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Ablation of Free Wall Accessory Pathways


Key Points

  • The atrioventricular (AV) annulus is mapped for atrial or ventricular accessory pathway (AP) insertion sites or the AP itself.

  • Ablation targets include the earliest site of atrial or ventricular activation by the AP, sites of AP potentials, and sites of electrogram polarity reversal (left free wall APs).

  • Special equipment includes preformed sheaths (especially for the transseptal approach), multielectrode halo mapping catheters, and steerable sheaths (especially for right free wall). Catheter navigation systems are useful, and electroanatomic mapping may play an important role in reduction of fluoroscopy.

  • Sources of difficulty are misdiagnosis of atrioventricular nodal reentry with eccentric atrial activation or atrial tachycardia as orthodromic reciprocating tachycardia, catheter stability (especially with right free wall APs), AP insertion sites away from the annulus, multiple insertion sites, and epicardial APs.

Free wall locations are the most common positions for accessory pathways (APs) in clinical practice. Right and left free wall APs account for 10% to 20% and 50% to 60% of all APs, respectively. These pathway locations each present distinct challenges to the electrophysiologist. Left free wall APs are very amenable to ablation and have the highest success rates and lowest incidences of recurrence. The left heart location is less accessible, however, necessitating arterial or transseptal approaches. In contrast, right free wall APs are readily approached from simple venous access but have the lowest success rates and highest incidences of recurrence.

Anatomy

The anatomy of the tricuspid annulus is different from that of the mitral annulus. The hinge of the mitral atrioventricular (AV) annulus is a well-formed and distinct cord of fibrous tissue around the annulus ( Fig. 23.1A ). This accretion of fibrous tissue is interposed between the atrial and ventricular myocardia. On the ventricular side of the mitral annulus, basal cords of ventricular myocardium may descend in a curtain-like fashion from the mitral hinge to insert into the trabeculations on the ventricular wall. These cords may limit catheter mobility beneath the valve during attempts at left free wall AP ablation using the retrograde aortic approach. In the limited human histologic descriptions of left free wall APs, the atrial connection is usually discrete and near the annulus. The pathways then skirt the annulus on its epicardial aspect and may cross at variable depths within the epicardial fat pad ( Fig. 23.1B ). The ventricular insertion usually branches into multiple connections with the ventricle that may be displaced away from the annulus, toward the apex. The histologically determined length of an AP is typically 5 to 10 mm, with a maximal diameter of 0.1 to 7 mm. The left-sided epicardial AV groove is shallow but contains the left circumflex artery near the annulus and the coronary sinus (CS) more remote from the annulus. Although the CS is useful for quickly mapping the mitral valve area, it runs an average of 10 to 14 mm on the atrial side of the true annulus. This separation from the annulus is more pronounced in the proximal 20 mm of the CS. Therefore during catheter mapping, the CS location and electrograms are best regarded as gross estimates of the true AP location on the annulus. The anterior limit of the left free wall is anatomically well demarcated by the aorto-mitral valve continuity, which rarely contains AP connections. The exact location of this continuity is difficult to recognize by fluoroscopy alone. The posterior limit of the left free wall is anatomically continuous with the posteroseptal area and is arbitrarily defined on fluoroscopy.

Fig. 23.1, A, Gross histologic section demonstrating a cross section of the atrioventricular (AV) valves along the free walls. Note the more apical position of the tricuspid valve (TO) compared with the mitral valve (MO). B, Histologic sections of the tricuspid (left) and mitral valve (right) annuli through the free walls. Along the tricuspid annulus, the atrial and ventricular myocardium folds over one another, separated by a poorly defined fibrous component (arrowheads) . The arrows show two cords supporting the base of the valve leaflet. Right : The distinct fibrous component to the mitral annulus creates a well-formed hinge (asterisk) for the mitral valve and separates the atrial and ventricular myocardia. Note the relation of the circumflex coronary artery (CA) and coronary sinus (CS) to the mitral annulus. C, Histologic sections of the mitral annulus in patients with a left posterior accessory pathway (left) and a left lateral accessory pathway (right) . In each case, the accessory pathways (arrows) cross in the epicardial fat pad (EF) on the epicardial aspect of the annulus fibrosus. Note the distant location of the CS to the accessory pathway ( left) . Right: atrial myocardium (AM) encircles the circumflex CA. AVS, Atrioventricular septum; IAS, interatrial septum; IVS, interventricular septum; LA, left atrium; limb, limbus; LV, left ventricle; MV, mitral valve; RA, right atrium; RV, right ventricle; VM, ventricular myocardium; VOF, foramen ovale.

