Conduction properties of the inferior vena cava-tricuspid annular isthmus in patients with typical atrial flutter

INTRODUCTION: A functional region of slow conduction located in the inferior right atrium has been postulated to be critical to the induction and maintenance of typical human atrial flutter. We reexamined the potential role of functional conduction delay in the annular isthmus between the tricuspid valve and the inferior vena cava; it is within this region that such delays have been postulated to occur, and where interruption of conduction by radiofrequency energy application has been shown to eliminate typical flutter. METHODS AND RESULTS: Thirty patients with type I atrial flutter (30 counterclockwise, 14 clockwise) were studied. Counterclockwise and clockwise isthmus activation times adjacent and parallel to the tricuspid valve were measured during three conditions: (1) atrial pacing in sinus rhythm, (2) atrial flutter, and (3) entrainment of atrial flutter. During pacing in sinus rhythm at progressively shorter cycle lengths, both counterclockwise and clockwise isthmus activation times remained unchanged; decremental conduction prior to flutter induction or loss of capture was not observed. Counterclockwise isthmus activation time did not significantly differ during flutter (68 +/- 23 msec), inferolateral tricuspid annulus pacing (71 +/- 23 msec), or entrainment of flutter (72 +/- 23 msec). Similarly, clockwise isthmus activation times did not significantly differ between flutter (65 +/- 22 msec), proximal coronary sinus pacing (73 +/- 21 msec), or entrainment of flutter (64 +/- 15 msec). CONCLUSION: Decremental conduction is not characteristic of activation through the isthmus when activation is assessed parallel and adjacent to the tricuspid annulus. Functional slowing or conduction delay does not develop in this region during typical atrial flutter.     

Effects of the novel antiarrhythmic agent azimilide on experimental atrial fibrillation and atrial electrophysiologic properties

OBJECTIVES: This study was designed to evaluate how the atrial electrophysiological and antiarrhythmic effects of azimilide compare with those of the specific rapid delayed rectifier (IKr) blocker dofetilide. BACKGROUND: Azimilide, a new class III drug, was initially believed to be a highly selective blocker of the slow delayed rectifier (IKs), but recent studies suggest that azimilide potently blocks IKr. Thus, it has been suggested that azimilide's in vivo effects may simply be due to IKr blockade. METHODS: Dose regimens producing stable effects over time were developed, and two dose levels of azimilide (10 and then 20 mg/kg) or dofetilide (0.08 and then 0.16 mg/kg) were administered to morphine/chloralose-anesthetized dogs during sustained vagal atrial fibrillation (AF). Epicardial mapping was used to measure conduction velocity and AF cycle length. RESULTS: Azimilide terminated AF in 13/14 dogs (93%), while dofetilide terminated AF in 6/12 (50%, P < 0.05). While dofetilide had strong reverse use-dependent effects on atrial ERP (e.g. at lower doses, dofetilide increased ERP by 51 +/- 3% at a basic cycle length, BCL, of 400 ms and by 17 +/- 3% at a BCL of 200 ms), azimilide's effects on ERP were rate-independent (ERP increased at lower dose by 38 +/- 6%, BCL 400 ms; 35 +/- 10%, BCL 200 ms). Neither drug affected conduction. CONCLUSIONS: Azimilide is effective against experimental AF, and increases ERP with a frequency dependence different from the IKr blocker dofetilide, suggesting that azimilide's actions on atrial tissue cannot be attributed exclusively to IKr block, and that effects on other currents (such as IKs) are likely to be important.     

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.     

