Abstract
Posteroseptal accessory pathways (APs) are actually not septal but reside in a complex region bordering the right atrium, right ventricle, left ventricle, left atrium and coronary sinus and its branches. Posteroseptal APs are among the most challenging to ablate given the complex anatomic relationships and the possible need to map in all of these locations. Distinguishing retrograde AV nodal conduction from retrograde septal AP conduction is yet another hurdle. Moreover, the risk of AV nodal or coronary arterial injury from ablation of posteroseptal accessory pathways is significant. Given these challenges the electrophysiologist should usually map all the potentially viable locations before proceeding with ablation.
Keywords
accessory atrioventricular bundle, accessory pathway potential, accessory pathway, antidromic atrioventricular reentrant tachycardia, atrioventricular reentrant tachycardia, catheter ablation, catheter ablation mapping, posteroseptal atrioventricular reentrant tachycardia, preexcitation, supraventricular tachycardia, Wolff-Parkinson-White syndrome
Key Points
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Posteroseptal accessory pathways (APs) are not true septal pathways but are located in the complex inferior pyramidal space involving the right atrium, right ventricle, left ventricle, left atrium, and coronary sinus and its branches.
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Mapping often needs to be performed in multiple regions including the septal tricuspid annulus, septal mitral annulus, proximal coronary sinus, and normal and abnormal branches of the coronary sinus including the middle cardiac vein, posterior cardiac vein, and possibly coronary sinus diverticula.
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Targets for catheter ablation are similar to other APs including anterograde or retrograde AP potentials, earliest local ventricular activation during preexcited rhythm, early atrial activation during orthodromic atrioventricular (AV) reentrant tachycardia —or possibly during ventricular pacing—but may also include coronary sinus muscular extension potentials analogous to AP potentials for these epicardial accessory connections.
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Equipment potentially needed for these mapping and ablation procedures include precurved or deflectable sheaths for positioning along the tricuspid annulus, equipment for trans-septal puncture possibly including intracardiac echocardiography, transseptal needles and sheaths and guidewires, preformed or deflectable sheaths for transseptal access, balloon occlusion angiographic catheters for coronary sinus venography, 4-mm-tip or irrigated radiofrequency catheters, or possibly cryoablation catheters for ablation adjacent to coronary arteries.
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Potential challenges include the very complex anatomic relationships, adjacent AV conduction system, the need for mapping along the tricuspid valve, mitral valve, and coronary sinus in many procedures before selecting an ablation target, oblique AP angulation as in other regions, abnormal anatomy such as coronary sinus diverticula, and proximity to the coronary artery branches such as the right coronary artery or AV nodal artery.
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The declining volume of AP ablations and the almost universal relationship of volume and outcomes emphasizes the importance of solid grounding in AP ablation during electrophysiologic training and maximizing the learning from these scarcer cases.
JPD reports the following relationships with industry: (1) Research grants to Duke University from Biosense-Webster, Medtronic, Boston Scientific, and Gilead (all are >10,000 USD); (2) Honoraria for lectures, advisory board, or consultation from: ARCA Biopharma, Biosense-Webster, Biotronik, Boston Scientific, Cardiofocus, Gilead, Medtronic, Orexigen, St. Jude, Spectranetics, and Vytronus (all are <15,000 USD); (3) Fellowship support to Duke University provided by: Biosense-Webster, Boston Scientific, Medtronic, and St. Jude (all are >10,000 USD).
