Atrial Flutter:

Entrainment Characteristics. Entrainment was first described based on observations during rapid (overdrive) pacing of type I atrial flutter. Entrainment is capture of the reentrant circuit of a tachycardia without interrupting the tachycardia, so that with cessation of pacing, the spontaneous reentrant tachycardia is still present. During entrainment, the orthodromic wavefront from the pacing impulse resets the tachycardia to the pacing rate, while the antidromic wavefront either collides with the orthodromic wavefront of the previous beat (usual case) or is blocked by some other mechanism (refractoriness or another cause of block). Entrainment may be either manifest or concealed. The principles of entrainment during type I atrial flutter have permitted identification of targets for successful ablation, of mapping sites within or outside the reentrant circuit, and of appropriate pacing rates to successfully interrupt atrial flutter and restore sinus rhythm.     

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.     

Further observations on transient entrainment: importance of pacing site and properties of the components of the reentry circuit

Transient entrainment of circus-movement tachycardia utilizing an atrioventricular (AV) bypass pathway was studied in 13 patients (nine with the orthodromic form, two with the antidromic form, and two with both the orthodromic and antidromic forms). All patients had a left-sided AV bypass pathway. Pacing at selected rates faster than the spontaneous rate was performed during the tachycardia at a site proximal or distal to the AV node, an area of slow conduction within the reentry loop. Rapid pacing from a site proximal to the AV node (from the right atrium during the orthodromic form of the arrhythmia or the right ventricle during the antidromic form of the arrhythmia) always demonstrated at least one of the three entrainment criteria: constant fusion beats except for the last captured beat, which was entrained but not fused (first criterion); progressive fusion (second criterion); localized conduction block to a site(s) for 1 paced beat associated with interruption of the tachycardia followed by activation of that site(s) by the next paced beat from a different direction and with a shorter conduction time (third criterion). In contrast, rapid pacing from a site distal to the AV node (from the right ventricle during the orthodromic form of the arrhythmia, or the right atrium during the antidromic form of the arrhythmia) transiently entrained the tachycardia, but never demonstrated any entrainment criteria because the antidromic wave front from the pacing impulse always blocked in the AV node (concealed entrainment). We conclude that the location of the pacing site relative to the components of a reentry loop is critical to the demonstration of the criteria of transient entrainment; i.e., if it is proximal to an area of slow conduction and/or unidirectional block within a reentry loop, transient entrainment should be demonstrable, but if it is distal, it will not be demonstrable.     

Entrainment of circus movement tachycardia utilizing an accessory pathway with long retrograde conduction times during ventricular and atrial stimulation

An unusual case is presented in which a circus movement tachycardia incorporating an accessory pathway with long retrograde conduction time was transiently entrained. Overdrive high right atrial stimulation produced entrainment without atrial fusion since collision of anterograde and retrograde impulses took place within the accessory pathway. Tachycardia termination occurred when, at a faster pacing rate, an atrial impulse that collided in the accessory pathway was blocked at the atrioventricular (AV) node. In contrast, the entrainment seen during right ventricular apical stimulation was characterized by the occurrence of both fusion and collision within the ventricles. The tachycardia was terminated when a pure paced impulse that collided in the normal pathway was blocked in a retrograde direction in the accessory pathway. These data indicate that: 1) transient entrainment of this arrhythmia (circus movement tachycardia) can be identified by the classical criteria used to diagnose it, provided that fusion and collision occur within the ventricles; and 2) the accessory pathway is the weak link for tachycardia termination only during ventricular pacing since the AV node is the weak link during atrial stimulation.     

