Onset of induced atrial flutter in the canine pericarditis model

To test the hypothesis that induced atrial flutter evolves from a transitional rhythm, the onset of 99 episodes of induced atrial flutter (mean cycle length 135 +/- 18 ms) lasting greater than 5 min in 40 dogs with sterile pericarditis was first characterized. In 85 (86%) of the 99 episodes, atrial flutter was preceded by a brief period (mean 1.4 +/- 0.9 s, range 0.4 to 42) of atrial fibrillation. Then, in 11 open chest studies, atrial electrograms were recorded simultaneously from 95 pairs of right atrial electrodes during the onset of 18 episodes of induced atrial flutter (mean cycle length 136 +/- 16 ms). Atrial flutter was induced by a train of eight paced atrial beats, followed by one or two premature atrial beats (7 episodes) or rapid atrial pacing (11 episodes). A short period of atrial fibrillation (mean cycle length 110 +/- 7 ms) induced by atrial pacing activated the right atrium through wave fronts, which produced a localized area of slow conduction. Then unidirectional conduction block of the wave front occurred for one beat in all or a portion of the area of slow conduction. This permitted the unblocked wave front to turn around an area of functional block and return through the area of slow conduction that had developed the unidirectional conduction block, thereby initiating the reentrant circuit. The location of the unidirectional block relative to the direction of the circulating wave fronts determined whether the circus movement was clockwise or counterclockwise. The area of slow conduction and unidirectional conduction block occurred where the wave front crossed perpendicular to the orientation of the atrial muscle fibers, suggesting a role for anisotropic conduction. These areas included the high right atrial portion of the sulcus terminalis (10 episodes), the low right atrial portion of the sulcus terminalis (4 episodes) and the pectinate muscle region (4 episodes). It is concluded that the development of a localized area of slow conduction in the right atrium followed by unidirectional conduction block in this area produced during a short period of atrial fibrillation or rapid atrial pacing is necessary for atrial flutter to occur in this model.     

Multiplexing studies of effects of rapid atrial pacing on the area of slow conduction during atrial flutter in canine pericarditis model

BACKGROUND. We report that rapid atrial pacing interrupts atrial flutter when the orthodromic wave front from the pacing impulse is blocked in an area of slow conduction in the reentry circuit. To characterize the area of slow conduction during atrial flutter and rapid pacing, we studied 11 episodes of induced atrial flutter, mean cycle length 157 +/- 20 msec, in eight dogs with sterile pericarditis. METHODS AND RESULTS. Atrial electrograms were recorded simultaneously from 95 pairs of right atrial electrodes during the interruption of atrial flutter by rapid atrial pacing, mean cycle length 139 +/- 21 msec. Areas of slow conduction during atrial flutter were demonstrated at one to three sites in the reentry circuit. After rapid pacing captured the reentry circuit, one area of slow conduction either disappeared (10 episodes) or the degree of slow conduction in an area of slow conduction decreased (one episode). Both changes were in association with activation of the region by a wave front from the pacing impulse that arrived from a direction different than that during the induced atrial flutter. Interruption of atrial flutter during rapid pacing occurred when the orthodromic wave front from the pacing impulse blocked in an area of slow conduction that had either newly evolved during rapid pacing (seven episodes) or that was previously present (four episodes). CONCLUSIONS. Areas of slow conduction present during atrial flutter and rapid pacing of atrial flutter are functional and depend on both the atrial rate and the direction of the circulating wave fronts. Interruption of atrial flutter by rapid pacing results from block of the orthodromic wave front of the pacing impulse in an area of slow conduction in the reentry circuit.     