Anatomy
Accessory pathways (APs) are located around the tricuspid or mitral atrioventricular (AV) valves with the exception of the aorto-mitral continuity in the left anterior septal aspect of the heart. Posteroseptal APs are the second most common variety of AV connection encountered clinically after left free wall APs. In general, they exhibit somewhat negative delta waves in the frontal plane electrocardiogram (ECG) leads and an early transition on the precordium (often in V 2 ). Neighbors of the posterior septal AP include left posterior free wall APs along the mitral annulus (MA), true midseptal APs along the tricuspid annulus (TA), and right posterior APs along the TA. Posteroseptal APs exhibit very complex anatomy consisting of several subtypes. Although the term posteroseptal is firmly entrenched in the electrophysiologic vocabulary, cardiac anatomists have long protested that these pathways are not truly septal in location. Furthermore from a true anatomic perspective, this region could be considered inferior rather than posterior. As opposed to most left free wall APs, which anatomically lie epicardial to a well-defined annulus fibrosis, tricuspid and posteroseptal APs lack the same robust annulus fibrosis as shown in Fig. 24.1 . Like other APs, they are now understood to course obliquely across the AV annulus rather than transversely, and this is appreciated in Fig. 24.1 with the atrial ventricular aspects of the AP residing in different sections ( A and C , respectively). Fig. 24.2A illustrates relevant right atrial endocardial anatomic relationships of posterior septal APs. The triangle of Koch is defined by the tendon of Todaro (TT), the septal leaflet of the tricuspid valve, and the coronary sinus (CS) orifice (see Fig. 24.2A ). The His bundle resides in the apex near the central fibrous body ( asterisk ) and the compact AV node outlined in yellow according to its typical location. Posterior septal pathways lie inferior (termed somewhat inaccurately as posterior) to the roof of the CS or within the CS ostium or proximal extent (about 2 cm), or along the posterior (inferior) septal aspect of the MA. It can easily be appreciated that these pathways are challenging in view of their proximity to the normal conduction system. Moreover, differentiating atrioventricular reentrant tachycardia (AVRT) caused by a posteroseptal AP from AV node reentry, wherein the earliest A can be mapped to a very similar area, may pose additional challenges. Patients, especially those with congenital anomalies, exhibit considerable variation in Koch’s triangle and location of the AV node. Fig. 24.2B illustrates this variation with a large CS orifice and small triangle of Koch. Fig. 24.2C–E further shows sections through the septal region demonstrating the AV node giving rise to the bundle of His and the relationships of the AV nodal artery. Because the TA lies slightly more apical than the MA and the interatrial septum slightly leftward to the interventricular septum, one must recall that the right atrium is anatomically juxtaposed with the left ventricle (LV) in this region ( Fig. 24.3 ). Fig. 24.4 exhibits progressively deeper dissection into the posterior septal region or inferior pyramidal space. Fig. 24.5 illustrates this inferior pyramidal space by computed tomography scan showing it is not true septal territory and illustrating the anatomic relationships including CS and AV nodal artery.
Epicardial accessory AV connections are an important subgroup of posteroseptal APs. The various endocardial as well as epicardial pathways are illustrated in Fig. 24.6 . Pathway type 1 (see Fig. 24.6 ) is an endocardial connection between the right atrium and right ventricle. Pathway type 2 is right atrial to left ventricular; this portion of the LV is termed the posterior superior process . Pathway 3 refers to an endocardial left atrial (LA) to left ventricular AV connection (see Fig. 24.6 ). Pathway type 4, an epicardial one, depicts a muscular connection between the LV and CS musculature in the middle cardiac vein; similar pathways can occur in slightly more distal coronary venous branches such as the posterior cardiac vein. Lastly, pathway type 5, another epicardial one, portrays a CS diverticulum, an anatomic anomaly, electrically connecting the LV and the CS musculature of the diverticulum. An additional schematic, Fig. 24.7 , delves further into the proposed anatomy of epicardial posteroseptal APs.
Pathophysiology
APs in the posterior septal region can exhibit all of the same pathophysiologic processes as other APs, plus some other unique ones as well. When manifest (that is exhibiting anterograde conduction), the surface QRS is a fusion of AP-generated ventricular muscle activation and activation over the His-Purkinje system. A rare but critical exception arises when anterograde AV nodal-His block occurs. Needless to say, this rare circumstance should be elucidated before ablating the AP! Pathways in the posterior septal region are not as apt to be concealed (retrograde-only), accounting for only 10% to 13% of posteroseptal APs as compared with 30% of left free wall ones.
Analogous to other AP locations, patients possessing posteroseptal APs may be asymptomatic, that is, thus far free from known or suspected arrhythmias. In the asymptomatic patient, the physician needs to consider the rare chance of cardiac arrest occurring in the future and implement risk stratification.
As for other APs, the most common arrhythmia produced by posteroseptal APs is orthodromic AVRT. A common mode of induction consists of a spontaneous or stimulated premature atrial beat that blocks (in a bidirectionally conducting AP) anterogradely, conducts slowly down the AV node, and then reenters the AP retrogradely ( Fig. 24.8 ).
Posteroseptal APs were notably absent in the Duke, Maastricht, and French publications collating true antidromic AVRT cases, that is, pathways using the AV node as the retrograde circuit. Posterior septal pathways may exhibit other preexcited tachycardias such as those using a second, retrogradely conducting AP. Conversely, in a large multicenter pediatric series including 1147 patients, antidromic AVRT was rarer than in adults (2.6% vs. 8%–10%), and interestingly, posteroseptal APs were represented like other locations; again, presumably these were true antidromic AVRT and not pathway-to-pathway reentry. Atrial fibrillation with preexcitation over posterior septal AP may be symptomatic or lead to sudden cardiac arrest.
