur during the prenatal stage. Drugs to slow conduction through the AV node may help to terminate the tachycardia. Radiofrequency ablation is a safe and effective treatment alternative to eliminate tachycardia.     

Dissimilar atrial rhythms in a patient with the Wolff-Parkinson-White syndrome

In this report, we present the findings in a patient who had paroxysmal supraventricular tachycardia and atrial flutter associated with the Wolff-Parkinson-White syndrome. During atrial flutter, localized atrial fibrillation was recorded in the coronary sinus (dissimilar atrial rhythms), near the accessory pathway; and during 90 minutes of observation, ventricular activation occurred solely over the normal pathway. We postulate that localized atrial fibrillation repetitively invaded the accessory pathway and rendered it refractory to conduction by flutter impulses.     

An Italian experience of radiofrequency transcatheter ablation in type-I atrial flutter: the results and follow-up

BACKGROUND: Type I atrial flutter (AF) is a supraventricular tachycardia that is notoriously disabling and resistant to antiarrhythmic drugs. The introduction of an effective non-pharmacologic technique, such as radiofrequency catheter ablation (RF), opened new therapeutic prospects for the management of this arrhythmia. The aim of our study was to evaluate the long-term efficacy of atrial flutter RF using a successful procedure marker of bi-directional conduction block in the isthmus. METHODS: In the last consecutive 50 patients (pts) who underwent RF procedure for AF at our Center (46 pts during spontaneous or induced AF and 4 in sinus rhythm) after the successful interruption of AF we performed the usual reinduction attempts and well atrial pacing from 2 sites in the right atrium (in 18 pts before and after RF and in 32 only after RF). The sites of pacing were site 1: low lateral right atrium (LRA); site 2: proximal coronary sinus (PCS). The 50 pts consisted of 13 females, 37 males with a mean age of 62.5 +/- 9.7 years (35-83). The end-point for the procedure was: 1) abrupt interruption of AF; 2) inability to reinduce AF; 3) recognition of atrial activation sequence during pacing in LRA and in PCS compatible with conduction block in the isthmus. RESULTS: The RF was successful in terminating AF in all pts after 11 +/- 7 applications of energy. After ablation, sustained AF was no longer inducible by atrial pacing. After RF, during pacing in sinus rhythm from LRA, the lower septum and PCS presented a delayed activation after the His region. Similarly, during pacing from PCS after ablation, the atrial activation sequence was modified: the low lateral right atrium was now activated by a single front after the high lateral atrium. No acute complications were noted in any pts during or after procedure. AF recurred in 9 pts. Four pts now present chronic atrial fibrillation. The mean follow-up period is 14.8 +/- 8 months. All the patients were discharged without antiarrhythmic therapy. CONCLUSIONS: The mechanism of successful ablation is the bi-directional conduction block in the isthmus with the evidence of the changes in the right atrial activation sequence during atrial pacing in sinus rhythm in LRA and in PCS before and after RF.     

Atrioventricular nodal reentrant tachycardia in patients with ventriculo-atrial conduction block

OBJECTIVE: To demonstrate the reversibility of retrograde ventriculo-atrial block by isoproterenol in patients with atrioventricular nodal reentrant tachycardia (AVNRT). DESIGN: Three case reports and their electrophysiological features. PATIENTS: Three patients with documented or suspected paroxysmal supraventricular tachycardia. INTERVENTIONS: At routine electrophysiology study, no supraventricular tachycardia was inducible in the baseline state. Infusion of isoproterenol (1 to 5 micrograms/min) was given and stimulation procedures were repeated. RESULTS: At baseline, all three patients had discontinuous antegrade atrioventricular (AV) nodal conduction, but very poor (two patients) or absent (one patient) ventriculo atrial conduction prevented induction of AVNRT. During infusion of isoproterenol, retrograde conduction was enhanced so that 1:1 retrograde occurred to cycle lengths of 300, 340 and 260 ms. AVNRT was then inducible in all patients, reproducing their clinical symptoms. CONCLUSION: Absent or poor ventriculo-atrial conduction in patients with suspected AV node reentry does not preclude the development of tachycardia with sympathomimetic enhancement. Isoproterenol should be given to attempt reversal of retrograde block in these patients.     