In contrast to the mitral annulus, the tricuspid valve annulus (TVA) is less well formed and frequently discontinuous. The right atrial and right ventricular myocardia tend to overlap or fold over one another as they insert on the tricuspid annulus (see Fig. 23.1 B ). Right free wall APs may cross discontinuities in the less distinct fibrous annulus or skirt the epicardial aspect of the annulus, as do left free wall APs. The less developed tricuspid annulus and acute angulation of the tricuspid leaflets toward the ventricle make catheter positions along the right free wall unstable. Fluoroscopic definition of the right free wall is difficult because there are no clear landmarks for guidance.

Because of the association of Ebstein anomaly with right-sided APs, the anatomy of this condition merits special consideration. In this disorder, the tricuspid valve leaflets are tethered to the ventricular wall for variable distances from the annulus. This contributes to catheter instability during mapping of the tricuspid annulus. Although not anatomically displaced, the true tricuspid annulus may be poorly developed, with extensive discontinuities of the fibrous architecture. Electrograms recorded from the annulus in Ebstein anomaly may be of low amplitude and fragmented owing to the disorganized tissue. This fragmentation adds to the difficulty in mapping the tricuspid annulus in this condition. APs in Ebstein anomaly are often multiple and may skirt the epicardial aspect of the annulus or pass subendocardially through gaps in the fibrous annulus.

A complete description of free wall accessory AV connections must also include those resulting from connections of the ventricle to the CS musculature, the ligament of Marshall, and the atrial appendage. Mahaim-type atriofascicular connections are described in Chapter 26 . The venous wall of the CS is surrounded by a continuous sleeve of atrial myocardium that extends 25 to 51 mm from the CS ostium. This muscle is continuous with the right atrial myocardium proximally but is usually separated from the left atrium by adipose tissue. This separation may be bridged by strands of striated muscle, however, producing electrical continuity between the CS musculature and the left atrium ( Fig. 23.2 ). These connections, which can be broad and very extensive, are reported in up to 80% of hearts in autopsy series. Electrical continuity of the CS musculature with the ventricle is less common, but it may provide the substrate for reciprocating tachycardias. Ventricular connections may result from CS musculature extensions over the middle cardiac vein, posterior cardiac vein, or AV groove branch of the distal left circumflex artery. Ventricular connections with the CS are described in 3% to 6% of hearts at autopsy. Sun and associates reported that 36% of patients (most with previously failed ablation) who had left posterior or left posteroseptal AV connections actually used the CS musculature as the intermediary between the atrium and ventricle in reciprocating tachycardias.

Fig. 23.2, Coronary sinus (CS) potentials recorded during mapping of the left lateral accessory pathway. The first complex represents orthodromic reciprocating tachycardia with earliest atrial activation at CS 7,8. The second complex is a premature ventricular stimulus that reverses the sequence of ventricular activation along the CS. This separates the atrial and ventricular potentials without altering the atrial activation sequence. After the ventricular electrogram on the CS tracings, there are low-amplitude, low-frequency, far-field atrial potentials (arrows) . After the atrial potentials on CS 5,6 through CS 9,10, there are high-amplitude, high-frequency CS musculature potentials (arrowheads) that are activated in a proximal-to-distal sequence. This is interpreted as activation of the proximal CS atrium by the accessory pathway with atrial conduction proximally to the point of connection to the CS musculature. The CS musculature then conducts proximally to distally along a portion of the CS catheter. CS 1,2, Distal CS; CS 9,10, proximal CS; HRA, high right atrium; RVA, right ventricular apex.

The ligament of Marshall is a vestigial fold of pericardium that carries the vein of Marshall from its origin as a branch of the distal CS to its termination near the left superior pulmonary vein. This structure may also contain bundles of muscle fibers that are continuous with the CS musculature. These fibers may end blindly, or they may insert directly into the left atrial musculature at the inferior interatrial pathway. With proximal connections between the CS musculature and the ventricle, the ligament of Marshall can support AV reciprocating tachycardia.

Another unusual form of AV connection is a direct epicardial muscular continuity between the atrial appendage and the ventricle. Several reports of connections between the right atrial appendage and ventricle are available, whereas left-sided connections appear even more rarely. The developmental basis for these connections is unknown. Because of epicardial ventricular insertions more than 1 cm apical to the annulus and atrial origins within the atrial appendage, endocardial mapping of the annulus for conventional APs is perplexing. For left-sided connections, mapping of the anterior coronary venous branches may demonstrate the earliest ventricular activation. At surgical division of one such right-sided connection, a broad band of myocardium under the epicardial fat pad was noted from the base of the atrial appendage to the base of the right ventricle. Case reports describe successful catheter ablation of these connections from the right atrial appendage.