Most pathways (about 75%) exhibiting the phenotype of permanent junctional reciprocating tachycardia (PJRT) are located in the posterior septal region. Permanent denotes that these arrhythmias tend to be incessant because of the relatively slow rate. Owing to the long retrograde conduction time, they fall under the “long-RP” classification. Fig. 24.9 shows electrocardiographic and electrogram data from a left posteroseptal, epicardial, decremental retrograde-only AP with incessant (long-RP), slow AVRT. Notably, this patient did exhibit a mild, tachycardia induced cardiomyopathy that resolved with successful catheter ablation. Tachycardia induced cardiomyopathy has been observed in nearly a quarter of PJRT patients in one large series. Notably, tachycardia is not the only mechanism for ventricular dysfunction. Posteroseptal APs, and right free wall ones, occasionally develop ventricular dysfunction secondary to a dyssynchronous contraction pattern engendered by the left bundle branch block (LBBB)-like conduction pattern. By eliminating preexcitation catheter ablation can resolve this cardiomyopathy.
RVA , right ventricular apex. Demographically, it is well appreciated that AV nodal reentrant tachycardia (AVNRT) is more common in females and APs slightly more common in males; one study showed that the main increase in prevalence of APs was for pathways located in the left posterior septal region.
Two other electrocardiographic phenomena, relating to depolarization and repolarization, respectively, are noteworthy. Preexcitation over a posteroseptal AP presents a “pseudo-infarct” pattern in the inferior leads because of the negative delta waves inferiorly. When preexcitation is eliminated, cardiac repolarization remains abnormal, typically exhibiting T wave inversion inferiorly—a process called cardiac memory . Resolving over a period of several months, cardiac memory is relatively conspicuous for posterior septal pathways.
Ebstein’s anomaly is another important association with posterior septal APs. Indeed, Wolff-Parkinson-White (WPW) syndrome may be demonstrated as a concomitant diagnosis in up to 10% of Ebstein’s anomaly patients. In Ebstein’s anomaly, the posteroseptal location is second most frequent behind the right free wall group. In a multicenter series, 19 of 34 Ebstein’s patients displayed multiple pathways, especially the combination of a right free wall and a posterior septal one.
Arrhythmia Diagnosis and Differential Diagnosis
Let us first consider the differential diagnosis for tachycardias associated with a posteroseptal AP, and then the preexcitation pattern as it relates to posteroseptal versus other APs. As noted, the most commonly observed arrhythmia is orthodromic ARVT. The usual differential diagnosis applies when confronted with a narrow QRS, regular tachycardia, namely AVNRT, (orthodromic) AVRT, and atrial tachycardia; automatic junctional tachycardia should not be neglected. Dissociation of the atrium and ventricle excludes AVRT. Armed with intracardiac recordings, bolstering the surface P wave timing, and examining the earliest atrial activation, the diagnosis is sometimes nearly obvious. For example, supraventricular tachycardia (SVT) with CS distal to proximal activation makes AVRT using a left lateral AP highly likely. In addition, the cycle length or ventriculoatrial (VA) interval changes associated with ipsilateral bundle branch block when present provide a clear diagnosis of a free wall APs involvement in a tachycardia ( Tables 24.1–24.3 ). Importantly, posteroseptal APs may exhibit an intermediate degree of VA interval prolongation with LBBB ( Fig. 24.10 ). Amongst posteroseptal APs, Haïssaguerre et al. have correlated LBBB-related VA prolongation with a positive delta wave in V 1 , indicative of an LV insertion.
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| Maneuver | Orthodromic AVRT | AVNRT | AT |
|---|---|---|---|
| Development of BBB | Lengthening the tachycardia CL by 35 ms indicates ipsilateral free wall AP a | No significant change in tachycardia CL | No significant change in tachycardia CL |
| Development of BBB | Lengthening the VA interval by 35 ms indicates ipsilateral free wall AP | No significant change in VA interval | No significant change in VA interval |
| Development of LBBB | Lengthening the tachycardia VA by 5–30 ms consistent with posteroseptal AP | No consistent change in VA interval | No significant change in VA interval |
| Development of RBBB | Minimal change in VA consistent with posteroseptal AP | No significant change in VA interval | No significant change in VA interval |
| VA dissociation | Disproves AVRT | 2 to 1 block below His not uncommon; 2 to 1 block above His in LCP rare; VA dissociation very rare | 2 to 1 and other non-1 to 1 AV conduction is common |
| Ventricular entrainment | V-A-V response | V-A-V response | V-A-A-V response b ; or dissociation of the As from the Vs. |
a Prolongation of the HV interval could theoretically lengthen the tachycardia CL.
