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.     

Atrial flutter. I. Electrophysiologic substrates and modes of initiation and termination

Forty-one of 525 consecutively studied patients had sustained (2 or more minutes) atrial flutter in response to programmed atrial simulation. Of these 41 patients, 31 had previously documented spontaneous atrial flutter or fibrillation, or both, and 10 had paroxysmal palpitations without documentation of the cause. Programmed atrial stimulation and atrial endocardial mapping were used to analyze the substrate of atrial conduction as well as the mode of initiation and termination of flutter. Atrial conduction defects were present in 36 of the 41 patients. Atrial flutter was induced by one or two atrial extrastimuli in 31 patients. In most of these patients the onset of flutter was characterized by a brief period of irregular atrial activity in one or more intracardial leads. Stimulation from the high right atrium was more successful (29 of 31 patients) than that from the coronary sinus (6 of 12 patients). Rapid atrial pacing at cycle lengths of 350 to 200 ms initiated flutter in 29 of 35 patients in whom it was attempted (in 27 of 35 from the high right atrium and in 10 of 18 from the coronary sinus). Termination of flutter was accomplished by rapid pacing in 34 patients at cycle lengths 20 to 55 ms less than the flutter cycle length. Failure to terminate flutter was associated with local areas of atrial fibrillation in one or more intracardiac leads.     

Use of procainamide with rapid atrial pacing for successful conversion of atrial flutter to sinus rhythm

Rapid atrial pacing is a useful technique and often the therapy of choice to terminate atrial flutter in patients. However, interruption of atrial flutter by rapid atrial pacing may not always produce sinus rhythm, but rather may result in atrial fibrillation. Twelve patients with spontaneous atrial flutter that had been present for greater than 24 h were studied to assess the efficacy of atrial pacing, alone and in combination with procainamide, to convert atrial flutter to normal sinus rhythm. Rapid atrial pacing for greater than or equal to 15 s from selected atrial sites at selected pacing rates were performed during atrial flutter. The initial pacing rate was always at a cycle length 10 ms shorter than the atrial flutter cycle length. If atrial flutter persisted after cessation of pacing, it was repeated at progressively shorter cycle lengths until either a rate of 400 beats/min was achieved or atrial fibrillation was induced. In two patients, atrial flutter was converted to sinus rhythm with pacing alone. Three patients developed sustained atrial fibrillation as a result of the rapid atrial pacing, this rhythm ultimately reverting back to atrial flutter in two. Ten patients received procainamide and 9 of the 10 had lengthening of the atrial flutter cycle length by a mean of 68 ms (1 patient continued to have atrial fibrillation). Then, using the same atrial pacing protocol, high right atrial pacing alone at a mean cycle length of 227 ms interrupted atrial flutter in all these patients, returning their rhythm to sinus rhythm. It is concluded that intravenous procainamide effectively augments the efficacy of rapid atrial pacing to convert atrial flutter to sinus rhythm.     

Effects of High-Frequency Atrial Pacing in Atypical Atrial Flutter and Atrial Fibrillation

Atypical atrial flutter has, hitherto, been relatively refractory totermination by rapid atrial pacing. High-frequency pacing (HFP) in theatrium, for termination of atrial flutter or atrial fibrillation (AF), andthe electrophysiologic effects related to it have not been examined. Weexamined the clinical efficacy, safety, and electrophysiologic mechanisms ofHFP using 50-Hz bursts at 10 mA applied at the high right atrium in patientswith atypical atrial flutter (group 1) or AF (group 2), using a prospectiverandomized study protocol. Four burst durations (500, 1000, 2000, and 4000ms) were applied at the high right atrium repetitively in random sequence in22 patients with spontaneous atrial flutter or AF. Local and distant rightand left atrial electrogram recordings were analyzed during and after HFP.HFP resulted in local and distant right and left atrial electrogramacceleration in 8 of 10 patients (80%) in group 1 but caused lessfrequent local atrial electrogram acceleration (6 of 12 patients) and nodistant atrial electrogram effects in group 2 (p < .05 versus group 1).The HFP protocol was effective in arrhythmia termination in 6 of 10patients in group 1 but in no patient in group 2 (p < .05 versus group1). Standard HFP protocol applied at the high right atrium can frequentlyalter atrial activation in both atria and can terminate atypical atrialflutter. Efficacy in AF is limited, probably due to limitedelectrophysiologic actions beyond the local pacing site.     