Pathophysiology

Diagnosis

As with APs at other locations, free wall APs may participate in reciprocating tachycardias or undergo bystander activation during tachycardias mechanistically unrelated to the presence of the AP. Free wall APs have been associated with specific electrophysiologic characteristics. Compared with septal and left free wall locations, right free wall APs are less likely to demonstrate retrograde conduction, to participate in reciprocating tachycardias, and to be associated with inducible atrial fibrillation. Pathways in the right free wall may be more likely to demonstrate decremental anterograde conduction than those in other locations. Compared with right free wall pathways, left free wall APs are more likely to demonstrate decremental retrograde conduction and have longer retrograde refractory periods. Right-sided pathways may worsen cardiac function by activating the RV early and causing a functional LBBB.

Surface electrocardiogram (ECG) localization of manifest free wall APs is imperfect and becomes less accurate if minimal preexcitation is present (QRS <120 ms). ECG algorithms for AP localization are most accurate for the diagnosis of left free wall APs compared with all other locations, achieving at least 90% sensitivity and almost 100% specificity. In using any localization algorithm one must be aware of the portion of the QRS complex on which the algorithm is based. Some algorithms use only the first 20 to 60 ms of the delta wave, whereas others are based on the morphology or polarity of the entire QRS complex. Provided that significant preexcitation is present, all left free wall APs should demonstrate a positive delta wave in V 1 , with the R wave greater than the S wave (R > S) in lead V 1 or V 2 at the latest ( Fig. 23.3 ). A negative delta wave in lead I, aVL, or V 6 is pathognomonic of a left lateral pathway. As the pathway location moves from posterior to lateral to anterior, the delta waves in the inferior leads, especially aVF and III, change from negative to isoelectric to positive in polarity. The ratio of the dominant amplitude in limb lead II and III can predict if a left free wall pathway is anterior lateral or posterior lateral. If the ratio II/III is greater than 1, the pathway is likely anterior, and if it is less than 1, it is likely posterior.

Fig. 23.3, Twelve-lead electrocardiogram in sinus rhythm from a patient with a manifest left lateral accessory pathway. The positive delta wave in V 1 with R greater than S wave indicates a left free wall location. The negative delta waves in leads I and aV L are pathognomonic of a left free wall position. The positive delta waves in leads II, III, and aV F suggest a position anterolateral on the annulus.

As opposed to left free wall APs, the ECG diagnosis of right free wall APs is the least accurate and least consistent among algorithms, with a sensitivity of 80% to 90% and a specificity of 90% to 100%. Confusion may arise in the interpretation of a positive delta wave in V 1 as indicating a left-sided AP ( Fig. 23.4 ). This finding is diagnostic of a left free wall AP only if R is greater than S; a positive delta wave with R less than S in V 1 is consistent with a right free wall AP or a minimally preexcited left free wall AP. A negative delta wave in V 1 is consistent with a septal AP. Therefore most algorithms identify right free wall APs by a positive initial delta wave in V 1 but a late transition to R greater than S in the precordial leads at V 3 or later, coupled with leftward orientation to the initial delta wave, such as delta wave positivity in lead I or aVL. As the pathway location moves from the right superior free wall to the right middle and right inferior free wall, the delta wave in inferior leads aVF and II changes from positive to isoelectric to negative. A useful algorithm for AP localization that is based on the initial 20 ms of the delta wave is shown in Fig. 23.5 .

Fig. 23.4, A, Twelve-lead electrocardiogram (ECG) in sinus rhythm from a patient with a manifest right free wall accessory pathway. The delta wave is positive in lead V 1 ; however, the transition to R greater than S wave in the precordial leads does not occur until V 5 , indicating a right free wall location. The delta waves are negative in leads II, III, and aV F , indicating a position inferiorly on the right ventricular free wall. B, ECG from the same patient during antidromic reciprocating tachycardia using the right free wall pathway. The QRS complex is fully preexcited.

Fig. 23.5, Algorithm for accessory pathway localization by surface electrocardiogram (ECG). This algorithm is based on the polarity of the first 20 ms of the delta wave. Left free wall pathways are readily identified by an isoelectric or negative delta wave in lead I or an R greater than S wave in V 1 . Note that with right free wall pathways, the initial component of the delta wave is positive in V 1 but with R less than S wave. Right free wall pathways are identified by a late transition to R greater than S usually in V 3 or later. AS, Anteroseptal; LAL, left anterolateral; LL, left lateral; LP, left posterior; LPL, left posterolateral; MS, midseptal; PSMA, posteroseptal mitral annulus; PSTA, posteroseptal tricuspid annulus; RA, right anterior; RAL, right anterolateral; RL, right lateral; RP, right posterior; RPL, right posterolateral.