b Knight et al. use the terms A-V and A-A-V to describe the events the last ventricular stimulus, but common parlance uses V-A-V and V-A-A-V. (Knight BP, Zivin A, Souza J, et al. A technique for the rapid diagnosis of atrial tachycardia in the electrophysiology laboratory. J Am Coll Cardiol . 1999;33:775-781.)
| Maneuver | Posteroseptal Orthodromic AVRT | AVNRT |
|---|---|---|
| Parahissian pacing | No change in Stim-A with loss of His capture; or change in atrial activation sequence | Increased Stim-A with loss of His capture; identical atrial activation sequence |
| PVC during His refractoriness a | Advances atrial activation; delays atrial activation; or terminates tachycardia without conduction to atrium | Unable to advance or delay atrial activation |
| Delta HA interval | HA pace – HA svt < –10 ms (i.e., more negative) | HA pace – HA svt > –10 ms (less negative or positive number) |
| Preexcitation index | 10–70 ms; overlaps with right free wall, anteroseptal and left free wall; left free wall not <50 ms | Usually > 100 ms |
| Difference between ventricular PPI and TCL | <115 ms | >115 ms |
| Corrected difference between ventricular PPI and TCL | <110 ms | >110 ms |
| Difference between VA during ventricular pacing at TCL and VA during tachycardia | <85 ms | >85 ms |
| VA pacing at ventricular base versus pacing at ventricular apex | VA shorter with pacing of base | VA shorter with pacing of apex |
| Ventricular entrainment without fusion | Acceleration of A to PCL within 1 beat of fully paced morphology | Acceleration of A to PCL in ≥ 2 beats of fully paced morphology |
| Ventricular entrainment with fusion | Atrial timing altered; or a fixed SA interval is established within the transition zone (fusion, i.e., before fully paced morphology) | Atrial timing not altered; nor a fixed SA interval established when fusion present |
a Failure of a premature ventricular complex (PVC) to affect the tachycardia (i.e., right column, under AVNRT) is consistent with atrioventricular nodal reentrant tachycardia (AVNRT) but does not exclude atrioventricular reentrant tachycardia (AVRT); demonstration of PVC advancing the tachycardia (i.e., left column, under AVRT) is consistent with AVRT and proves the existence of an accessory pathway (AP), but theoretically the rhythm could be AVNRT or atrial tachycardia (AT) with a bystander AP. Perturbing the atrium with a PVC during His refractoriness and advancing the next His (i.e., advancing the tachycardia) does prove existence of an AP and participation in the tachycardia as does delaying the atrial activation (i.e., that it is AVRT).
Conversely, because of the concentric pattern (i.e., midline atrial activation) with orthodromic AVRT using a posteroseptal AP, retrograde AV nodal activation is not easily excluded. Although atrial recordings at the CS ostium should be earliest in AVRT via a posteroseptal AP, it can be similar with retrograde slow pathway activation, and for right posteroseptal APs, the His atrial and CS proximal atrial may be nearly tied. Further challenging the clinician, recall that retrograde AV nodal activation may appear eccentric because of left-sided AV nodal exits (LA slow pathway exit or leftward inferior extension).
Next steps in diagnosing a narrow QRS, 1:1 SVT reside with the stimulator. Maneuvers during tachycardia comprise programmed single ventricular extrastimuli and ventricular entrainment. Pacing during sinus rhythm includes differential pacing (base vs. apex) or parahissian pacing. The key principles to understanding the different response centers around the situation in AVRT where a ventricular stimulus is potentially able to engage the retrograde AP at a time when the His bundle has just conducted anterogradely. This cannot occur in AVNRT or atrial tachycardia (except for the theoretical use of a bystander retrograde AP). Advancing the timing of the retrograde atrial with a His-refractory premature ventricular complex (PVC) or with surface QRS fusion during entrainment (fusion referring to orthodromic activation via His plus ventricular pacing) are two manifestations of the same phenomenon. Another principle relates to ventricular pacing being able to engage an AV AP earlier when pacing from near its insertion (more basally in general, but also theoretically in the LV for a left-sided one) as opposed to the mode of retrograde engagement of the AV node via the right bundle branch, which terminates in the right ventricular (RV) apical septal region (see Table 24.2 ). Comparing VA or His-to-atrial intervals during SVT and during pacing relies on the concept that in AVNRT anterograde activation of the ventricle occurs concurrently with retrograde conduction to the atrium, whereas in AVRT there is sequential activation (ventricular-AP-atrial-AV node-His); with pacing, it is sequential from ventricular to atrial over either the AVN or the AP (see Table 24.2 ). Finally, parahissian pacing evaluates whether atrial activation timing is dependent upon or independent of His bundle activation (see Table 24.2 ).