Prednisone prevents inducible atrial flutter in the canine sterile pericarditis model

Background: Atrial fibrillation (AF) and atrial flutter (AFL) are common following cardiac surgery and are associated with significant morbidity. We tested the hypothesis that suppression of the inflammatory response with steroids would significantly modify the inducibility of postoperative AF/AFL in the canine sterile pericarditis model.
Methods: Twenty-three dogs were studied daily from creation of pericarditis to the fourth postoperative day: 11 dogs were treated with oral prednisone (PRED) starting 2 days preoperatively until the end of the study; 12 dogs were controls (CON). EP testing was performed daily using epicardial electrodes placed at initial surgery. High-resolution (404 sites) epicardial mapping was performed during the terminal study. Baseline and daily CRP levels were obtained in all dogs.
Results: Sustained AFL was absent in PRED (0%) versus CON dogs (91%; P < 0.001); AF induced in the early postoperative course in PRED dogs was of very short CL (mean 66 ms). Tissue inflammation was significantly attenuated in PRED dogs. Thresholds were lower in PRED versus CON dogs, significantly so on postoperative day (POD) 3. There was a trend toward lower ERPs in the PRED group at all CLs. CRP levels were markedly reduced in PRED versus CON dogs (peak CRP 78 ± 7 mg/L vs 231 ± 21 mg/L, P < 0.001), and returned to baseline in PRED dogs by POD 4, correlating with a virtual absence of sustained arrhythmia. During open chest mapping studies on POD 4, PRED dogs showed only nonsustained AF/AFL.
Conclusions: Prednisone eliminated postoperative AFL, affected all EP parameters studied, and attenuated the inflammatory response associated with pericarditis.     

峡部依赖性心房扑动心房间传导途径及其与心房扑动波的关系

目的探讨峡部依赖性心房扑动（房扑）心房间传导途径及其与心房扑动（FL）波的关系，以及冠状静脉安（CS）和Halo导管激动时间与FL波的对应关系。方法对20例峡部依赖性房扑患者行电生婵柃查，常规放置CS、His、Halo电极导管，观察CS、Halo导管激动顺序及其与FL波在时间上的对应关系。结果4例为顺时针房扑（clockwise—AFL，CW—AFL），其中3例心电图下壁及V6导联FL波以正相为主；16例为逆时针房扑（counterclockwise—AFL，CCW—AFL），其中13例心电图下壁导联h波以负相波为主。CW—AFL患者2例冲动由CS近端向远端传导，2例冲动由CS远、近两端向中部传导；13例CCW—AFL患者冲动由CS近端向远端传导。仅1名（25％）CW—AFL患者CS激动时间对应体表心电图下壁导联FL波的升支，冲动由冠状静脉窦口（CSO）向上传导至右心房前侧壁的时间对应下壁导联FL波降支；13例CCW—AFL患者CS激动时间对应体表心电图下壁导联FL波降支，冲动自右心房前侧壁向CSO传导时问对应下壁导联FL波升支和正相切迹。结论CCW—AFL时冲动主要经CSO传导至左心房，CW—AFL时冲动町经CSO或Bachmann束（BB）传导至左心房。FL波的极性主要取决于心房间传导途径和左心房激动顺序。CCW—AFL时FL波与心房内特定部位激动时间有一定对应关系，但在CW—AFL时这种对应关系并不常见。     

Circus movement atrial flutter in the canine sterile pericarditis model: Relation of characteristics of the surface electrocardiogram and conduction properties of the reentrant pathway

Objectives. This study was designed to elucidate the basis for the electrocardiographic (ECG) appearance of atrial flutter in the canine sterile pericarditis model.Background. During atrial flutter, the surface ECG may show typical F waves or isolated P waves of any polarity.Methods. Electrocardiographic leads II, III and aVF and epicardial atrial activation maps constructed from 127 simultaneously recorded bipolar electrograms were compared in 20 dogs with sterile pericarditis and inducible atrial flutter.Results. In 10 dogs with F wave atrial flutter, single loop reentry occurred around combined functional/anatomic obstacles that included one or both caval veins and a vertically oriented arc of functional conduction block. In 10 dogs with P wave atrial flutter, a merely functional (n = 4) or combined (n = 6) obstacle involving any atrial vessel and more vertically (n = 5) or more horizontally (n = 5) oriented arcs of block was present. The isoelectric interval between P waves corresponded to the conduction time within the slow zone of the reentrant circuit (96 ± 27 vs. 100 ± 24 ms, mean ± SD). Slow conduction accounted for 65 ± 8% of the cycle length in P wave atrial flutter, but for only 29 ± 7% in F wave atrial flutter (p < 0.05). Slow conduction was usually associated with activation of fewer than five epicardial electrodes per 10-ms isochronal interval, reflecting only a small amount of atrial tissue. The polarity of P or F waves was determined by the direction of the major wave front activating the most electrodes per 10-ms isochronal interval, irrespective of whether the right or the left atrium was activated.Conclusions. The F waves result from reentrant activation at a relatively constant speed around a vertically oriented functional/ anatomic obstacle involving one or both caval veins. The P waves occur when the circuit contains a marked area of slow conduction.     