Entrainment of ventricular tachycardia by atrial depolarizations

Four patients in whom rapid atrial pacing resulted in transient entrainment of a sustained ventricular tachycardia (VT) are reported. Ventricular fusion was seen in 3 of the 4. The following new observations were made: (1) A single atrial depolarization resulted in ventricular fusion and resetting of a VT, while atrial pacing at a faster rate entrained the same VT but without detectable fusion. This suggests that fusion during entrainment may be a rate-dependent phenomenon. (2) The interval between the last paced beat and the first nonpaced VT beat was different from the pacing cycle length in 3 patients. Two mechanisms accounted for this: the initial forces of each entrained QRS occurring as a result of the pacing wavefront, with fusion taking place only during the terminal forces, and the last entrained cycle exceeding the pacing cycle length by an amount related to the nonfused portion of the QRS, and delay in the presumed reentrant circuit responsible for the tachycardia. One VT was entrained with atrial pacing while ventricular pacing at the same rate resulted in termination, suggesting "site specificity" for termination. It is concluded that entrainment can occur without the criteria previously described as characteristic of it and that additional phenomena may be observed after stimulation that further support reentry as the mechanism of VT.     

Linking by collision initiated in the absence of preexisting reentrant tachycardia

Dynamic functional block in 1 limb of a reentrant circuit ("linking") can be maintained by either repetitive interference or collision of successive impulses entering the circuit. Occurrence of linking by collision during attempted overdrive pacing of reentrant tachycardias accounts for the entrainment phenomenon. To investigate whether linking by collision can be initiated in the absence of preexisting tachycardia, a human reentrant circuit model was studied. The model consisted of the atrioventricular node and His-Purkinje system as anterograde limb and an electronic stimulator that served as "retrograde limb" by initiating a paced atrial impulse at a predetermined ventriculoatrial interval following each sensed ventricular depolarization. In 3 patients with intact ventriculoatrial conduction, "reentrant tachycardia" was initiated by a ventricular extra-stimulus (V2), which retrogradely blocked bilaterally below the His bundle. When this same V2 was followed, instead, by a paced V2V2 train at a cycle length equal to the programmed ventriculoatrial interval of the "tachycardia," it could be shown that each beat of the train not only "traversed" the simulated "retrograde limb" but also retrogradely collided with a prior circulating impulse in the anterograde limb of the circuit, thereby constituting linking by collision at a supra-Hisian level with inability of even a single "reentrant cycle" to be completed; "tachycardia" became manifest only after termination of the V2V2 train. The findings suggest the existence of a unique mechanism for initiation of certain clinical reentrant tachycardias during incremental pacing.     

Interactions between paced wavefronts and monomorphic ventricular tachycardia: implications for antitachycardia pacing

Objectives: Interactions between paced wavefronts and monomorphic ventricular tachycardia (VT) dictate antitachycardia pacing outcomes. We used optical mapping to assess those interactions during single and dual site pacing of rabbit ventricular epicardium. Methods and Results: Monomorphic VTs were initiated in six isolated rabbit hearts that were endocardially cryoablated to limit viable tissue to visible epicardium and establish apical tissue as the anatomic anchor. Preparations were optically mapped during single (n = 39) and dual (n = 43) site pacing at 50%–90% of VT cycle length (CL) with eight pulses per trial. Overall, we found six pulses that abruptly terminated VT. This occurred because the VT wavefront collided with the antidromic portion of the paced wavefront and the orthodromic portion of paced wavefront blocked in the VT's refractory region. When effective, dual site pacing that captured tissue at both leads simultaneously terminated the VT immediately, while single site pacing or dual site pacing that captured tissue at only one lead terminated the VT after resetting advanced the orthodromic wavefront. We found 12 pulses that induced polymorphic VT, with 11 of those pulses occurring during capture at only one lead. Expansion of the combined antidromic‐VT wavefront around one or both ends of the arc of conduction block formed by the interaction of the orthodromic wavefront with the VT's refractory region initiated functional reentry. Six of these polymorphic VTs were nonsustained because the underlying wavefronts self‐terminated. The wavefronts did persist for 4.2 ± 3.5 cycles before self‐terminating in these trials, and the post‐pacing cycles presented a 146% increase in CL variability, compared with the variability prior to pacing. These temporal characteristics are similar to those of delayed termination in patients with ICDs. Conclusions: The main difference between pulses that terminated abruptly and pulses that induced polymorphic VT was the effective separation of the antidromic and orthodromic portions of the paced wavefront from one another.     