Response of atrial flutter to overdrive atrial pacing and intravenous disopyramide phosphate, singly and in combination.

Ten patients who suffered spontaneous paroxysms of atrial flutter were investigated by electrophysiological techniques. Two had overt Wolff-Parkinson-White syndrome; three Lown-Ganong-Levine syndrome; and one a concealed accessory atrioventricular connection. Atrial flutter was initiated, at study, by right atrial pacing and electrograms from the right atrium and coronary sinus were observed for at least five minutes to ensure stable flutter in both atria. Atrial flutter was terminated by 2.5 s or 5 s bursts of atrial pacing at rates 10, 50, or 100 beats/min faster than the intrinsic flutter rate in only two patients. Atrial flutter, which was reinitiated in two patients, was then treated with intravenous disopyramide phosphate, 2 mg/kg body weight, infused over five minutes. In all 10 patients the atrial rate slowed from a mean of 310 +/- 39 beats/min to 217 +/- 27 beats/min and atrial flutter terminated in one case. Though the mean ventricular rate fell from 161 +/- 52 beats/min to 156 +/- 45 beats/min the atrioventricular conduction ratio fell from 2.17 +/- 0.86 to 1.55 +/- 0.59 and four patients were left with symptomatically significant increases of ventricular rate. In seven of nine patients overdrive atrial pacing, repeated after disopryamide, resulted in the conversion of atrial flutter to sinus rhythm. In this study, overdrive atrial pacing and intravenous disopyramide, singly and in combination, terminated atrial flutter in nine of the 10 patients and it is suggested that this method may provide an effective alternative to direct current cardioversion.     

One to one atrioventricular conduction during atrial pacing at rates of 300/minute in absence of wolff-parkinson-white syndrome

One to one atrioventricular (A-V) or atrio-His bundle (A-H) conduction occurred during right atrial pacing at rates of 300/min in two patients with short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias. Patient 1 had episodes of reciprocating A-V tachycardia and of atrial fibrillation with very fast rates (270 to 290/min) that were slowed to 100 to 135/min after administration of intravenous verapamil. Enhanced A-V (A-H) conduction was exposed only during stimulation from the high right atrium, but not from the low lateral right atrium or coronary sinus. Patient 2 had episodes of atrial flutter with 1:1 A-V conduction and rates of 290/min. The H-V interval was short (25 ms) during sinus rhythm and atrial pacing presumably because conduction occurred through an atrio-“distal” His bundle (atriofascicular) tract. In contrast, the H-V interval was normal (40 ms) in echo beats or when the “proximal” His bundle was stimulated.In these two patients, having as “common denominators” short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias, enhanced A-V (A-H) conduction was (1) possibly due to different electrogenetic mechanisms; (2) pacing-site dependent; (3) manifested, during atrial fibrillation and atrial flutter, by extremely fast ventricular rates; and (4) unrelated to the rate of reciprocating A-V tachycardias because the latter was predominantly a function of anterograde conduction through the “slow” nodal pathway.     

Predictors of failure of transoesophageal cardioversion of common atrial flutter.

BACKGROUND: Common atrial flutter is due to a re-entry circuit in the right atrium. It is possible to entrain and interrupt this arrhythmia with transoesophageal pacing (TEAP) in a substantial percentage of patients. The aim of this study is to evaluate factors associated with failure of transoesophageal cardioversion of common atrial flutter. METHODS: One hundred consecutive patients underwent an attempted transoesophageal cardioversion of their common atrial flutter. In order to detect factors associated with failure of this procedure, the following were considered: (a) age and gender; (b) underlying heart disease; (c) time of onset of the arrhythmia; (d) antiarrhythmic treatment at the time of cardioversion; (e) flutter cycle length, (f) A/V deflection ratio at the site of transoesophageal pacing; and (g) longitudinal and transverse diameters of right and left atrium on the echocardiogram. RESULTS: In 84 of 100 patients, TEAP modified the atrial flutter circuit: in 23 of these, sinus rhythm was restored; in 31 patients, flutter was converted into atrial fibrillation which spontaneously reverted to sinus rhythm; and in remaining 30 patients, persistent atrial fibrillation was obtained. In 16 cases, no modification in atrial flutter circuit was obtained by TEAP (Group 2). Using univariate analysis, this group of patients showed no significant difference in flutter cycle length, a smaller A/V ratio at the site of TEAP, a longer transverse diameter of left atrium and a shorter transverse diameter of right atrium. Analysis of the therapy at cardioversion shows that no Group 2 patients was on intravenous amiodarone, while a greater percentage of patients of the former group was on chronic amiodarone treatment. A logistic regression model applied to the data showed that flutter cycle length, transverse diameter of left atrium and A/V deflection ratio at the site of TEAP were independent variables with influence on the failure rate. CONCLUSION: Transoesophageal pacing is able to modify the circuit of common atrial flutter in a large percentage of patients, and can convert this arrhythmia to sinus rhythm in more than 50% of cases. Failure of this procedure is associated with electrophysiological parameters (flutter cycle length, A/V ratio at the site of TEAP), anatomical factors (left and right atrial diameters) and treatment in use at the time of TEAP.     