Circus movement atrial flutter in the canine sterile pericarditis model. Differential effects of procainamide on the components of the reentrant pathway

To evaluate the mechanisms of action of procainamide on the components of the reentrant pathway, drug-induced changes in activation patterns, effective refractory periods (ERPs), and stimulation thresholds were analyzed in nine dogs with sterile pericarditis and sustained atrial flutter. Activation maps were based on 127 close bipolar recordings from a special "jacket" electrode. From the control map, 22 +/- 2 sites covering the slow zone and the normal zone of the reentrant circuit were selected to measure ERPs and thresholds. The excitable gap was estimated from the longest ERP during pacing at the tachycardia cycle length. During atrial flutter, epicardial activation proceeded as a single wave around an arc of functional conduction block in the proximity of the atrioventricular (AV) ring or around a combined functional/anatomic obstacle, with the arc being contiguous with one of the venae cavae. An area of slow conduction, which accounted for 53 +/- 15% of the revolution time within 35 +/- 15% of the total length of the reentrant pathway, was bordered by the arc of block and the AV ring or a caval vein and the AV ring, respectively. Procainamide (5-10 mg/kg i.v.) prolonged the cycle length of atrial flutter from 144 +/- 17 to 190 +/- 24 msec (p less than 0.05) and then terminated the arrhythmia in all studies. The increase in cycle length was due to an increase in conduction time in the slow zone by 37 +/- 11 msec (86 +/- 17% of the total cycle length increase). During the last reentrant beat, conduction failed in the slow zone, with the arc of block joining the AV ring. At termination, procainamide had prolonged conduction time, stimulation threshold, and ERP in the normal zone by 11 +/- 18%, 40 +/- 80%, and 5 +/- 15%, respectively, compared with 51 +/- 16%, 86 +/- 93%, and 14 +/- 21%, respectively, in the slow zone (p less than 0.05 for all three parameters). The duration of the excitable gap did not change significantly. We conclude that procainamide preferentially affected the slow zone of single loop reentrant circuits. The drug terminated circus movement atrial flutter without abolishing the excitable gap, and its effect on conduction seemed the major determinant of the antiarrhythmic action.     

Relationship between surface electrocardiogram characteristics and endocardial activation sequence in patients with typical atrial flutter

OBJECTIVES: The relationships that exist between endocardial and surface electrocardiogram (ECG) activity in patients with AFl have not been satisfactorily delineated. The aim of the study was to determine the relationships that exist between the atrial endocardial activity and the surface ECG in patients with atrial flutter (AFl). METHODS: In 40 patients with AFl, a 64-electrode basket catheter (BC) was deployed in the right atrium (RA). A decapolar catheter was inserted into the coronary sinus (CS) to record from the left atrium. The temporal relationship between endocardial and surface ECG activity was determined by means of electronic calipers. RESULTS: In counterclockwise AFl, the activation of the lateral wall of RA coincided with the positive deflections in lead I, V1 and V6 and the upstroke component in inferior leads. Plateau duration in lead III (121 +/- 27 ms) correlated strongly with isthmus conduction time (117 +/- 23 ms) (r = 0.91). Septal and left atrial conduction coincided with negative components in lead I, inferior leads and V6 and positive deflections in leads aVL and V1. In clockwise AFl, the F wave was notched in all ECG leads. The first component resulted from the activation of the septum and posterior wall of the RA. The second component was coincident with activity recorded in CS electrograms. The interval between the two deflections (60 +/- 18 ms) correlated strongly with interatrial conduction time (57 +/- 19 ms) (r = 0.84). Interatrial conduction interval was prolonged during AFl as compared to sinus rhythm (60 +/- 18 ms vs 43 +/- 13 ms, p = 0.04). Activation of the lateral wall of RA coincided with the negative components in lead I, inferior leads and V6. CONCLUSIONS: The electrical activity in surface ECG closely correlates with conduction in specific parts of the atria. Polarity of the F wave in an ECG lead is determined by a resultant of opposing activities from the lateral wall of the RA and the left atrium.     