Electropharmacologic effects of class I and class III antiarrhythmia drugs on typical atrial flutter: insights into the mechanism of termination

BACKGROUND: Acute effects of class I and class III antiarrhythmia drugs on the reentrant circuit of typical atrial flutter are not fully studied. Furthermore, the critical electrophysiologic determinants of flutter termination by antiarrhythmia drugs are not clear. METHODS AND RESULTS: The study population consisted of 36 patients (mean age, 53+/-17 years) with clinically documented typical atrial flutter. A 20-pole "halo" catheter was positioned around the tricuspid annulus. Incremental pacing was performed to measure the conduction velocity along the isthmus and lateral wall, and extrastimulation was performed to evaluate atrial refractory period in the baseline state and after intravenous infusion of ibutilide, propafenone, and amiodarone. Efficacy of these drugs in conversion of typical atrial flutter and patterns of termination were also determined. Ibutilide significantly increased the atrial refractory period and decreased conduction velocity in the isthmus at short pacing cycle length. It terminated atrial flutter in 8 (67%) of 12 patients after prolongation of flutter cycle length due to increase (86+/-19%) of conduction time in the isthmus. Propafenone predominantly decreased conduction velocity with use dependency and significantly increased atrial refractory period, but it only converted atrial flutter in 4 (33%) of 12 patients. Amiodarone had fewer effects on atrial refractory period and conduction velocity than did ibutilide and propafenone, and it terminated atrial flutter in only 4 (33%) of 12 patients. Termination of typical atrial flutter was due to failure of wave front propagation through the isthmus, which occurred with cycle length oscillation, abruptly without variability of cycle length, or after premature activation of the reentrant circuit. CONCLUSIONS: Ibutilide, with a unique increase in atrial refractoriness, was more effective in conversion of atrial flutter than were propafenone and amiodarone.     

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.     

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.     

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.     

Electrophysiological properties in patients undergoing atrial compartment operation for chronic atrial fibrillation with mitral valve disease

AIMS: Surgical treatment for atrial fibrillation is now feasible in selective cases. The aim of this study was to assess the electrophysiological properties of patients undergoing atrial compartment operation for chronic atrial fibrillation. METHODS AND RESULTS: Electrophysiological studies were performed in 20 mitral valve patients with atrial fibrillation who had been maintained in sinus rhythm for more than 1 year after atrial compartment operation. Intra-cardiac recording and programmed electrical stimulation were performed in various atrial compartments. The parameters studied included sinus node function, atrial conduction and refractoriness, atrioventricular conduction function and inducible arrhythmias if any. Intra-cardiac recordings showed that the rhythm was of sinus origin in all cases, with the earliest atrial activity located in the high right atrium. The mean sinus cycle length was 750 +/- 110 ms, AH time 106 +/- 29 ms, and HV time 53 +/- 7 ms. The sinus node function was normal in 18 patients (90%), and only two patients had prolonged sinus node recovery and sino-atrial conduction. The right atrial appendage compartment was driven by the sinus node in all patients. However, the conduction time from the high right atrium to the right atrial appendage compartment was markedly prolonged in 12 of 15 patients (80%) undergoing the three-compartment operation in which an incision was placed between the high right atrium and right atrial appendage compartments. On the other hand, the electrical activities in the left atrial compartment were much more varied. In 13 of 20 patients (65%), the left atrial compartment was driven by the sinus node; 11 of the 13 patients had a normal or mildly prolonged conduction time (ranged 75 to 146 ms), whereas two patients had a marked delay in conduction (200 ms and 266 ms, respectively). In the remaining seven patients, the left atrial compartments were dissociated from the rest of the heart; five of them had a quiescent left atrium, one a fluttering left atrial rhythm, and one a slow left atrial rhythm. The effective refractory period was longer in the left atrial compartment (242 +/- 47 ms) as compared to that of the high right atrium (224 +/- 26 ms, P < 0.01) and right atrial appendage compartments (219 +/- 25 ms, P < 0.01). Programmed electrical stimulation could not induce atrial fibrillation in any patient, whereas two patients had inducible atrial flutter and three repetitive atrial responses. CONCLUSIONS: (1) Atrial compartment operation does not impair sinus node function in most cases. (2) Elimination of atrial fibrillation while maintaining the electrical connection between different atrial compartments is feasible.     