Significance of pacing cycle lengths in manifest entrainment of orthodromic circus movement tachycardia by ventricular pacing

The physiology of entrainment of orthodromic circus movement tachycardia (CMT) was studied using ventricular pacing during 18 episodes of induced CMT in 7 patients with atrioventricular (AV) accessory pathways. The first paced impulse was delivered as late as possible in the tachycardia cycle (mean 88 +/- 5% of the spontaneous cycle length [CL]). Entrainment was demonstrated by the following criteria: 1:1 retrograde conduction via the accessory pathway; capture of atrial, ventricular and His bundle electrograms at the pacing rate; and resumption of tachycardia at its previous rate after cessation of pacing. The number of ventricular paced impulses ranged from 5 to 14 (mean 8 +/- 3), and entrainment occurred in 2 to 7 paced cycles (mean 4 +/- 2). Orthodromic activation of a major part of the reentry circuit (manifest entrainment) was demonstrated during 9 episodes by the occurrence of His bundle electrogram preceding the first CMT QRS at the time anticipated from the last paced beat. In the 9 other episodes, persistent retrograde His bundle activation and AV nodal penetration by each paced impulse caused a delay (mean 79 +/- 25 ms) in activation of the His bundle preceding the first CMT QRS after the last paced beat. The mean pacing CL achieving manifest entrainment was 92 +/- 3% of the tachycardia CL, compared with 84 +/- 3% for retrograde AV nodal penetration (p less than 0.01). In conclusion, manifest entrainment of orthodromic CMT can be demonstrated by ventricular pacing at very long CLs; shorter CLs may cause CMT termination due to retrograde AV nodal penetration.     

Frequency and implications of resetting and entrainment with right atrial stimulation in atrial flutter.

Thirty-three patients (24 with typical and 9 with atypical flutter-wave morphology) were studied to evaluate the incidence and implications of resetting and entrainment of atrial flutter with right atrial stimulation. Resetting with single extrastimulus was present in 23 cases (group A) and absent in 10 (group B). Most cases of reset flutter were typical (20 of 23). Fixed fusion indicative of entrainment was observed in all 29 cases with pacing trains. Groups A and B did not differ significantly in flutter cycle length (230 +/- 20 vs 223 +/- 19 ms), atrial functional refractory period (165 +/- 18 vs 167 +/- 22 ms) or longest paced cycle length producing entrainment (213 +/- 19 vs 210 +/- 19 ms). In contrast, the return cycle after the longest paced cycle length producing entrainment was significantly shorter in group A (228 +/- 27 vs 284 +/- 56 ms; p = 0.001). The return cycle in group A was virtually identical to the flutter cycle length, whereas in group B it was greater (p = 0.002 compared with group A). Resetting was more frequent in typical than atypical flutter (20 of 24 vs 3 of 9; p = 0.01). Both typical and atypical flutter can be transiently entrained by right atrial pacing. Lack of resetting and longer return cycle, suggesting a longer conduction time between the reentrant circuit and the stimulation site, were mostly observed in atypical flutter. The data suggest a different location for both types of flutter, and may have implications for ablation techniques. A more cautious approach, with more extensive mapping, appears appropriate for ablation attempts of atypical flutter.     

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.     