Atrial flutter with inapparent flutter waves on the surface electrocardiogram

A case with inapparent flutter waves on surface electrocardiogram are described. Typical atrial flutter activity could be seen on right atrial monophasic action potential recordings, His bundle electrograms and echocardiograms. During long pauses induced by carotid sinus massage the atrial activity on endocavitary tracings and echocardiograms was unchanged while isoelectric lines were recorded on the twelve surface electrocardiographic leads.     

Circus movement atrial flutter in canine sterile pericarditis model. Activation patterns during entrainment and termination of single-loop reentry in vivo

BACKGROUND. Recently, we used a custom designed "jacket" electrode with 127 bipolar electrodes in a flexible nylon matrix to map the total atrial epicardial surface in the in situ canine heart. Atrial flutter in dogs with sterile pericarditis was shown to be due to a single wave front circulating around a combined functional/anatomic obstacle, with the arc of functional conduction block contiguous with one or more of the atrial vessels. METHODS AND RESULTS. In the present study, this model was used to analyze the activation pattern during pacing-induced entrainment and termination of single reentrant loops in a syncytium without anatomically predetermined pathways. Sustained atrial flutter was induced in five dogs with 3-5-day-old sterile pericarditis. Atrial pacing at a cycle length 5-30 msec shorter than the spontaneous cycle length entrained the arrhythmia and could result in a "classical" activation pattern, characterized by an antidromic stimulated wave that collided with the reentrant orthodromic wave front of the previous beat at a constant site. However, two variations of this classical activation pattern were also observed: 1) Pacing at short cycle lengths could lead to localized conduction block in antidromic direction, forcing a change in the pathway of the antidromic wave front. This could prevent the expected shift of the site of collision in antidromic direction. 2) The stimulated orthodromic wave front could also use a pathway different from that of the original reentrant impulse, so that a different circuit was active during the pacing period. Termination of atrial flutter by rapid atrial stimulation was associated with progressive slowing and finally blocking of the paced orthodromic wave front and a progressive shift of the site of collision in antidromic direction. The occurrence of conduction block was determined by the cycle length of stimulation and the number of stimulated beats. A longer train at the critical cycle length or the critical number of beats at a shorter cycle length could reinduce the same reentrant circuit or a different reentrant circuit, respectively, during stimulated cycles following the beat that terminated reentry. CONCLUSIONS. The epicardial activation sequence during entrainment of reentrant arrhythmias does not necessarily follow a standard activation pattern. Instead, the stimulated orthodromic as well as the antidromic wave front might use a pathway different from that of the original reentrant wave front. The mechanisms of termination, failure of termination, and reinitiation of single-loop reentry are similar to those in the "figure-eight" reentrant circuit.     

Antiarrhythmic effects of JTV-519, a novel cardioprotective drug,on atrial fibrillation/flutter in a canine sterile pericarditis model