Simultaneous occurrence of atrial fibrillation and atrial flutter

INTRODUCTION: Early reports suggested that some patients with "atrial fibrillation/flutter" might have atrial fibrillation in one atrium and atrial flutter in the other. However, more recent conceptions of atrial fibrillation/flutter postulate that the pattern is due to a relatively organized (type I) form of atrial fibrillation. We report the occurrence and ECG manifestations of simultaneous atrial fibrillation and flutter in patients undergoing attempted catheter ablation of atrial flutter. METHODS AND RESULTS: In patients undergoing radiofrequency ablation for atrial flutter, an attempt was made to entrain atrial flutter by pacing in the right atrium. The arrhythmias observed occurred following attempts at entrainment, or spontaneously in one case. Twelve transient episodes of simultaneous atrial fibrillation and flutter were observed in five patients. The atrial fibrillation was localized to all or a portion of one atrium, during which the other atrium maintained atrial flutter. In each case, the surface 12-lead ECG reflected the right atrial activation pattern. No patients had interatrial or intra-atrial conduction block during sinus rhythm, suggesting functional intra-atrial block as a mechanism for simultaneous atrial fibrillation/flutter. CONCLUSION: In certain patients, the occurrence of transient, simultaneous atrial fibrillation and flutter is possible. In contrast to prior studies in which it was suggested that left atrial or septal activation determines P wave morphology, the results of the present study show that P wave morphology is determined by right atrial activation. Functional interatrial block appears to be a likely mechanism for this phenomenon.     

右房峡部传导特性与心房扑动诱发的关系

在 10例室上性心动过速消融后及 2例窦性心动过缓心脏电生理检查中 ,依次进行低侧右房和冠状静脉窦口刺激 ,检出右房峡部双向阻滞 6例、双向传导 2例、单向阻滞 4例。在 3例峡部逆钟向阻滞者 ,低侧右房刺激诱发出短阵顺钟向心房扑动 (简称房扑 ) ;在 1例峡部顺钟向阻滞者 ,冠状静脉窦口刺激诱发出短阵逆钟向房扑。提示在无临床房扑史但有右房峡部单向阻滞者 ,可诱发短阵房扑 ,诱发房扑的类型与峡部阻滞方向及刺激位点有关。     

Further observations on entrainment of atrial flutter in the dog

To determine whether the first postpacing interval after entrainment was affected by recording and pacing sites, overdrive atrial pacing was undertaken in 13 episodes of atrial flutter with a mean flutter cycle length (FCL) of 140 +/- 8 msec induced in seven dogs. Atrial flutter was induced by means of an anatomic obstacle. Seven recording sites, four in the right atrium and three in the left atrium, and three pacing sites, two in the right atrium and one in the left atrium, were selected. After entrainment from the right atrium at pacing cycle lengths that were 94% of the FCL, the first postpacing interval was not significantly different from the intrinsic FCL at each recording site, but it tended to be shorter than the FCL at the recording sites near pacing sites. For entrainment from the left atrium, the first postpacing interval was longer than the FCL at recording sites in the left atrium (p less than 0.001), but it was not different from the FCL at recording sites in the right atrium. These results are due to differences in placement of recording and pacing electrodes relative to the reentrant circuit. Also we observed that activation sequences involving three appropriately selected recording sites were always identical when paced from two different pacing sites at a single constant pacing cycle length. This new phenomenon may best be explained by postulating reentry as the mechanism for atrial flutter.     