Characteristics of entrainment during autodecremental atrial and ventricular stimulation

The entrainment characteristics of orthodromic circus movement tachycardias occurring during autodecremental atrial and ventricular stimulation were studied in 9 patients with manifest Wolff-Parkinson-White syndrome. The phenomenon occurred in 34 of 38 episodes of tachycardia during autodecremental atrial stimulation. It was not seen in 4 episodes because the first impulse penetrating the circuit terminated the arrhythmia. Invariably, the HH and VV intervals were not equal to, but longer than, the stimulus-stimulus intervals, thus not fulfilling the definition of "classic" (constant cycle length) entrainment postulated by Okumura et al. Furthermore, the first 2 of the 3 diagnostic criteria were not demonstrated and the third only could be demonstrated in 7 episodes. Tachycardia termination was achieved in all 38 episodes. Entrainment occurred during autodecremental ventricular stimulation in 79 of 80 episodes, with the AA and H-H- intervals (when visible) being equal to the corresponding paced cycle lengths. Moreover, the intervals between the last paced ventricular beat and the first ventricular beat of the resumed tachycardia were invariably longer than the last stimulus-stimulus intervals. These characteristics were those which Okumura et al attributed to "concealed" entrainment. Tachycardia termination was achieved in 77 of 80 episodes. In summary: (1) autodecremental atrial pacing produced a specific form of entrainment that did not fulfill the "classic" definition of Okumura et al; (2) autodecremental ventricular pacing consistently produced "concealed" entrainment; and (3) autodecremental stimulation was very effective in terminating 115 of 118 (98%) of episodes of circus movement tachycardias.     

心室起搏拖带对房室结折返性和间隔旁路参与的房室折返性心动过速的鉴别作用

目的　研究心动过速时心室起搏拖带对房室结折返性心动过速 (AVNRT )和间隔旁路参与的顺向型房室折返性心动过速 (间隔旁路ORT)的鉴别意义。方法　 30例AVNRT和 2 5例间隔旁路ORT病人在心动过速发生后 ,采用较心动过速的周长 (TCL)短 10～ 4 0ms的周长行右心室起搏拖带心动过速。测量右心室起搏之前的心室 心房 (VA)间期和TCL。停止起搏后 ,测量最后一次刺激信号至最后起搏拖带的心房激动 (SA)间期 ,以及起搏后间期 (PPI)。结果　所有 30例AVNRT病人的SA -VA间期 >85ms、PPI-TCL >115ms,而 2 5例ORT病人的SA -VA间期 <85ms、PPI-TCL <115ms。结论　PPI TCL和SA VA间期是鉴别AVNRT和间隔旁路ORT的非常可靠的指标 ,具有较高的特异性。     

Characterization of return cycle responses predictive of successful pacing-mediated termination of ventricular tachycardia

Objectives. The purpose of this study was to characterize response patterns during overdrive pacing that predict successful termination of ventricular tachycardia.Background. Overdrive pacing during ventricular tachycardia typically results in entrainment at slow pacing rates and in termination or acceleration at faster rates. The factors that determine the critical paced cycle length that results in tachycardia termination have not been extensively studied.Methods. Ventricular tachycardias in 14 patients with coronary artery disease were studied with overdrive pacing at several cycle lengths. Return cycles were measured after each additional paced beat at each paced cycle length. The return cycle responses during pacing trials that resulted in tachycardia termination and those that resulted in entrainment were compared.Results. Three return cycle responses were identified: flat, plateau and increasing. Twenty trials of overdrive pacing resulted in tachycardia termination; all were characterized by an increase in the return cycle with the delivery of each successive beat in the pacing drive until the tachycardia terminated (increasing response). Thirty-four pacing trials resulted in entrainment and not termination; these were characterized either by a constant return cycle (flat response) or an initial increase in return cycle followed by a longer, constant return cycle (plateau response) with the delivery of additional paced beats. The longest paced cycle length that resulted in tachycardia termination correlated with the relative refractory period of the circuit, defined as the tachycardia cycle length minus the fully excitable gap (r²= 0.764, p = 0.0001). Tachycardia termination was not observed unless the paced cycle length was shorter than the relative refractory period of the circuit.Conclusions. The critical paced cycle length that causes termination of ventricular tachycardia depends on the relative refractory period of the circuit because this factor determines whether the nth + 1 beat of the pacing drive will encounter partially recovered tissue. These data provide insights into the mechanism of pacing-mediated tachycardia termination and entrainment and are applicable to the development of improved antitachycardia pacing algorithms.     