Detection of BK polyomavirus genotypes in healthy and HIV-positive children

BACKGROUND: Atrial flutter is a common arrhythmia which frequently recurs after cardioversion and is relatively difficult to control with antiarrhythmic agents. AIMS: To evaluate the success rate, recurrence rate and safety of radiofrequency, (RF) ablation for atrial flutter in a consecutive series of patients with drug refractory chronic or paroxysmal forms of the arrhythmia. METHODS: Electrophysiologic evaluation of atrial flutter included activation mapping with a 20 electrode halo catheter placed around the tricuspid annulus and entrainment mapping from within the low right atrial isthmus. After confirmation of the arrhythmia mechanism with these techniques, an anatomic approach was used to create a linear lesion between the inferior tricuspid annulus and the eustachian ridge at the anterior margin of the inferior vena cava. In order to demonstrate successful ablation, mapping techniques were employed to show that bi-directional conduction block was present in the low right atrial isthmus. RESULTS: Successful ablation was achieved in 26/27 patients (96%). In one patient with a grossly enlarged right atrium, isthmus block could not be achieved. Of the 26 patients with successful ablation, there has been one recurrence of typical flutter (4%) during a mean follow-up period of 5.5 +/- 2.7 months. This patient underwent a successful repeat ablation procedure. Of eight patients with documented clinical atrial fibrillation (in addition to atrial flutter) prior to the procedure, five continued to have atrial fibrillation following the ablation. There were no procedural complications and all patients had normal AV conduction at the completion of the ablation. CONCLUSIONS: RF ablation is a highly effective and safe procedure for cure of atrial flutter. In patients with chronic or recurrent forms of atrial flutter RF ablation should be considered as a first line therapeutic option.     

Circus movement in rabbit atrial muscle as a mechanism of tachycardia. II. The role of nonuniform recovery of excitability in the occurrence of unidirectional block, as studied with multiple microelectrodes

Periods of tachycardia were induced in isolated segments (15 X 15 mm) of rabbit left atrium by local application of a properly timed premature stimulus. We used a special device for multiple synchronous microelectrode recordings of responses of more than 100 fibers during the initiation of tachycardia. We clearly demonstrated circus movement of the impulse through a small area of atrial muscle as the underlying mechanism. The premature impulse was conducted antegrade in only one direction, whereas in the other directions antegrade conduction failed. The local responses of the fibers in the blocked area served as a temporary obstacle for return of the premature impulse. When these fibers recovered their excitability before extinction of the premature impulse, they were reentered in a retrograde direction, and the impulse traveled in a circular route. During the propagation of a premature beat, local block, which set the stage for circus movement, was caused by nonuniform recovery of excitability of the atrium. We related the spread of activation of a premature impulse to the naturally occurring spatial dispersion in refractory periods and found that local conduction block invariably was associated with an area of delayed restoration of excitability. Artificial induction of differences in refractory periods by regional application of carbamylcholine made it clear that a disparity in refractory periods of only 11-6 msec between adjacent areas may be sufficient to cause local conduction block of a properly timed premature impulse.     

Laparoscopic assisted spine surgery

A neonate presented with atrial flutter complicating acute Coxsackie B2 myocarditis. The tachyarrhythmia was successfully terminated with electrocardioversion followed by digoxin administration. The infant survived with no long-term cardiac sequelae. Atrial flutter is an unusual complication of Coxsackie myocarditis that has not previously been reported.     