Bi-atrial mapping of atrial arrhythmias

Cardiac mapping of atrial activation was originally performed in animals during open chest preparations, using epicardial electrodes. The development of endocardial egg-shaped multiple electrodes provided detailed assessment of the minimum number of wavelengths required to sustain atrial fibrillation (AF), as well as the role of interatrial connections during AF. Subsequently, several studies on bi-atrial epicardial high-density mapping in animals and humans also reported on the importance of interatrial connections, as well as the specific characteristics of the left atrium as compared with the right atrium during chronic AF. Endocardial bi-atrial mapping studies using electrode catheters were reported using basket-shaped catheters carrying 64 electrodes. Animal studies suggested that septal activation was asynchronous and discordant, while a human study outlined the multiple origins of atrial ectopic beats following DC cardioversion in patients with chronic atrial fibrillation. The advent of non-fluoroscopic mapping systems significantly changed our approach to percutaneous endocardial mapping. Simultaneous bi-atrial studies using electroanatomic mapping were performed in sinus rhythm as well as in atrial flutter. These studies demonstrated the predominance of interatrial conduction over Bachmann's Bundle and the coronary sinus-left atrial connection during respectively, sinus rhythm and atrial flutter. Simultaneous bi-atrial non-contact mapping was initially performed during porcine studies and later in humans, demonstrating asynchronous and discordant septal activation both during sinus rhythm or left lateral atrial pacing. Preliminary studies from simultaneous bi-atrial non-contact mapping in humans in whom AF occurred spontaneously or was induced suggests three main types of atrial activation, consisting of left atrial drivers causing the right atrium to fibrillate following conduction over interatrial connections, the right atrium independently sustaining AF, even after pulmonary vein disconnection, and both atria fibrillating independently without activation over interatrial connections. Bi-atrial mapping has been essential for our understanding of normal and abnormal atrial activation, and ultimately may provide new approaches for ablation of atrial fibrillation.     

Electrophysiological and clinical characterization of left atrial macroreentrant tachycardia]

BACKGROUND AND OBJECTIVE: We are reporting the characteristics of 9 patients with left atrial macroreentrant tachycardia, an arrhythmia not well studied in man. PATIENTS AND METHOD: Mean age was 60 years and 7 were men. Tachycardia was spontaneous in 6 and induced in 3. Two had no heart disease, 2 sick sinus syndrome, 3 aortic prosthesis, 2 hypertension, 1 cardiomyopathy and 1 chronic bronchitis. Simultaneous recordings from right atrial, coronary sinus and right pulmonary artery were obtained at baseline and with atrial pacing. Macroreentrant tachycardia was diagnosed when entrainment with fusion was documented. RESULTS: Cycle length was 230-440 ms (287 67). The ECG showed atypical flutter in 3 patients and P waves with flat baseline in 6. Coronary sinus activation was distal to proximal in 7. Right atrial activation was circular in 3 with previous typical flutter ablation. Entrainment from the right atrium produced long return cycles in the right atrial recordings, but equal to basal tachycardic cycle in coronary sinus recordings. Entrainment from the coronary sinus produced local return cycles equal to basal cycle in 8 and prolonged in 1. After stimulation, 4 recovered sinus rhythm, 4 went to atrial fibrillation and 1 had no change. After a follow-up of 9-19 months 5 remain in sinus rhythm treated with antiarrhythmic drugs and/or atrial pacing. CONCLUSIONS: Left atrial macroreentrant tachycardia is associated with organic heart disease. The ECG most frequent pattern tends to show P waves with flat baseline at a relatively slow rate. Most circuits turn clockwise in anterior view. Atrial stimulation is not very effective for cardioversion to sinus rhythm. The prognosis of long term rhythm is uncertain.     

