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Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3849_Библиотеки_им_академика_М_И_Перельмана

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6 Wol-Parkinson-White (WPW) Syndrome
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One of the biggest pitfalls with mapping in WPW is the possi­bility of fusion between pathway and nodal conduction, which can occur when mapping in sinus, atrial paced, and ventricular paced rhythms. This can be partially avoided by carefully adjust­ing the rhythm to promote pathway conduction, for example by accelerating the pacing rate, changing the pacing site to be closer to the pathway (best demonstrated by comparing the degree of preexcitation in right vs left atrial pacing at the same cycle length), or even administering medication (e.g. phenylephrine) to slow AV nodal conduction. Mapping in AVRT completely eliminates this concern. Mapping in orthodromic AVRT provides an additional advantage of crisper ventricular electrograms (due to His-Purkinje activation), sometimes resulting in more easily interpreted sig­nals. Alternatively, differential pacing from either side of the path­way can be performed so that the electrical wavefront is from the opposite direction from the presumed path of a slanted pathway. This technique separates the local electrogram components resulting in easier interpretation of electrograms and the resulting map. This approach is also reported to often unmask accessory pathway potentials, which are appealing targets for ablation.
Regardless of mapping strategy, it is critical to target the abso­lute earliest electrogram in the targeted chamber relative to a xed reference point such as a coronary sinus bipole (for retrograde mapping) or a surface lead with a clearly identiable deection (for antegrade mapping). Although tempting, it can be quite mis­leading to target sites with short local A-V interval (for antegrade mapping) or V-A interval (for retrograde mapping); while this local “fusion” is frequently present at successful sites (see Figs.6.10, 6.11c, 6.12b, 6.13c, 6.14a, 6.15, 6.16a), it can also be present at distant sites where both components of the local elec­trogram are delayed to similar degrees. Similar to mapping PVCs, the relevance of a suspected site can be conrmed independent of the relative timing data by analyzing precocity relative to surface QRS onset, and local unipolar electrogram timing and morphol­ogy.
Because almost all pathways are direct AV connections cross­ing the mitral or tricuspid annulus, interpretation of the maps is usually straightforward, with the earliest area being a point (or a
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Fig. 6.10 Surface and intracardiac electrograms at the site of successful ablation from mapping earliest ventricular activation in sinus rhythm, note the very early ventricular component recorded from the ablation catheter. Artifact in CS7,8 and ABLd channels relates to onset of RF delivery
Fig. 6.11 (a) Right atrial activation map (RAO and LAO/cranial views) of earliest atrial activation in AVRT of the patient in Fig.6.8 with an anteroseptal pathway. Yellow markers indicate sites where His potential was recorded; white/pink coloration indicates the area of earliest activation; blue markers indicate site of successful cryoablation. (b) Corresponding uoroscopy (RAO and LAO views) of catheter positions at the successful site. (c) Electrograms from the surface ECG, His, coronary sinus, right ventricle, and ablation cath­eter at the successful site
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Fig. 6.12 (a) Right atrial activation map (LPO and LAO views) of earliest ventricular activation in atrial pacing of a patient with a right posteroseptal pathway. White/pink coloration indicates the area of earliest activation. (b) Electrograms from the surface ECG, His catheter, coronary sinus catheter, and roving/ablation catheter at the site indicated by the green marker. Although only 16msec prior to QRS onset, early activation was well brack­eted and unipolar tip recording showed a QS morphology. Ablation at this site eliminated the pathway within 1s
small line running across the atrioventricular groove), and with progressively later points to either side along the annulus (see Figs.6.11a, 6.12a, 6.13a, b). A broad area of earliest electrograms suggests (1) imprecise electrogram interpretation that may benet from careful manual review or switch to a different mapping strat­egy, (2) fusion between pathway and nodal conduction if plausi­ble in the rhythm being used, (3) fusion between multiple pathways, and/or (4) that the true earliest area has not been
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Fig. 6.13 (a) Right atrial activation map (RAO view) of earliest atrial activa- tion during ventricular pacing of a patient with WPW and two bidirectional accessory pathways. The right anterolateral pathway’s antegrade conduction was weak and prone to mechanical suppression but retrograde conduction was readily mapped after change in strategy. (b) Right atrial activation map (LAO/caudal view) of earliest atrial activation during orthodromic AVRT in the same patient. Antegrade conduction was not readily mapped due to com­plex difcult-to-annotate electrograms through a large portion of the poste­rior annulus, but retrograde conduction was readily mapped after change in strategy. (c) Electrograms from the same patient. First beat, site where abla­tion eliminated the anterolateral pathway within 1s. Remaining beats, site where ablation eliminated the posterior pathway within 3s
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Fig. 6.14 Surface and intracardiac electrograms (a) before and (b) just after successful ablation performed during ventricular pacing in a patient with WPW via a left lateral accessory pathway. Note the change from eccentric retrograde conduction (coronary sinus activation distal to proximal) to absent retrograde conduction exposing V-A dissociated sinus rhythm. Displayed channels are as in Fig. 6.15
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explored, for example on the opposite side of the atrial septum, or (rarely) within an atrial appendage or coronary sinus.