Neurohumoral and hemodynamic mechanisms of diuresis during atrioventricular nodal reentrant tachycardia

Thirty-two consecutive patients with paroxysmal supraventricular tachycardias, with previously defined mechanisms of the tachycardias, were interviewed by noninvestigators about whether they experienced symptoms of diuresis during or at the termination of the tachycardias, to test the hypothesis that patients with AV nodal reentrant tachycardia would have a feeling of diuresis, polyuria, or both during or at the termination of the tachycardia. Twelve of the 13 patients with AV nodal reentrant tachycardia (92%), two of the 15 patients with AV reentrant tachycardia (13%), and one of the 4 patients with atrial flutter associated with 2:1 AV conduction (25%) felt diuresis during or at the termination of the tachycardias (AV nodal reentrant tachycardia vs other forms of tachycardia; P < 0.001). In 14 of the 32 patients, the right atrial pressure and plasma atrial natriuretic peptide (ANP) concentration were measured during both the tachycardias and sinus rhythm. The mean right atrial pressure during AV nodal reentrant tachycardia was significantly elevated compared to that during other forms of tachycardia (P < 0.01). The plasma ANP concentration during AV nodal reentrant tachycardia was also elevated significantly compared to that during other forms of tachycardias (P < 0.001). There were no significant differences in the cycle lengths of the tachycardias, age, left atrial dimensions, or the left ventricular ejection fraction between the AV nodal reentrant tachycardia and the other forms of tachycardia. We concluded that the feeling of diuresis during or at the termination of tachycardia was a more common symptom in patients with AV nodal reentrant tachycardia. The higher secretion of plasma ANP from the right atrium might be involved in the mechanism of this symptom.     

Induction of atrioventricular node reentrant tachycardia with adenosine: differential effect of adenosine on fast and slow atrioventricular node pathways

OBJECTIVES: This study sought to evaluate the sensitivity of fast and slow atrioventricular (AV) node pathways to incremental doses of adenosine in patients with typical AV node reentrant tachycardia. BACKGROUND: Although adenosine is known to depress conduction through the AV node, the relative sensitivity to adenosine of the anterograde fast and slow pathways in patients with dual AV node pathways and typical AV node reentrant tachycardia has not previously been studied. METHODS: Sixteen patients with dual AV node physiology and typical AV node reentrant tachycardia and 10 control patients were given incremental doses of adenosine during atrial pacing. RESULTS: In 14 of 16 patients with dual-AV node physiology, administration of small doses of adenosine during atrial pacing led consistently to transient block of impulse conduction in the fast pathway before block in the slow pathway, resulting in abrupt prolongation of the AH interval with continued 1:1 AV conduction. The mean (+/- SD) doses of adenosine required to cause conduction block in the fast and slow pathways were 2.7 +/- 3.0 and 7.2 +/- 4.7 mg, respectively (p = 0.004). In 9 of 16 patients, administration of low dose adenosine led to initiation of AV node reentrant tachycardia. The control patients showed no abrupt increases in AH interval with administration of adenosine during atrial pacing. CONCLUSIONS: In most patients with dual AV node pathways and typical AV node reentrant tachycardia, the fast pathway is more sensitive than the slow pathway to the effects of adenosine.     

Coronary sinus pacing initiates counterclockwise atrial flutter while pacing from the low lateral right atrium initiates clockwise atrial flutter. Analysis of episodes of direct initiation of atrial flutter

INTRODUCTION: Rapid atrial pacing in sinus rhythm may directly induce atrial flutter without provoking intervening atrial fibrillation, or initiate atrial flutter indirectly, by a conversion from an episode of transient atrial fibrillation provoked by rapid atrial pacing. The present study was performed to examine whether or not the direct induction of clockwise or counterclockwise atrial flutter was pacing-site (right or left atrium) dependent. METHODS AND RESULTS: We analyzed the mode of direct induction of atrial flutter by rapid atrial pacing. In 46 patients with a history of atrial flutter, rapid atrial pacing with 3 to 20 stimuli (cycle length = 500 - 170 ms) was performed in sinus rhythm to induce atrial flutter from 3 atrial sites, including the high right atrium, the low lateral right atrium, and the proximal coronary sinus, while recording multiple intracardiac electrograms of the atria. Direct induction of atrial flutter by rapid atrial pacing was a rare phenomenon and was documented only 22 times in 15 patients: 3, 11, and 8 times during stimulation, respectively, from the high right atrium, low lateral right atrium, and the proximal coronary sinus. Counterclockwise atrial flutter (12 times) was more frequently induced with stimulation from the proximal coronary sinus than from the low lateral right atrium (8 vs 1, P = .0001); clockwise atrial flutter (10 times) was induced exclusively from the low lateral right atrium (P = .0001 for low lateral right atrium vs proximal coronary sinus, P = .011 for low lateral right atrium vs high right atrium). CONCLUSIONS: Direct induction of either counterclockwise or clockwise atrial flutter was definitively pacing-site dependent; low lateral right atrial pacing induced clockwise, while proximal coronary sinus pacing induced counterclockwise atrial flutter. Anatomic correlation between the flutter circuit and the atrial pacing site may play an important role in the inducibility of counterclockwise or clockwise atrial flutter.     