Atrial fibrillation and atrial enlargement in patients with mitral stenosis

The present study was designed to assess the relative contribution of atrial fibrillation and left atrial pressure to changes in the size of the left and right atria in patients with mitral stenosis. The study included 155 subjects, 102 of whom underwent prospective echocardiography and Doppler cardiography, and 69 of whom underwent cardiac catheterization. The size of the atria was determined by two-dimensional echocardiography. There were no significant hemodynamic differences between patients with mitral stenosis who were in either sinus rhythm or atrial fibrillation. The left atrium was larger (p less than 0.001) in patients with mitral stenosis and atrial fibrillation (37.6 +/- 10.8 cm2) than in patients in sinus rhythm (27.8 +/- 7.7 cm2) or normal subjects (15 +/- 3.3 cm2). The size of the right atrium was larger (p less than 0.001) in patients with mitral stenosis and atrial fibrillation (21.7 +/- 5.2 cm2) than in patients in sinus rhythm (13.4 +/- 3.9 cm2) or normal subjects (13.8 +/- 3.7 cm2). Multiple regression analysis showed that the severity of mitral stenosis accounted for 38%, age for 7%, and atrial fibrillation for 11% of the change in the size of the left atrium. Atrial fibrillation accounted for 24%, age for 11, and mitral valve area for 3% of the change in the size of the right atrium. The analysis suggests that the onset of left atrial dilatation in mitral stenosis is the result of an early increase in left atrial pressure. Atrial fibrillation, which develops irrespective of the severity of the mitral stenosis, contributes to a further enlargement of the left and right atria.     

Transesophageal stimulation in the treatment of atrial flutter and tachysystole

Transoesophageal left atrial pacing was used to reduce 102 episodes of ectopic atrial rhythms (79 common flutters and 23 ectopic tachycardias) in 83 patients (64 men, 19 women) aged 33 to 85 years (average 61 years). Overdrive pacing, at a faster rate than that of the spontaneous rhythm, was delivered via a bipolar pacing catheter introduced nasally and positioned behind the atrium under fluoroscopic and/or electrocardiographic control. Long pulse durations (up to 20 ms) were used to capture the atria with intensities of less than 20 mA for better tolerance. The overall results were: a) conversion to sinus rhythm in 60.8 p. 100 of cases (47 p. 100 directly and 13.8 p. 100 after transient atrial fibrillation), b) atrial fibrillation lasting over 24 hours in 7.8 p. 100 of cases, c) failure (31.4 p. 100) due to non-capture or intolerance (20.6 p. 100) or recurrence of the arrhythmia after transient atrial fibrillation (10.8 p. 100). Atrial flutter is more accessible to pacing than tachycardia (restoration of sinus rhythm in 63.3 p. 100 and 52.2 p. 100, respectively). Arrhythmias in the postoperative period of cardiac surgery, and isolated and recent arrhythmias were more easily converted. Prior antiarrhythmic therapy did not seem to improve results. Fifty per cent of failures of oesophageal pacing were converted to sinus rhythm by endocavitary pacing. These results show that atrial flutter or tachycardia may be successfully treated by oesophageal pacing in over 50 p. 100 of cases without having to use other forms of electrotherapy (endocavitary pacing or cardioversion).     

射频消融心房扑动拖带刺激的电生理特征

探讨射频消融心房扑动 (简称房扑 )拖带刺激的电生理特征 ,更好的理解房扑机制 ,以期提高消融成功率、减少复发率。 5例阵发性典型房扑患者 ,诱发房扑后 ,在高位、低位右房 ,冠状窦口 (CSO)及右房下部的峡部分别进行拖带刺激 ,分析心房激动顺序 ,然后进行三尖瓣环至下腔静脉之间的线性消融。 5例房扑折返环均为逆钟向旋转 ,峡部 ,高位、低位右房及CSO呈现隐匿拖带 ,左房和卵圆窝呈现显性拖带 ,平均放电 9± 6次 ,均达到右房峡部双向阻滞。CSO起搏时体表心电图Ⅱ、Ⅲ、aVF导联P波形态发生改变。结论 :隐匿、显性拖带对判断峡部依赖性逆钟向房扑有较高价值 ,CSO起搏时心内电图激动顺序和体表心电图P波改变可做为判断峡部消融达到双向阻滞的标志     

High-density mapping of left atrial endocardial activation during sinus rhythm and coronary sinus pacing in patients with paroxysmal atrial fibrillation

