Orthodromic Wavefront Research Articles

Challenges and Pitfalls of Entrainment Mapping of Ventricular Tachycardia: Ten Illustrative Concepts.

The use and interpretation of entrainment mapping, or continuous resetting, of a reentrant tachycardia has been regarded as the gold standard for delineation of the components of a reentrant circuit.1,2 The response during and after overdrive pacing, whereby 2 wavefronts enter the circuit antidromically (with fusion) and orthodromically, is used to confirm reentry as the arrhythmia mechanism and determine the relationship of the pacing site to the circuit. The fulfillment of classical criteria outlined by Waldo and colleagues3,4 were synthesized into an anatomic concept for scar-related ventricular tachycardia (VT) by Stevenson et al5 to portray the structural and architectural basis of circuit conduction meandering between regions of fibrosis. In this construct, a central corridor, or protected isthmus, is bordered between 2 regions of dense scar with a single entrance that is distinct from a single exit, which yields the QRS morphology.6 This reentrant model has been central to our current mechanistic understanding of scar-mediated VT and is critically important for differentiating critical sites from bystander sites and regions that are unlikely to interrupt or eliminate reentry.7 However, the nature of reentrant VT in man is more complex than our idealized working construct for many reasons. In clinical practice, the majority of VT is hemodynamically unstable, which precludes the ability to perform entrainment mapping and activation mapping of the entire circuit.8 Differences in the circuit between patients with untolerated and tolerated VT are not well understood. VT circuits are 3 dimensionally complex with transmural conduction and circuit conduction is unlikely to be planar, as depicted by electroanatomic mapping of the myocardial surface. Exits may be multiple9,10 and patterns other than loop reentry around scar are likely. Channels of preserved myocardium are frequently not “normal” in voltage (>1.5 mV) …

Misleading Long Post-Pacing Interval After Entrainment of Typical Atrial Flutter From the Cavotricuspid Isthmus

The purpose of this study was to evaluate the prevalence and mechanism of a misleading long post-pacing interval (PPI) upon entrainment of typical atrial flutter (AFL) from the cavotricuspid isthmus (CTI). In typical AFL, the PPI from entrainment at the CTI is expected to closely match the tachycardia cycle-length (TCL). Sixty patients with confirmed CTI-dependent AFL were retrospectively analyzed and grouped into short (≤30 ms) or long (>30 ms) PPI-TCL. Thereafter, we prospectively studied 16 patients to acquire the PPI-TCL at 4 CTI sites with entrainment at pacing cycle-lengths (PCLs) 10 to 40 ms shorter than the TCL. Conduction times during AFL and entrainment were compared in 5 segments of the AFL circuit. Eleven patients (18%) in the retrospective analysis had a long PPI-TCL after entrainment from the CTI. Subjects with long PPI-TCL had similar baseline characteristics but greater beat-to-beat TCL variability. In the prospective cohort, PPI-TCL was influenced by the difference between PCL and TCL and site of entrainment. Conduction delays associated with a long PPI-TCL were located predominantly in the segment activated first by the paced orthodromic wave front, and were mainly due to local pacing latency, as confirmed by the use of monophasic action potential catheters. A long PPI upon entrainment of typical AFL from the CTI is common and due to delayed conduction with entrainment. Whether these findings apply to other macro-re-entrant tachycardias warrants further investigation.

Another Way to Prove the Presence and Participation of an Accessory Pathway in Supraventricular Tachycardia?

Another Way to Prove the Presence and Participation of an Accessory Pathway in Supraventricular Tachycardia?

Interactions Between Paced Wavefronts and Monomorphic Ventricular Tachycardia: Implications for Antitachycardia Pacing

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. 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. 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.

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.

Characterization of the excitable gap in a functionally determined reentrant circuit. Studies in the sterile pericarditis model of atrial flutter.