Effect of JTV-519 on AF. INTRODUCTION: A new cardioprotective drug, JTV-519, blocks Na+ current and inwardly rectifying K+ current and inhibits Ca2+ current. However, its role in atrial electrophysiology is unknown. We investigated the antiarrhythmic effects of JTV-519 on atrial fibrillation/flutter in the canine sterile pericarditis model. METHODS AND RESULTS: In nine dogs with sterile pericarditis, 38 episodes of sustained (>30 sec) atrial fibrillation (8 dogs) and 24 episodes of sustained atrial flutter (7 dogs) were induced by rapid atrial pacing. When atrial fibrillation or atrial flutter was sustained >15 minutes, it was cardioverted and reinduced. The inducibility of atrial fibrillation/flutter, the atrial effective refractory period, and the intra-atrial conduction time were compared before and after the continuous infusion of JTV-519 (0.03 mg/kg/min). JTV-519 significantly decreased the mean number of sustained atrial fibrillation episodes (from 4.2 +/- 2.9 to 0 +/- 0, P < 0.01). In contrast, atrial flutter was still inducible in 4 dogs after JTV-519 (from 2.7 +/- 2.5 to 1.6 +/- 2.1, P = NS). JTV-519 significantly prolonged effective refractory period (from 123 +/- 18 to 143 +/- 14 msec, from 127 +/- 18 to 151 +/- 12 msec, and from 132 +/- 13 to 159 +/- 9 msec at basic cycle lengths of 200, 300, and 400 msec, respectively, P < 0.01), but it did not affect the intra-atrial conduction time (from 47 +/- 11 msec to 48 +/- 11 msec, P = NS). CONCLUSION: JTV-519 had significant protective effects on atrial fibrillation in the canine sterile pericarditis model, mainly by increasing effective refractory period, suggesting that it may have potential as a novel antiarrhythmic agent for atrial fibrillation.     

典型逆钟向心房扑动特征性扑动波的电解剖研究

目的 通过对典型逆钟向心房扑动(房扑)左右心房的电解剖标测,阐明其体表扑动波的产生机制.方法 2012年10月至2014年2月于南京医科大学第一附属医院住院患者中入选15例典型逆钟向房扑患者,平均年龄(60±14)岁,男性14例,女性1例.对15例患者进行心脏超声检查、电生理检查及三维标测系统指导下的双心房激动标测,观察体表扑动波的形成与左右心房心内膜激动模式的关系.结果 15例患者的平均左心室射血分数为(60.8±6.6)％,平均左心房内径为(39.0±3.4)mm,平均扑动周期为(220±24) ms,均完成房扑节律下右心房、左心房的电解剖重建.在下壁导联,可将体表扑动波分为3个部分:缓慢下降区,快速下降区及终末正向成分,分别对应心腔内右心房峡部、间隔由下而上和左心房激动及右心房游离壁由上而下的激动.左心房激动始于快速下降区,终于终末正向成分.结论 典型逆钟向房扑体表扑动波与其特殊的大折返激动组成部分一一对应,是其特征性激动模式的心电反映.左心房激动参与了扑动波中下降部分的形成.     

Circus movement atrial flutter in the canine sterile pericarditis model. Activation patterns during initiation, termination, and sustained reentry in vivo

The mechanisms of single-loop reentry in a syncytium without anatomically predetermined pathways have not been shown. Using a "jacket electrode" with 111 bipolar electrodes in a nylon matrix, we mapped in situ the atrial epicardial surface during atrial flutter in dogs with sterile pericarditis. Of 21 episodes of reentrant atrial flutter, only four showed double-loop ("figure-eight") reentry, whereas in 17 episodes a single loop was present. During initiation of single-loop reentry, an arc of functional block extended to the atrioventricular (AV) ring. This forced activation to proceed as a single wave around the free end of the arc, before breaking through the arc close to the AV ring. Activation continued as one loop around an arc close to the AV ring (in eight episodes) or around a combined functional and anatomic obstacle (in nine episodes) when the arc joined an atrial vessel. A zone of slow conduction was consistently bordered by the arc of block and the AV ring or by the anatomic obstacle and the AV ring. Spontaneous termination occurred when conduction failed in this area and the arc rejoined the AV ring. High-density recordings (2 mm) along the arc of block showed double potentials separated by an isoelectric interval, interpreted as local activation and electrotonus due to activation on the opposite side of the arc. Histologically, a diffuse inflammatory reaction involved 50-80% of the atrial wall. A transitional layer of myocardial bundles with preserved cross striation, but separated by edema and inflammatory cells, was enclosed between an epicardial layer of fragmented myocytes and an endocardial layer of grossly intact myocardium. There were no distinctive features at sites of functional conduction block or slowed conduction. In conclusion, single-loop reentry is the common pattern during atrial flutter in this model. Its induction depends on an interaction of the AV ring, a functional arc of block, and a zone of slow conduction. The location of the inferior vena cava predisposes the lower right atrium to this type of reentry.     