Radiofrequency catheter ablation in patients with common atrial flutter

BACKGROUND: Type 1 atrial flutter is produced by a reentry circuit located in the right atrium that can be interrupted applying radiofrequency in the inferior cava-tricuspid valve isthmus. AIM: To report our experience in the treatment of atrial flutter with radiofrequency ablation. PATIENTS AND METHODS: Nine patients (eight male) whose ages ranged from 6 to 72 years old were studied. Two patients had an operated congenital cardiopathy, two had high blood pressure, one was subjected previously to radiofrequency ablation due to a left paraspecific pathway, one developed a cardiac failure secondary to tachycardia and three did not have evidences of cardiopathy. RESULTS: In two patients, atrial flutter was not interrupted. In the other seven patients, radiofrequency ablation was successful. There were three relapses in the first month after the procedure, of these, two patients were successfully treated again. After a mean follow up of 4.5 months, these patients are asymptomatic and without antiarrhythmic drugs. Analysis of obtained signals, showed that radiofrequency that interrupted atrial flutter always occurred in zones of double potentials. CONCLUSIONS: Radiofrequency ablation is an effective treatment for atrial flutter and the zone of successful ablation is associated to the presence of double atrial potentials.     

Mechanisms and medical management of patients with atrial flutter

Type I atrial flutter is due to reentrant excitation, principally in the right atrium. The standard ECG remains the cornerstone for its clinical diagnosis. Acute treatment should be directed at control of the ventricular response rate and, if possible, restoration of sinus rhythm. Radiofrequency catheter ablation therapy provides the best hope of cure, although atrial fibrillation may subsequently occur after an ostensibly successful ablative procedure. Alternatively, antiarrhythmic drug therapy to suppress recurrent atrial flutter episodes may be useful, recognizing that occasional recurrences are common despite therapy. Radiofrequency ablation of the His bundle ablation with placement of an appropriate pacemaker system may be useful in selected patients.     

Atrial macroreentry involving the myocardium of the coronary sinus: a unique mechanism for atypical flutter

Atrial flutter involving either clockwise or counterclockwise rotation around the tricuspid annulus utilizing the subeustachian isthmus has been well described. However, macroreentrant atrial circuits in atypical atrial flutter in patients who have not undergone previous surgery or without atrial disease are not well defined. We describe a patient without structural heart disease who presented with an atrial macroreentrant rhythm. Entrainment mapping demonstrated a critical isthmus within the coronary sinus. Activation mapping demonstrated double potential throughout the length of the coronary sinus with disparate activation sequences. A circuit involving the myocardium of the coronary sinus, exiting in the lateral left atrium, down the interatrial septum, and reentering into the coronary sinus was identified. Successful ablation of the rhythm was accomplished by a circumferential radiofrequency application within the coronary sinus.     