Entrainment of reentrant tachycardia in a computer model

Capture of the cardiac rate by pacing followed by an immediate return to the original rate after pacing has been proposed as characteristic of reentrant rhythms. In this study, such entrainment has been demonstrated using computer-model simulations of propagated excitation and of reentry associated with structural and functional obstacles. With structural obstacles, the mechanism of entrainment was bidirectional propagation of paced excitation in reentry circuits, with collision of the reentrant and paced excitation in one direction and continued propagation of paced excitation in the other direction. The time of pacing onset, rate, and location all affected the QRS waveform during entrainment. With a particular time of onset and rate of pacing, the duration of time during which the QRS waveform underwent dynamic change was directly related to the distance between the pacing site and reentrant circuit. The location of reentry associated with functional obstacles moved so that the relationship between pacing-induced and reentrant excitation varied. In some cycles, pacing did not alter reentrant circuits, that is, entrainment did not occur, while other cycles were entrained, but by a different mechanism than that with structural obstacles. Leading circle reentry circuits, consisting of propagation away from and returning to reentry sites, did not have an excitable gap and paced excitation did not enter those circuits. Paced excitation did, however, enter the propagation paths between leading circle reentry circuits and modified the circuits by affecting the recovery of excitability.     

Preferential effect of procainamide on the reentrant circuit of ventricular tachycardia

Transient entrainment was used to test the hypotheses that 1) procainamide prolongs the cycle length of ventricular tachycardia in patients with coronary artery disease because it has a preferential effect on the reentrant tachycardia circuit, and 2) regions of slow conduction in the reentrant circuit are more susceptible to the effect of procainamide than are other areas of the ventricles. In five patients with prior myocardial infarction, sustained ventricular tachycardia with identical QRS configuration was inducible before and after intravenous infusion of procainamide. Transient entrainment of ventricular tachycardia was demonstrated at two or more cycle lengths by rapid pacing in the baseline state and after procainamide. Rapid pacing was performed from the same site during sinus rhythm at the cycle lengths that demonstrated transient entrainment of ventricular tachycardia. The conduction interval to the transiently entrained site during ventricular tachycardia (orthodromic interval) was compared with the conduction interval to the same site during pacing in sinus rhythm (antidromic interval). The mean tachycardia cycle length increased by 27% after procainamide administration (p = 0.002). The antidromic conduction intervals were prolonged by 9% (p = 0.06) compared with a 28% increase in the mean orthodromic conduction interval (p = 0.002). The difference between the orthodromic and antidromic conduction intervals increased by 40% (p = 0.003). Prolongation of the tachycardia cycle length after procainamide administration correlated positively with increases in the orthodromic conduction intervals (r = 0.94, p = 0.02) but not with changes in the antidromic intervals (r = -0.08, p = NS). The effect of procainamide on the difference between correlated strongly with changes in the cycle length of ventricular tachycardia (r = 0.97, p = 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

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.     

Endocardial Mapping of Reentry Around an Anatomical Barrier in the Canine Right Atrium:

Flecainide and Atrial Reentry. Introduction: Flecainide is effective in terminating stable atrial flutter in the conscious dog with a Y-shaped right atrial lesion. In this model, flutter is due to circus movement of the impulse around a fixed anatomical barrier. Methods and Results: To investigate the mechanism of flecainide-induced termination of this type of reentry, we determined the pattern of endocardial activation of the right and left atria before and during administration of flecainide by recording simultaneously from 192 electrode pairs in the isolated blood perfused heart. At least five consecutive flutter beats were analyzed before and during flecainide for each of eight termination episodes in five hearts. In all, flecainide increased flutter cycle length (164 ± 24 msec) by 89% to 309 ± 77 msec (P < 0.05) before termination. Atrial refractory period and conduction time during paced beats were also increased by flecainide. In flve episodes, termination was due to conduction block of the impulse at critical sites within the reentrant circuit (mode 1). Cycle length oscillations (± 30 msec) at sites proximal to site of block preceded termination in three of these episodes. In three other episodes, interruption of the original circuit occurred when there was failure of a lateral boundary, giving rise to an impulse that reset the original circuit (mode 2). In these episodes, long-short cycle length oscillations led to return reexcitation by the impulse within the primary path and suhsequent termination. Conclusion: In summary, similar to our previous findings with the Class III agent, d-sotalol, two different modes of termination of atrial reentry were observed with flecainide.     