Mechanism of double potentials recorded during sustained atrial flutter in the canine right atrial crush-injury model.

BACKGROUND. During atrial flutter, double potentials may be recorded at specific sites in the atria. It has been suggested that double potentials represent sequential activations at the center of the reentrant circuit. An alternative hypothesis is that double potentials represent electrical activity in an area of slow conduction. Understanding their mechanism is important because double potentials have been considered a possible indicator of target sites for catheter ablation. METHODS AND RESULTS. We systematically studied double potentials in our canine model of atrial flutter produced by right atrial crush injury using a 64-channel computerized mapping system with 56 electrodes on the right atrium in seven mongrel dogs under general anesthesia. Activation maps were recorded during sinus rhythm before and after crush injury, during rapid pacing above and below the crush injury, and during sustained atrial flutter, entrainment of atrial flutter, and termination of atrial flutter induced with D-sotalol (2 mg/kg). During sinus rhythm before crush injury, activation was uniform, and double potentials were not recorded in any dog. After crush injury, activation proceeded up to and around the crush injury, and narrowly split double potentials were recorded in two of seven dogs. During rapid pacing above and below the crush injury, double potentials were recorded in five dogs. During 14 episodes of atrial flutter (mean cycle length, 140 +/- 16 msec), double potentials were recorded at electrodes along the crush injury. The activation time of the early x component of the double potentials (25 +/- 13 msec) was similar to that of adjacent electrodes above the crush injury (24 +/- 11 msec), and the activation time of the late y component (89 +/- 13 msec) was similar to that of adjacent electrodes below the crush injury (91 +/- 14 msec). The timing of the x and y components was dependent on the location of the recording electrode, with x and y widely spaced at the end of the crush injury near the area of earliest atrial activation during atrial flutter, more equally timed at the center of the crush injury, and more closely timed at the end of the crush injury opposite the area of earliest activation. During transient entrainment, double potentials were accelerated to the pacing rate, but their activation time relative to adjacent electrodes was maintained. During abrupt termination of atrial flutter, the early x component of the double potential was always recorded, but the late y component was not, because of conduction block below the posterior end of the crush injury. CONCLUSIONS. This study has shown in our canine model of atrial flutter that double potentials are recorded from the center of the reentrant circuit and that they represent sequential activations as the reentrant wave front passes on either side of the crush injury.     

体表心电图P波极性改变对典型心房扑动射频消融结果的评估价值

目的 :探讨在心房扑动 (AF)射频消融 (RFCA)过程中体表心电图P波极性改变对峡部发生传导阻滞的评估价值。方法 :17例典型AF患者在成功RFCA前后分别行低右房间隔部和侧壁起搏 ,起搏下同步记录体表 12导联心电图 ,分析测量RFCA前后P波电轴、极性和宽度的变化。结果 :RFCA后低右房间隔部起搏 ,体表心电图P波电轴宽度与RFCA前相比差异均无统计学意义 [(- 95± 18)°∶(- 99± 2 1)° ,t=- 1.6 92 ,P >0 .0 5和 (12 7± 33)ms∶(118± 2 4 )ms ,t =- 1.4 2 5 ,P >0 .0 5 ]。RFCA后低右房侧壁起搏 ,体表心电图P波电轴较RFCA前显著右偏 [(14± 32 )°∶(- 6 9± 2 7)° ,t=- 9.16 6 ,P<0 .0 1];14例患者肢体Ⅱ导联P波的极性由RFCA后的负向波变为RFCA前的正向波 ;P波宽度RFCA后和RFCA前相比明显延长 [(173± 33)ms∶(130± 2 6 )ms,t=- 6 .4 70 ,P <0 .0 1]。结论 :三尖瓣环与下腔静脉之间的峡部形成传导阻滞仅使低右房侧壁起搏下体表 12导联心电图发生变化。提示低右房侧壁起搏下肢体Ⅱ导联P波极性的变化可作为典型AF在RFCA中逆时针传导阻滞的无创评价指标     