A study comparing several algorithms was not able to duplicate the accuracy of the original papers. Wren et al. looked at the accuracy of seven well known algorithms to predict AP location in children. In 100 children ages 3.8 to 17 years (mean age 11.7 years) the accuracy of prediction was 30% to 49% for exact location and 61% to 68% including adjacent locations. The algorithms were least accurate in predicting midseptal or right anteroseptal AP locations. The accuracy of algorithms may vary with ECG lead position, degree of preexcitation, patient body habitus, heart rotation, and prior QRS abnormalities.

The location of the AP can also be inferred from the surface ECG by the polarity of the retrograde P waves during orthodromic reciprocating tachycardia (ORT). A negative P wave in lead I is highly suggestive of a left free wall location, with a 95% positive predictive value. A negative P wave in lead V 1 is highly suggestive of a right-sided AP. The presence of a positive retrograde P wave in lead I suggests a right free wall AP with a positive predictive value of 99%. For either right or left free wall APs, the presence of negative P waves in all three inferior leads indicates an inferior location, whereas positive P waves in these leads indicate a superior location. Isoelectric or biphasic P waves in any of the inferior leads suggest a middle free wall location.

At electrophysiologic testing, the hallmark of any ORT is the demonstration of obligatory 1:1 atrial and ventricular activation for persistence of the tachycardia ( Box 23.1 ). The diagnosis of ORT using a free wall AP also requires an eccentric atrial activation sequence earliest along the right or left atrial free wall. Coupled with such an eccentric atrial activation sequence, ORT is highly suggested by demonstration of the shortest QRS-to-atrium time of 60 ms or more, constant ventricle-to-atrium times despite changes in the tachycardia cycle length, and the ability to advance atrial activation by a premature ventricular stimulus delivered during His bundle refractoriness. The last finding indicates the presence of an AP but does not prove participation in the tachycardia. A preexcitation index greater than 70 ms is consistent with a left lateral AP. The preexcitation index is the difference between the tachycardia cycle length and the longest coupling interval of a right ventricular apical premature stimulus that advances the atrium. Diagnostic of a free wall pathway is prolongation of the QRS-to-atrium (or His-to-atrium) time during reciprocating tachycardia (and usually of the tachycardia cycle length as well) by 35 to 40 ms or longer with ipsilateral bundle branch block. Left anterior fascicular block also prolongs the QRS-to-atrium time in patients with left free wall APs. Coupled with an eccentric atrial activation sequence, the ability to reproducibly terminate the tachycardia with a premature ventricular stimulus delivered during His bundle refractoriness but that does not result in atrial activation also proves an ORT. Parahissian pacing techniques consistently indicate the presence of retrograde conduction over right free wall APs. The response of left free wall APs to parahissian pacing is more complex. In about 25% of cases of left free wall APs, parahissian pacing is consistent with retrograde conduction over only the AV node. His capture may lead to a paradoxical shortening of the ventricle-to-atrium times, with left lateral APs because of the more rapid activation of the left free wall through the His-Purkinje system than occurs with septal ventricular capture alone.

BOX 23.1
Diagnostic Criteria

Orthodromic Tachycardia

  • Obligatory 1:1 AV relationship with earliest atrial activation on AV free wall

    • Shortest V-to-A time ≥60 ms

    • Constant V-to-A conduction times despite TCL variations

    • Advance atrial activation during His refractoriness (proves pathway presence but not participation in tachycardia)

    • Preexcitation index >70 ms (left lateral AP)

    • Ipsilateral bundle branch block prolongs His- (or V-) to-A time (and usually TCL) by ≥35 ms a

      a Proves free wall AP-mediated tachycardia.

    • Reproducible tachycardia termination by premature ventricular stimuli during His refractoriness without conduction to atrium b

      b Proves AP-mediated tachycardia.

Antidromic Tachycardia

  • Obligatory 1:1 AV relationship with earliest ventricular activation on free wall

    • QRS morphology in tachycardia consistent with maximal preexcitation

    • Tachycardia QRS morphology reproduced by atrial pacing near pathway insertion

    • Each limb of tachycardia circuit supports conduction at TCL

    • Advance ventricular activation by atrial extrastimuli near insertion with advancement of subsequent His and atrial activation b

    • Changes in V-to-His interval precede changes in TCL

    • Exclusion of ventricular tachycardia and bystander participation, especially AV nodal reentry (His-to-A time in tachycardia ≤70 ms consistent with AV nodal reentry)

A, Atrium; AP, accessory pathway; AV, atrioventricular; His, bundle of His; TCL, tachycardia cycle length; V, ventricle.

The diagnostic features of antidromic reciprocating tachycardia are given in Box 23.1 . Preexcited reciprocating tachycardias may use the AV node or a second AP as the retrograde limb. There are no surface ECG features that are diagnostic of antidromic tachycardia, but the diagnosis is excluded by demonstration of an atrial-to-ventricular relationship other than 1:1.

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