Entrainment
Although WPW supports SVT via a reentrant mechanism, it can be mapped like a focal tachycardia by following the activation pattern towards the earliest site, which should correspond to where the pathway crosses the atrioventricular groove. Thus, entrainment maneuvers are not critical to mapping of WPW. However, they can occasionally be useful diagnostically (e.g. in evaluating whether an SVT is AVRT) or when there is uncertainty about whether the pathway is left-sided or right-sided (although usually this is evident from the retrograde atrial activa-
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Fig. 6.15 Surface and intracardiac electrograms showing loss of preexcita­tion (between rst and second beats) due to ablation performed during atrial pacing in a patient with WPW.Note the very early local ventricular activation recorded from the ablation catheter on the rst beat, compared to the well­separated atrial and ventricular electrograms on the later beats
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tion sequencing, see Fig.6.17). When performed, the maneuvers are comparable to those used for AVRT.
Ablation
Correct, precise mapping is the cornerstone of successful WPW ablation. Most pathways are delicate and can be easily eliminated with energy delivery at the correct location. However, there are important considerations with regard to the rhythm in which ablation is performed (see Table6.1). Because cardiac lling can vary with heart rate and A-V relationship, the exact location of the pathway may differ in different rhythms and therefore mapping and ablation are ideally performed in the same rhythm.
Catheter stability can be an issue with abrupt rhythm changes at the moment of ablation success, such as when AVRT breaks to sinus rhythm with elimination of pathway conduction. This dif­culty can be minimized by mapping in AVRT and then ablating in V-entrained AVRT. By carefully entraining just slightly faster
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Fig. 6.16 Surface and intracardiac electrograms (a) before and (b) just after successful ablation performed during sinus rhythm in a patient with WPW. Note again the very early local ventricular activation recorded from the ablation catheter during preexcitation, compared to the well-separated atrial and ventricular electrograms during nodal conduction. Unlike the previ­ous gure, this patient has relatively subtle preexcitation so the changes in surface PR interval and coronary sinus AV interval are less prominent than the local change at the ablation site. Displayed channels are as in Fig. 6.15
than the tachycardia (often achieving sustained fusion in QRS morphology), the map remains accurate, but at the time of path­way success there is only a small change in hemodynamics (from fused tachycardia to fully paced tachycardia) and thus less chance of catheter dislodgement. However, this precludes the possibility of monitoring antegrade AV node function during ablation. Conversely, catheter stability is less likely to be an issue when
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Fig. 6.17 Orthodromic AVRT with LBBB aberrancy and earliest atrial acti­vation at the His position, in a patient with an anteroseptal pathway
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ablating in sinus or paced rhythm, except in the situation of V paced rhythm with no retrograde nodal conduction, when V-A dissociation can result in cannon A waves and intermittent sinus capture beats. In this situation, quickly switching to simultaneous V and A pacing can improve stability. Finally, when stability is a persistent issue, cryoablation (with its ability to adhere to tissue) can be helpful even if far from the normal conduction system. Force- sensing catheters and intracardiac echo can both be helpful in determining whether stability and contact are appropriate, par­ticularly in challenging locations such as the right free wall.
When ablating near the AV node, antegrade properties of the normal conduction system should be continuously monitored. This is easy in orthodromic AVRT (see Fig.6.11c) as antegrade conduction is exposed during both SVT and sinus rhythm after successful termination. However, it is impossible during ventricu­lar pacing (including V-entrained AVRT), except by alternating between V pacing and A pacing in an attempt to monitor both antegrade nodal and retrograde pathway conduction (a technique
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that is much easier and safer with cryoablation, due to catheter adherence and reversibility of effect). The normal conduction sys­tem can also usually be assessed during sinus or atrial paced rhythm, as elimination of both nodal and pathway conduction results in AV block, and elimination of nodal conduction alone results in QRS widening (maximal preexcitation). However, when preexcitation is maximal at baseline (due to rapid atrial pacing, see Fig.6.1c, or when nodal conduction times are long or the pac­ing site is much nearer to pathway than node), it is possible to injure the normal conduction without any outward sign. Unfortunately, this results in a tradeoff between optimal mapping, in which maximal preexcitation is helpful, and safest ablation, where fused conduction is required.
Once a mapping strategy has been chosen and executed, an appropriate site identied, and an ablation strategy selected, the catheter is carefully positioned and energy is delivered. It is important to anticipate which aspects of the rhythm need to be monitored during ablation to assess effect and, potentially, AV node conduction); usually success is obvious (see Figs.6.14 and
6.15) but occasionally it can be fairly subtle (see Fig.6.16). At an
optimal site, pathway conduction can frequently be eliminated within a second or two of RF delivery. Ongoing ablation (beyond 5 or at most 10s) should be avoided at ineffective sites; although “success” will sometimes be achieved late, this is often due to partial heating from the periphery of the lesion, increasing the risk of early recurrence either later in lesion delivery or immediately after energy delivery is completed. Additionally, these lesions can result in tissue edema and local electrogram fragmentation, both of which can interfere with subsequent mapping and ablation.