Novel form of atrial tachycardia originating at the atrioventricular annulus

We report two patients with reentrant atrial tachycardia that originated at the AV annulus. Atrial tachycardia originated in the posterior portion of mitral annulus in one patient (case 1) and the posterolateral portion of tricuspid annulus in one patient (case 2). Tachycardia was successfully eliminated by RF catheter ablation in both patients, with the catheter placed underneath the mitral valve in case 1 and on the tricuspid annulus in case 2. Spiky potentials were recorded in the diastolic phase of the atrium during tachycardia at the sites of successful ablation. Spiky potentials were also recorded after atrial electrogram during sinus rhythm, and showed decremental properties during atrial pacing. An accelerated atrial rhythm was observed during RF application, and tachycardia could not be induced after ablation in either patient. Tachycardia in these patients seemed to be due to reentrant tachycardia originating in the accessory AV node (Mahaim fiber) without ventricular connection.     

Characterization of the excitable gap in human type I atrial flutter

OBJECTIVES: We sought to characterize the excitable gap of the reentrant circuit in atrial flutter. BACKGROUND: The electrophysiologic substrate of typical atrial flutter has not been well characterized. Specifically, it is not known whether the properties of the tricuspid valve isthmus differ from those of the remainder of the circuit. METHODS: Resetting was performed from two sites within the circuit: proximal (site A) and distal (site B) to the isthmus in 14 patients with type I atrial flutter. Resetting response patterns and the location where interval-dependent conduction slowing occurred were assessed. RESULTS: Some duration of a flat resetting response (mean +/- SD 40.1 +/- 20.9 ms, 16 +/- 8% of the cycle length) was observed in 13 of 14 patients; 1 patient had a purely increasing response. During the increasing portion of the resetting curve, interval-dependent conduction delay most commonly occurred in the isthmus. In most cases, the resetting response was similar at both sites. In three patients, the resetting response differed significantly between the two sites; this finding suggests that paced beats may transiently change conduction within the circuit or the circuit path, or both. CONCLUSIONS: Some duration of a flat resetting response was observed in most cases of type I atrial flutter, signifying a fully excitable gap in all portions of the circuit. The isthmus represents the portion of the circuit most vulnerable to interval-dependent conduction delay at short coupling intervals.     

Radiofrequency catheter ablation in type I atrial flutter: preliminary experience of 10 cases

Common atrial flutter results from macroreentry in the right atrium. Catheter ablation of slow conduction, between tricuspid annulus and inferior vena cava (TA-IVC) or tricuspid annulus and coronary sinus ostium (TA-CS os) has been reported to terminate and prevent recurrence of this arrhythmia. We reported 10 consecutive patients, 7 men and 3 women, who underwent radiofrequency catheter ablation of common atrial flutter. The mean age was 59.4 +/- 11.2 years (range 42-82 years). During the paroxysmal atrial flutter, all patients had palpitation, 4 had dyspnea on exertion, 3 patients had syncope and 1 patient had presyncope. The mean duration of symptoms was 5.7 +/- 4.9 years (range 0.5-13 years). Two patients had dilated cardiomyopathy, 1 Ebstein's anomaly and 1 chronic obstructive pulmonary disease. Four patients (40%) had history of atrial fibrillation (AF) before ablation. The mean cycle length of atrial rhythm was 257.2 +/- 36.6 ms. Ablation was done by anatomical approach and could terminate arrhythmia in 9 patients (90%), 7 from TA-IVC, 2 from TA-CS os without major complication. The mean number of applications was 20.4 +/- 16.9 and turned atrial flutter to normal sinus rhythm in 13.5 +/- 10.7 seconds. Fluoroscopic and procedure times were 38.4 +/- 31.4 and 157.2 +/- 68.8 minutes, respectively. During the follow-up period of 24.0 +/- 28.7 weeks, 2 patients had recurrent atrial arrhythmia, 1 atrial fibrillation and 1 atrial flutter type I, giving the final success rate of 70 per cent. All patients who had recurrence or failure had a history of paroxysmal AF before ablation. In conclusion, radiofrequency catheter ablation in atrial flutter type I, using anatomical approach, is an effective treatment to terminate and prevent this arrhythmia in short term follow-up. It may be considered as an alternative treatment in patients with atrial flutter who were refractory to antiarrhythmic agents.