Electrogram polarity and cavotricuspid isthmus block during ablation of typical atrial flutter

INTRODUCTION: The atrial activation sequence around the tricuspid annulus has been used to assess whether complete block has been achieved across the cavotricuspid isthmus during radiofrequency ablation of typical atrial flutter. However, sometimes the atrial activation sequence does not clearly establish the presence or absence of complete block. The purpose of this study was to determine whether a change in the polarity of atrial electrograms recorded near the ablation line is an accurate indicator of complete isthmus block. METHODS AND RESULTS: Radiofrequency ablation was performed in 34 men and 10 women (age 60 +/- 13 years [mean +/- SD]) with isthmus-dependent, counterclockwise atrial flutter. Electrograms were recorded around the tricuspid annulus using a duodecapolar halo catheter. Electrograms recorded from two distal electrode pairs (E1 and E2) positioned just anterior to the ablation line were analyzed during atrial flutter and during coronary sinus pacing, before and after ablation. Complete isthmus block was verified by the presence of widely split double electrograms along the entire ablation line. Complete bidirectional isthmus block was achieved in 39 (89%) of 44 patients. Before ablation, the initial polarity of E1 and E2 was predominantly negative during atrial flutter and predominantly positive during coronary sinus pacing. During incomplete isthmus block, the electrogram polarity became reversed either only at E2, or at neither E1 nor E2. In every patient, the polarity of E1 and E2 became negative during coronary sinus pacing only after complete isthmus block was achieved. In 4 patients (10%), the atrial activation sequence recorded with the halo catheter was consistent with complete isthmus block, but the presence of incomplete block was accurately detected by inspection of the polarity of E1 and E2. CONCLUSION: Reversal of polarity in bipolar electrograms recorded just anterior to the line of isthmus block during coronary sinus pacing after ablation of atrial flutter is a simple, quick, and accurate indicator of complete isthmus block.     

Atrial reentry around an anatomic barrier with a partially refractory excitable gap. A canine model of atrial flutter

We have characterized, in dogs, a model of inducible regular atrial tachycardia that resembles atrial flutter. The model involves creating a Y-shaped lesion comprised of an intercaval incision and a connected incision across the right atrium. It is suitable for serial studies of the effects of pacing or antiarrhythmic drugs in chronically instrumented animals studied in the awake state for at least several months. The postoperative cycle length of the induced tachycardia varies from 143 to 188 msec, depending on the size of the dog. The tachycardia cycle length was consistent for each dog, and the rhythm--once induced--was very stable until terminated by pacing. The mechanism of the tachycardia was reentry due to circus movement based on the ability to induce and terminate it by premature impulses or overdrive, the ability to reset the tachycardia by single premature stimuli, the pattern of entrainment during overdrive stimulation, and the ability to terminate the tachycardia by interrupting the conduction pathway. The window of reset determined by the range of coupling intervals of premature stimuli that were able to enter and reset the tachycardia ranged from 56 to 82 msec. There appears to be incomplete recovery of excitability by the end of the excitable gap as evidenced by the fact that even late premature impulses that enter the reentrant circuit conduct more slowly than the tachycardia impulse, and because stimulation of muscarinic receptors that shortens the duration of the action potential and refractoriness also reduces the cycle length of the tachycardia. Epicardial and endocardial activation mapping during tachycardia showed the reentrant pathway does not merely encircle the lesion, particularly over the left atrial epicardium near the intercaval lesion. Rather, the impulse appears to travel around the atrial tissue just above the tricuspid ring, including a portion that travels through the right side of the lower intraatrial septum. Thus, the model involves circus movement around an anatomic barrier through normal tissue that contains no depressed segments. During the circus movement, there is a relatively long excitable gap during which there is incomplete recovery of excitability. This model should be useful for studies of the mechanism of antiarrhythmic drug action and the responses to premature stimulation in this particular subclass of reentrant rhythms, and for comparison with the behavior and responses of other forms of reentry.