Evolution of flightless land birds on southern continents: transferrin comparison shows monophyletic origin of ratites

In 34 successive patients with Wolff-Parkinson-White syndrome premature beats were induced from the right ventricular apex during reciprocating tachycardia (RT) at progressively shorter coupling intervals. The presence of an accessory pathway was confirmed by a reduction in the atrial cycle length (A-A interval) during which the premature ventricular beat was introduced. This retrograde preexcitation occurred at a time when the His-AV node pathway was refractory; i.e. there was premature activation of the atria over a pathway other than the His-AV node. 3 patients were excluded because of unsatisfactory or unstable H-H intervals. In the remaining 31 patients with constant preceding H-H intervals, the A-A interval shortened; (a) 35-65 msec in 4 patients with right-sided pathways and normal conduction during RT and by 110 msec in a 5th patient with a right-sided pathway, in whom bundle branch block aberration persisted during RT, (b) 45 msec in the single patient with both a right-sided and a septal accessory pathway, (c) 35-65 msec in 5 patients with septal pathways, and (d) 15-35 msec in only 4/20 patients with left-sided pathways and normal conduction during RT. Left-sided ventricular premature beats were introduced in 5 patients with left-sided pathways and normal conduction in RT. In 4/5, left-sided premature beats shortened the A-A interval 40-75 msec whereas right-sided premature beats at the same coupling interval failed to do so. In the fifth case, the left-sided premature resulted in a 65 msec abbreviation of the A-A interval compared to 30 msec from the right ventricular outflow tract and 15 msec from the right ventricular apex. In 5 patients with left-sided pathways, right ventricular premature beats were introduced during RT with left bundle branch block aberration, and shortened the A-A interval 30-50 msec in all of these, whereas right-sided premature beats in 4 of the 5 during normal conduction failed to do so. This technique is useful to confirm the participation of accessory pathways in reciprocating tachycardias associated with the preexcitation syndromes, and emphasizes the importance of the site of stimulation used relative to the location of the accessory pathway. Because of the possibility of multiple accessory pathways, stimulation of the left ventricle should be performed in patients undergoing surgery for preexcitation unless the left ventricle is already inplicated by right-sided studies.     

Differential effect of adenosine on anterograde and retrograde fast pathway conduction in patients with atrioventricular nodal reentrant tachycardia

INTRODUCTION: Several studies have shown that the fast pathway is more responsive to adenosine than the slow pathway in patients with AV nodal reentrant tachycardia. Little information is available regarding the effect of adenosine on anterograde and retrograde fast pathway conduction. METHODS AND RESULTS: The effects of adenosine on anterograde and retrograde fast pathway conduction were evaluated in 116 patients (mean age 47 +/- 16 years) with typical AV nodal reentrant tachycardia. Each patient received 12 mg of adenosine during ventricular pacing at a cycle length 20 msec longer than the fast pathway VA block cycle length and during sinus rhythm or atrial pacing at 20 msec longer than the fast pathway AV block cycle length. Anterograde block occurred in 98% of patients compared with retrograde fast pathway block in 62% of patients (P < 0.001). Unresponsiveness of the retrograde fast pathway to adenosine was associated with a shorter AV block cycle length (374 +/- 78 vs 333 +/- 74 msec, P < 0.01), a shorter VA block cycle length (383 +/- 121 vs 307 +/- 49 msec, P < 0.001), and a shorter VA interval during tachycardia (53 +/- 23 vs 41 +/- 17 msec, P < 0.01). CONCLUSION: Although anterograde fast pathway conduction is almost always blocked by 12 mg of adenosine, retrograde fast pathway conduction is not blocked by adenosine in 38% of patients with typical AV nodal reentrant tachycardia. This indicates that the anterograde and retrograde fast pathways may be anatomically and/or functionally distinct. Unresponsiveness of VA conduction to adenosine is not a reliable indicator of an accessory pathway.     

Conduction properties of the crista terminalis in patients with typical atrial flutter: basis for a line of block in the reentrant circuit

INTRODUCTION: Previous mapping studies in patients with typical atrial flutter have demonstrated the crista terminalis to be a posterior barrier of the reentrant circuit forming a line of block. However, the functional role of the crista terminalis in patients with or without a history of atrial flutter is not well known. The aim of this study was to determine whether the conduction properties of the crista terminalis are different between patients with and those without a history of atrial flutter. METHODS AND RESULTS: The study population consisted of 12 patients with clinically documented atrial flutter (group 1) and 12 patients with paroxysmal supraventricular tachycardia as well as induced atrial flutter (group 2). A 7-French, 20-pole, deflectable Halo catheter was positioned around the tricuspid annulus. A 7-French, 20-pole Crista catheter was placed along the crista terminalis identified by the recording of double potentials with opposite activation sequences during typical atrial flutter. After sinus rhythm was restored, pacing from the low posterior right atrium near the crista terminalis was performed at multiple cycle length to 2:1 atrial capture. No double potentials were recorded along the crista terminalis during sinus rhythm in both groups. In group 1, the longest pacing cycle length that resulted in a line of block with double potentials along the crista terminalis was 638 +/- 119 msec. After infusion of propranolol, it was prolonged to 832 +/- 93 msec without change of the interdeflection intervals of double potentials. In group 2, the longest pacing cycle length that resulted in a line of block with double potentials along the crista terminalis was 214 +/- 23 msec. After infusion of procainamide, it was prolonged to 306 +/- 36 msec with increase of interdeflection interval of double potentials. CONCLUSION: The crista terminalis forms a line of transverse conduction block during typical atrial flutter. Poor transverse conduction property in the crista terminalis may be the requisite substrate for clinical occurrence of typical atrial flutter.     