Electrophysiologic basis of catheter ablation in atrial flutter

A reentrant mechanism is believed to be responsible for atrial flutter. The recent development of the entrainment criteria further supports this theory, and there is a general consensus that circus movement is the underlying abnormality that supports this arrhythmia. In most clinical studies, abnormal fragmented (or double spike) electrograms, suggesting the presence of areas of localized slowing of conduction or block, have been reported. They are almost always recorded in the lower and posterior portion of the right interatrial septum, but also frequently in the high lateral portion of the right atrium. The determination of their involvement in the reentry pathway is important for designing curative procedures such as surgery or ablation. The low atrial septal area surrounding the mouth of the coronary sinus was suspected as being the critical area of slow conduction in atrial flutter. Rapid pacing at that site can yield a surface electrocardiographic pattern similar to the clinically occuring arrhythmias. Additionally, the flutter circuit can be accelerated during atrial pacing at fixed and slightly faster rates than the intrinsic tachycardia rate—the so-called entrainment phenomenon. When entrainment criteria are fulfilled, tachycardla termination being by definition ruled out, any concomitant recorded local type II block identifies an area that must be outside the circuit. Such local block may be recorded either spontaneously or during entrainment and therefore helps in identifying atrial slow conduction areas that do not belong to the reentrant path. This approach was applied to identify the optimal ablation site in 8 patients with long-standing drug resistant atrial flutter. In 7 of 8 patients, we were able to identify a fragmented potential in the low posteroseptal area during sustained atrial flutter. Fulguration shocks were delivered at this site without complications, and after a mean follow-up of SSA weeks atrial flutter was controlled in 5 of 8 patients without the need of His bundle atrioventricular node ablation.     

Bystander cavo-tricuspid isthmus activation during post-incisional intra-atrial reentrant tachycardia.

We describe a case of post-incisional atrial tachycardia resembling typical atrial flutter on the surface ECG. Typical atrial flutter reentry was ruled out by the results of activation and entrainment mapping. Nevertheless, overdrive pacing from the lateral edge of the cavo-tricuspid isthmus produced tachycardia entrainment with concealed fusion associated with post-pacing and stimulus-to-P wave onset intervals exactly matching the tachycardia cycle length duration and the electrogram-to-P wave onset interval, respectively. Therefore, that site was firstly severed by sequential radiofrequency pulses. However, a transformation of the tachycardia P wave morphology and endocardial activation sequence, not associated with tachycardia termination or cycle length modification occurred. After additional mapping manoeuvres, a relatively small reentrant circuit was identified in the low and mid aspect of the lateral right atrium with the critical isthmus located between the lower border of a cannulation atriotomy and the crista terminalis, close to the inferior vena cava orifice. A single radiofrequency pulse at that site terminated the tachycardia. Both the electrocardiographic pattern and the endocardial mapping data obtained in our case might be explained by a split of the reentrant wavefront into a secondary wavelet which freely propagated through the cavo-tricuspid isthmus without completing the peritricuspid loop. In conclusion, bystander cavo-tricuspid isthmus activation during atrial tachycardia may simulate a typical atrial flutter pattern on the surface ECG. Further studies should evaluate the prevalence of this propagation pattern in post-incisional atrial reentry and atypical atrial flutters, and identify its implications for ablation strategy.