Single premature beats were introduced in the reentrant circuit during stable atrial flutter in the canine sterile pericarditis model to test the hypotheses that (1) despite the fact that the reentrant circuit is functionally determined, there is a fully excitable gap; (2) the excitable gap in the reentrant circuit is not uniform; and (3) inhomogeneities of conduction in the reentrant circuit explain the effects of premature beats. A multiplexing system was used to record 190 unipolar electrograms from the right atrial free wall during 18 atrial flutter episodes in 9 dogs. In all 18 episodes, premature stimuli captured the atrial flutter reentrant circuit. At the longest coupling intervals, the return cycle at the site closest to the pacing site did not prolong. As the coupling interval of the premature stimulus decreased, the return cycle then progressively increased, associated with changes in conduction in the reentrant circuit that were not uniform. The result was that coupling intervals associated with introduction of the premature beat also were not constant. The mean duration of the total (ie, fully plus partially) excitable gap was 12 +/- 4 ms in areas of slow conduction, and it was always shorter than the total excitable gap in other areas (22 +/- 6 ms, P < .001). The mean duration of the fully excitable gap based on analysis of the return cycle was 4 +/- 1 ms in the reentrant circuit. In 13 of 18 atrial flutter episodes, a premature stimulus terminated atrial flutter by causing block of the orthodromic wave front of the premature beat in an area of slow conduction. The mean coupling interval that caused orthodromic block was 113 +/- 5 ms (recorded at the site just proximal to the area of block), and it was always longer than the delivered stimulus coupling interval at the pacing site (96 +/- 8 ms, P < .001). We conclude that in this functionally determined atrial flutter reentrant circuit in the canine sterile pericarditis model, (1) a fully excitable gap is present in at least part of the reentrant circuit; (2) the duration of the excitable gap in the reentrant circuit is shortest in areas of slow conduction; and (3) when a premature beat encounters the partially excitable gap of the reentrant circuit, it results in changes in conduction such that the coupling intervals are not uniform throughout in the reentrant circuit.

Patterns of interruption of atrial flutter induced by rapid atrial pacing.

We evaluated the patterns of interruption of atrial flutter (AFl) induced by rapid atrial pacing in 10 patients using standard electrophysiologic techniques. We observed 3 patterns of interruption of AFl: 1) interruption resulting from block of an orthodromic wavefront within the reentry loop in 5 patients; 2) interruption when pacing impulses no longer captured all of the recording sites in the atrium during rapid atrial pacing in 2 patients, and 3) interruption with 1 echo wave after the cessation of pacing in 3 patients. These findings suggest that there are patterns of interruption of AFl other than that resulting from a simple block of an orthodromic wavefront within the reentry loop.

Characterization of double potentials in a functionally determined reentrant circuit: Multiplexing studies during interruption of atrial flutter in the canine pericarditis model

Objectives. We tested the hypothesis that double potentials recorded during atrial flutter in a functionally determined reentrant circuit reflect activation of the reentrant wave front around an area of functional conduction block.Background. The center of the atrial flutter reentrant circuit in the sterile pericarditis canine model is characterized by double potentials.Methods. We studied 11 episodes of atrial flutter in eight dogs during interruption of atrial flutter while pacing the atria. A multielectrode mapping system was used to record simultaneously from 190 electrodes on the right atrium (location of reentry).Results. Interruption of atrial flutter occurred when the orthodromic wave front from the pacing impulse blocked in an area of slow conduction in the reentrant circuit. The response of the double potential with interruption of atrial flutter depended on the location of the recording site relative to this area of block. Two types of response were seen. When the double potential was recorded orthodromically distal to this area of block, interruption of atrial flutter was associated with disappearance of the second deflection, and continued pacing after interruption of atrial flutter was not associated with reappearance of the second potential. When the double potential was recorded at a site orthodromically proximal to the area of block, interruption of atrial flutter was not associated with disappearance of the second potential, and when rapid atrial pacing was continued, the double potential remained despite disappearance of the atrial flutter reentrant circuit.Conclusions. Double potentials represent functional conduction block in the center of the reentrant circuit, with each deflection of the double potential reflecting activation on either side of the area of functional block. The data also demonstrate that double potentials are not limited to a reentrant circuit, as they were recorded on either side of an area of block in the absence of such a circuit.