Posterior fast atrioventricular node pathways: implications for radiofrequency catheter ablation of atrioventricular node reentrant tachycardia

OBJECTIVES: This study sought to present evidence that fast atrioventricular (AV) node pathways with posterior exit sites may participate in typical AV node reentry. BACKGROUND: Catheter ablation of the slow AV node pathway in the posteroseptal right atrium is the preferred therapeutic approach in patients with AV node reentrant tachycardia. Despite the success achieved with this approach, electrophysiologic changes consistent with fast pathway ablation are occasionally observed. One potential explanation is the presence of an aberrant posterior fast pathway. METHODS: The location of fast and slow AV node pathways was determined by atrial activation mapping along the tricuspid valve annulus during tachycardia and was further confirmed by the effect of radiofrequency catheter ablation. RESULTS: Seven patients with AV node reentrant tachycardia had evidence of a posterior fast pathway near the coronary sinus os. Abolition of anterograde and retrograde fast pathway conduction followed radiofrequency ablation in the posteroseptal region in six patients. Consistent with fast pathway ablation, the AH interval increased from 70 +/- 24 to 195 +/- 35 ms (mean +/- SD), and tachycardia was no longer inducible. Selective slow pathway ablation was performed in one other patient with a posterior fast pathway. CONCLUSIONS: Functionally fast AV node pathways may be located in the posteroseptal right atrium, where slow pathway modification is performed. These data delineate the limitation of an anatomically guided slow pathway ablative approach and emphasize the importance of detailed mapping and localization of the retrograde fast pathway exit site before ablation. Failure to recognize the presence of posterior fast AV node pathways may account for sporadic examples of AV block, complicating posteroseptal ablation in patients with AV node reentry.     

A case of AV reentrant tachycardia due to a concealed accessory pathway with retrograde conduction manifested by isoproterenol

Retrograde conduction of the concealed accessory pathway (AP) is a prerequisite for the induction of atrioventricular reentrant tachycardia (AVRT). In patients with AVRT due to a concealed AP, the absence of retrograde conduction of the AP in the baseline state has rarely been reported. We report a case of AVRT due to a concealed left lateral AP, in which the retrograde conduction was absent in the baseline state and manifested by isoproterenol infusion. A 61-year-old man had suffered from intermittent palpitation for 17 years. A narrow QRS complex tachycardia with a retrograde P wave in the ST segment was recorded in 24-h Holter monitoring. An electrophysiologic study was performed while he was in a nonsedated state. No ventriculoatrial conduction over either the normal atrioventricular conduction system or the AP was demonstrated in the baseline state. Isoproterenol was infused at a rate of 1.0 microg/min. Retrograde conduction over the AP became manifest and AVRT was induced. The AP was ablated with radiofrequency energy at the left free wall. After ablation of the AP, no tachycardia was induced. To the authors'best knowledge, only 1 other similar case has been reported in the literature.     

Characterization of low right atrial isthmus as the slow conduction zone and pharmacological target in typical atrial flutter

BACKGROUND: Previous electrophysiological studies in patients with typical atrial flutter suggested that the slow conduction zone might be located in the low right atrial isthmus, which is a path formed by orifice of inferior vena cava, eustachian valve/ridge, coronary sinus ostium, and tricuspid annulus. The conduction characteristics during atrial pacing and responses to antiarrhythmic drugs of this anatomic isthmus were unknown. METHODS AND RESULTS: Forty-four patients, 20 patients with paroxysmal supraventricular tachycardia (group 1) and 24 patients with clinically documented paroxysmal typical atrial flutter (group 2), were studied. A 20-pole halo catheter was situated around the tricuspid annulus. Incremental pacing from the low right atrium and coronary sinus ostium was performed to measure the conduction time and velocity along the isthmus and lateral wall in the baseline state and after intravenous infusion of procainamide or sotalol. In both groups, conduction velocity in the isthmus during incremental pacing was significantly lower than that in the lateral wall before and after infusion of antiarrhythmic drugs. Furthermore, gradual conduction delay with unidirectional block in the isthmus was relevant to initiation of typical atrial flutter. Compared with group 1, group 2 had a lower conduction velocity in the isthmus and shorter right atrial refractory period. Procainamide significantly decreased the conduction velocity, but sotalol did not change it. In contrast, sotalol significantly prolonged the atrial refractory period with a higher extent than procainamide. After infusion of procainamide, the increase of conduction time in the isthmus accounted for 52+/-19% of the increase in flutter cycle length, and 5 of 12 patients (42%) had spontaneous termination of typical flutter. After infusion of sotalol, typical flutter was induced in only 6 of 12 patients (50%) without significant prolongation of flutter cycle length. CONCLUSIONS: The low right atrial isthmus with rate-dependent slow conduction properties is critical to initiation of typical human atrial flutter. It may be the potentially pharmacological target of antiarrhythmic drugs in the future.