INTRODUCTION: This study was designed to record global high-density maps of left atrial endocardial activation during sinus rhythm and coronary sinus pacing. METHOD AND RESULTS: Noncontact mapping of the left atrium was performed in nine patients with paroxysmal atrial fibrillation undergoing pulmonary vein ablation procedures. High-density isopotential and isochronal activation maps were superimposed on three-dimensional reconstructions of left atrial geometry. Mapping was repeated during pacing from sites within the coronary sinus. Earliest left atrial endocardial activation occurred anterior to the right pulmonary veins in seven patients and on the anterosuperior septum in two patients. A line of conduction block was seen in the posterior wall and inferior septum in all patients. The direction of activation in the left atrial myocardium overlying the coronary sinus was different from the electrogram sequence in the coronary sinus catheter in 6 of 9 patients. During coronary sinus pacing, activation entered the left atrium a mean (SD) of 41 (13) ms after the pacing stimulus at a site 12 (10) mm from the endocardium overlying the pacing electrode. Lines of conduction block were present in the posterior wall and inferior septum. CONCLUSION: In patients with paroxysmal atrial fibrillation, lines of conduction block are present in the left atrium during sinus rhythm and coronary sinus pacing. Electrograms recorded in the coronary sinus infrequently correspond to the direction of activation in the overlying left atrial myocardium.     

Characterization of double potentials in human atrial flutter: studies during transient entrainment

Double potentials, defined as atrial electrograms with two discrete deflections per beat separated by an isoelectric interval or a low amplitude baseline, have been observed during right atrial endocardial mapping of human atrial flutter. In this study, bipolar atrial electrograms were recorded during atrial flutter (mean cycle length 235 +/- 27 ms [+/- SEM]) from the high right atrium, the His bundle region, the coronary sinus and at least 30 right atrial endocardial mapping sites in 10 patients. Double potentials were recorded from the right atrium in all patients during atrial flutter. Double potentials were evaluated during transient entrainment of atrial flutter by rapid high right atrial pacing in 5 of the 10 patients. In four of these five patients during such transient entrainment 1) one deflection of the double potential was captured with a relatively short activation time (mean interval 89 +/- 45 ms) and the other deflection was captured with a relatively long activation time (mean interval 233 +/- 24 ms), producing a paradoxical decrease in the short interdeflection interval from a mean of 75 +/- 20 ms to a mean of 59 +/- 24 ms; and 2) the configuration of the double potential remained similar to that observed during spontaneous atrial flutter. On pacing termination 1) the two double potential deflections were found to be associated with two different atrial flutter complexes in the electrocardiogram (ECG); 2) the previous double potential deflection relation resumed; and 3) when sinus rhythm was present, the double potentials were replaced by a broad, low amplitude electrogram recording at the same site.(ABSTRACT TRUNCATED AT 250 WORDS)     

Activation patterns in experimental canine atrial flutter produced by right atrial crush injury.

OBJECTIVES. This study was designed to localize and characterize the atrial flutter reentrant circuit and the electrophysiologic effects of right atrial crush injury in a new canine model. BACKGROUND. In previous studies sustained atrial flutter was induced in the canine heart by rapid atrial pacing after a linear crush injury was placed in the right atrial free wall. METHODS. Eight dogs (group 1) with three electrode plaques on the right and left atria and Bachmann's bundle and seven dogs (group 2) with a single high density electrode plaque on the right atrium were studied with use of a 64-channel computerized mapping system. RESULTS. At baseline, during sinus rhythm and right and left atrial pacing, activation spread uniformly without areas of slow conduction. Crush injury produced marked conduction delay or complete block during sinus rhythm, increasing the mean difference in activation times across the injury compared with control values (group 1, 31 +/- 4 vs. 14 +/- 5 ms, p less than 0.01; group 2, 28 +/- 10 vs. 7 +/- 2 ms, p less than 0.01). Rapid atrial pacing (S1S1 200 ms) above and below the crush injury revealed a line of complete block across which adjacent electrodes recorded markedly different activation times (33 +/- 5 and 38 +/- 12 ms difference, respectively) and around which activation wave fronts proceeded, colliding opposite the stimulating electrodes. The mean atrial flutter cycle length of 11 episodes induced in group 1 and 14 episodes in group 2 was 157 +/- 16 and 140 +/- 16 ms, respectively (p = NS). Activation mapping revealed a reentrant circuit in the right atrium around the crush injury in all episodes. Although the reentrant circuit did not contain a discrete area of slow conduction, activation time below was longer than that above the crush injury (92 +/- 14 vs. 66 +/- 8 ms and 82 +/- 12 vs. 59 +/- 9 ms in groups 1 and 2, respectively, p less than 0.01 for both). Rapid atrial pacing or premature stimuli produced progressive conduction delay and unidirectional block between the crush injury and the tricuspid anulus, inducing atrial flutter directly in 9 of 25 episodes. In 16 episodes, atrial flutter developed after transient induction of atrial fibrillation. CONCLUSIONS. 1) Atrial flutter in this model is due to reentry in the right atrium; 2) the crush injury functions as an anatomic obstacle around which reentry may occur; and 3) the reentrant circuit does not contain a discrete area of slow conduction but, rather, generally slower conduction below the crush injury.     