Significance of ventricular pacing site in manifest entrainment during orthodromic atrioventricular reentrant tachycardia with left-sided accessory pathway.

We examined entrainment by ventricular pacing in six patients during orthodromic atrioventricular reentrant tachycardia (AVRT) utilizing a left-sided lateral accessory pathway. Constant fusion and progressive fusion were demonstrated in all patients by left ventricular pacing during tachycardia, but in none of the patients by right ventricular pacing. When left ventricular pacing was performed during AVRT, the antidromic wave front from the pacing impulse (n) collided with the orthodromic wave front of the previous pacing beat (n - 1) within the ventricle, therefore, constant fusion and progressive fusion were demonstrated in the surface electrocardiographic QRS complexes. On the other hand, when right ventricular pacing was performed during orthodromic AVRT, the antidromic wave front from the pacing impulse (n) collided with the orthodromic wave front of the previous paced beat (n - 1) within the normal atrioventricular pathway, and constant fusion and progressive fusion were therefore not demonstrated. These phenomena were explained by the relationship of the ventricular pacing site and the reentrant circuit. This study demonstrates the importance of the pacing site in manifest entrainment of orthodromic AVRT during ventricular pacing.

Determinants of Antidromic Wave Front Propagation During Entrainment of Reentrant Arrhythmias

Antidromic Conduction. During entrainment or resetting of ventricular tachycardia, the distance a stimulated antidromic wave front propagates determines the degree of QRS fusion observed. Determinants of antidromic wave front propagation distance during stimulation at reentry circuit sites were studied in computer simulations of figure eight reentry circuits. When not limited by refractory tissue, antidromic propagation distance depended on the stimulus timing, the conduction velocity in the antidromic direction away from the stimulus site, and the time available for propagation before collision with a returning orthodromic wave front. The latter was determined by the conduction time through the circuit in the orthodromic direction from the stimulus site. Faster conduction from the stimulus site in the orthodromic direction relative to the antidromic direction diminished antidromic wave front propagation distance. Consequently, in circuits with heterogeneous conduction velocities, antidromic propagation distance was dependent on the location of the stimulus site. Stimulation in slow areas limited antidromic propagation distance, although increasing stimulus prematurity increased antidromic propagation distance markedly if the antidromic wave front reached faster tissue. These findings explain the ability of rapid or premature stimuli to entrain or reset tachycardia without producing detectable antidromic wave front effects (QRS fusion) on the surface electrocardiogram when the stimulation site is located centrally within slowly conducting areas in the reentry circuit. However, greater antidromic propagation occurs with stimulation at or near more rapidly conducting sites increasing the likelihood that antidromic effects will be seen on the surface electrocardiogram.

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

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. 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. 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.

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

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. 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). 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.

Activation mapping of reentry around an anatomic barrier in the canine atrium. Observations during entrainment and termination.

We determined total right atrial activation sequences during entrainment and termination of flutter induced in dogs with a surgically induced atrial lesion. This type of atrial flutter is due to circus movement of an impulse around the tricuspid valve orifice. We recorded simultaneously from 96 bipolar intracavity electrodes in the right atrium of the isolated, perfused heart. By constructing isochronal maps, we demonstrated the pattern of atrial activation during atrial pacing protocols that either entrained or entrained and then terminated the reentrant rhythm. We show that during pacing the antidromic wavefront from the paced impulse (An) collides with the orthodromic wavefront from the previous paced impulse (On-1). During entrainment, the site of collision of the orthodromic and antidromic wavefronts was constant during pacing at a fixed rate but shifted in the antidromic direction as the pacing rate increased. Furthermore, the last paced beat was entrained only up to the site of collision of the previous paced beat. During one period of entrainment, termination of the reentrant arrhythmia occurred because On-1 blocked in the reentrant pathway due to refractory tissue left by On-2. However, subsequent An did not collide directly with On as was expected, but rather On blocked by an interaction with tissue left refractory by An. Because On was blocked, no reentry occurred when pacing ended.