Posteroseptal APs can participate in wide QRS tachycardias of several types. In addition to a narrow QRS morphology, orthodromic AVRT can exhibit bundle branch block aberrancy as discussed earlier and in Table 24.1 . Antidromic AVRT using the AP anterogradely and the His bundle-AV node retrogradely was not observed for posteroseptal APs in three of four large series but was seen in one pediatric series. However, pathway-to-pathway tachycardias, that is, using a second AP as the retrograde limb, were noted. Either of these tachycardias will be wide, have a slurred QRS onset, and regular cycle length; some SVT versus ventricular tachycardia (VT) ECG criteria will classify these as VT since they resemble VT by having a myocardial activation pattern rather than a bundle branch to Purkinje rapid activation mode; other algorithms may prove more accurate for detecting preexcitation versus VT. Other preexcited tachycardias include atrial flutter, atrial tachycardia, or atrial fibrillation as well as, more rarely, AV node reentry with a bystander AP.
Turning to preexcitation, differentiating posteroseptal APs from neighboring ones can be difficult as can be expected from the anatomy. Challenges include the proximity to the AV conduction system and possible need to consider multiple locations. Predicting the location of an AP before electrophysiologic study has great value in preprocedural planning. Understanding the likelihood that a pathway is left-sided or near the conduction system on the interatrial septum modifies informed consent and optimizes selection of catheters and sheaths. Fortunately, a number of algorithms have been designed that use the 12-lead ECG and examine the axis of the delta wave or the polarity of the QRS morphology through certain leads.
The first attempt at classification and ECG localization was published in 1945 by Rosenbaum et al. who divided preexcitation patterns into either left or RV pathways. In type A, or left ventricular pathways, the delta wave was upright in all precordial leads. In type B, or RV pathways, the delta wave was negative, with prominent S waves in the right precordium.
In 1987, Milstein et al. reported an algorithm that used previously described ECG features of AP locations and refined these features with an analysis of 97 patients with a single known AP. Their algorithm used the polarity of delta waves, the presence of isoelectric periods in certain leads, or an LBBB-like pattern (Rosenbaum B) to localize single pathways to one of four locations: right lateral, left lateral, anterior septal, and posterior septal. Milstein et al. tested their algorithm on the ECGs of 141 patients with WPW who had invasive AP location verification and reported an accuracy of 90% to 91%. Two other algorithms, both published in 1995, attempted more specific anatomic localization dividing AP locations into eight or nine zones and reporting >90% accuracy.
Fig. 24.11 shows one of the most commonly used algorithms for determining the ventricular insertion of an AP developed by the Oklahoma team. It focuses on the initial 20 to 40 ms of the delta wave. First, left free wall pathways are identified by a negative or isoelectric delta wave in lead I and/or a dominant R wave in V 1 (R>S). Next, relevant to the posteroseptal space, a negative delta in II classifies the AP as subepicardial (middle cardiac vein, CS-associated diverticulum or possibly left posterior cardiac venous branch); subsequent data disclose that a negative delta wave in II is specific for subepicardial pathways, but the finding has only moderate sensitivity of 68%, that is, absence of it does not rule out the middle cardiac vein (MCV) region. If neither the findings for left free wall nor subepicardial pathways are present, the septum or right free wall are implicated. The next branch point considers V 1 , and if positive, the right free wall is the site, but if negative or isoelectric, the pathway should be septal. Note that the right free wall APs have a positive delta wave but an overall negative QRS in V 1 and a transition at V 3 or later. Breaking down the septal pathways (V 1 isoelectric or negative), the algorithm considers aVF: negative pointing to posteroseptal TA, isoelectric compatible with posteroseptal TA or MA, and positive characteristic of midseptal or anteroseptal site. Subepicardial APs, the most inferior or posterior, have negative delta waves in II, III, and aVF; next most inferiorly, the posteroseptal TA negative (or isoelectric) in aVF and III but not II. On the other hand, the most anteriorly located (anteroseptal) APs have positive delta waves in II, III, and aVF; the midseptal and posteroseptal MA are intermediate.