Dependence of electrogram duration in right posteroseptal atrium and atrium-pulmonary vein junction on pacing site: mechanism and implications regarding atrioventricular nodal reentrant tachycardia and paroxysmal atrial fibrillation

INTRODUCTION: The fractionated atrial electrogram, a signal helpful in identifying the target site for radiofrequency catheter ablation of the slow AV nodal pathway, is considered to arise from nonuniform anisotropic electrical activity. However, the effects of pacing sites and radiofrequency ablation on these electrograms are not clear. Similarly, the nature of the fractionated atrial electrogram in the atrium-pulmonary vein junction has yet to be determined. METHODS AND RESULTS: Two experiments were performed in this study. Experiment 1 evaluated the fractionated atrial electrogram at target sites before and after slow AV nodal pathway ablation during sinus rhythm or during pacing from different sites. Group 1A consisted of 16 patients with dual AV nodal pathway physiology and AV nodal reentrant tachycardia who underwent successful ablation without residual slow AV nodal pathway. Group 1B consisted of 7 patients who underwent successful elimination of AV nodal reentry but with residual dual AV nodal pathway physiology. Group 1C consisted of 6 patients who still had AV nodal reentrant tachycardia after two applications of radiofrequency energy. In group 1D, there were 16 patients with dual AV nodal pathway physiology, but without inducible AV nodal reentrant tachycardia. In group 1E, there were 15 patients without dual AV nodal pathway physiology. Experiment 2 investigated the fractionated atrial electrogram in the ostium of the left and right superior pulmonary veins in 18 patients with paroxysmal atrial fibrillation (2A) and in 8 patients without paroxysmal atrial fibrillation (2B). Before radiofrequency ablation, electrogram duration in the right posteroseptal atrium during pacing from the middle coronary sinus or the right posterolateral atrium was shorter than that during pacing from the high right atrium (HRA) in all group 1 patients. After the successful elimination of the slow AV nodal pathway conduction in group 1A, atrial electrogram duration during HRA pacing was shorter than that before ablation. In experiment 2 patients, electrogram duration during pacing from the proximal or distal coronary sinus was shorter than that during pacing from HRA or sinus rhythm. CONCLUSION: These findings suggest that the fractionated atrial electrograms in the right posteroseptal atrium and ostium of left or right superior pulmonary veins are potentially consistent with nonuniform anisotropic propagation. Alternations of electrogram characteristics after successful radiofrequency ablation of the slow AV nodal pathway may arise from the changes of nonuniform anisotropic activity in the right posteroseptal atrium.     

不同部位及不同方式心房起搏对心房激动的影响

目的 了解不同部位、不同方式心房起搏时P波、P－R间期以及心房激动顺序的特点，从而寻找最佳的心房单部位起搏方式。方法 对20例射频消融成功后的患者，分别放置高位右房、右心耳、Koch三角、希氏束以及冠状窦电极，若为左侧旁路则加置左心房电极，行不同部位、不同方式心房起搏。结果 Koch三角、Koch三角＋高位右房、左房、双房起膊时P波宽度、P－R间期无差异，但右心耳起搏时各导联P波增宽，P－R间期延长。从心房激动顺序分析，右心耳起搏时，激动传至希氏束区及冠状窦区的时间最长，而Koch三角、Koch三角＋高位右房及双房起搏时则较短，尤其是Koch三角、Koch三角＋高位右房起搏缩短更明显。另外，不同部位、不同方式起搏时右心房压力无差异。结论 Koch三角起搏在某种程度上可替代高位右房＋冠状窦起搏及双房起搏。