7/5/23, 10:45 AM Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome - UpToDate Official reprint from UpToDate www.uptodate.com 2023 UpToDate, Inc. and/or its affiliates. All Rights Reserved. Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome : Bradley P Knight, MD, FACC : Peter J Zimetbaum, MD : Susan B Yeon, MD, JD, FACC All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jun 2023. This topic last updated: Dec 06, 2021. INTRODUCTION Conduction from the atria to the ventricles normally occurs via the atrioventricular (AV) node/His-Purkinje system. Patients with a preexcitation syndrome have an additional or alternative pathway, known as an accessory pathway, which directly connects the atria and ventricle and bypasses the AV node. AV conduction through an accessory pathway (most commonly a direct AV connection) results in the earlier activation of the ventricles than if the impulse had traveled through the AV node; hence the term preexcitation. Accessory pathway is a generic term which may indicate either a "tract" which bypasses the AV node but inserts into the specialized conduction system (eg, the bundle of His, right or left bundles, or one of the fascicles), or a "connection" which bypasses the AV node and terminates directly within the myocardium. Other names that may be used include anomalous AV pathway, connection, or tract; accessory AV bypass pathway, connection, or tract; or simply AV bypass, tract, or pathway. (See "General principles of asynchronous activation and preexcitation".) At other times, the specific sites of origin and termination are used. Examples include accessory AV connection, atrio-Hisian pathway or connection, or atriofascicular pathway or connection ( table 1). Preexcitation through an AV bypass tract, the bundle of Kent, during sinus rhythm produces the electrocardiographic (ECG) pattern described by Wolff, Parkinson, and White in 1930 [1]. The terms preexcitation and Wolff-Parkinson-White (WPW) pattern are often used interchangeably. https://www.uptodate.com/contents/anatomy-pathophysiology-and-localization-of-accessory-pathways-in-the-preexcitation-syndrome/print 1/40 7/5/23, 10:45 AM Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome - UpToDate The ECG pattern of WPW should be differentiated from the "WPW syndrome," since patients with the latter have both the ECG pattern of preexcitation and paroxysmal tachyarrhythmias [2]. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis".) This topic will review the anatomy and electrophysiologic properties of the accessory pathways. These accessory pathways are clinically important because they can serve as one limb of a reentrant circuit during AV reentrant tachycardia, either orthodromic and antidromic, or can allow for frequent rapid conduction to the ventricles during atrial fibrillation leading to ventricular fibrillation and cardiac arrest. The related issue of asynchronous activation, the arrhythmias associated with WPW, and the pharmacologic and nonpharmacologic treatments of patients with this syndrome are discussed separately. A detailed discussion of electrophysiologic mapping techniques is found elsewhere. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis" and "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome" and "Invasive diagnostic cardiac electrophysiology studies", section on 'Mapping and ablation'.) ANATOMIC CONSIDERATIONS There are several types of accessory pathways ( table 1 and figure 1) [3,4]: The classic accessory pathway is the AV bypass tract or bundle of Kent in patients with Wolff-Parkinson-White pattern. This pathway directly connects atrial and ventricular myocardium, bypassing the AV node/His-Purkinje system. James fibers, atrionodal tracts, connect the atrium to the distal or compact AV node. (See "Lown-Ganong-Levine syndrome and enhanced atrioventricular nodal conduction".) Atrio-Hisian tracts connect the atrium to His bundle. Various types of Hisian-fascicular tracts, also known as Mahaim fibers, connect the atrium (atriofascicular pathways), AV node (nodofascicular pathways) or His bundle (fasciculoventricular) to distal Purkinje fibers or ventricular myocardium. (See "Atriofascicular ("Mahaim") pathway tachycardia".) The gross anatomy of AV accessory pathways should be considered in two planes that run transversely at the level of and parallel to the AV groove and longitudinally perpendicular to the AV groove [5]. https://www.uptodate.com/contents/anatomy-pathophysiology-and-localization-of-accessory-pathways-in-the-preexcitation-syndrome/print 2/40 7/5/23, 10:45 AM Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome - UpToDate Transverse plane In the transverse plane, bypass tracts can cross the AV groove anywhere except between the left and right fibrous trigones where the atrial myocardium is not in direct juxtaposition with ventricular myocardium. The remainder of the transverse plane can then be divided into quadrants consisting of the left free wall, posteroseptal, right free wall, and anteroseptal spaces ( figure 2) [5,6]. The distribution of accessory pathways within these regions is not homogeneous [7,8]: 46 to 60 percent of accessory pathways are found within the left free wall space 25 percent are within the posteroseptal space 13 to 21 percent of pathways are within the right free wall space 2 percent are within the anteroseptal space The left and right free wall spaces can be subdivided into anterior, anterolateral, lateral, posterolateral, and posterior zones. Distinctive 12-lead ECG patterns of fully preexcited QRS morphology have been validated during surgical mapping and ablation of accessory pathways within each of these subdivisions [9-13] Detailed knowledge of accessory pathway location within the free wall regions is of critical importance to the interventional electrophysiologist performing catheter ablation procedures [14]. Longitudinal plane Accessory pathway anatomy in the longitudinal plane can be most easily understood by studying a longitudinal section of the left free wall region ( figure 3). AV accessory pathways exist only between the annulus fibrosus and the epicardial reflection off the atrial and ventricular walls, confined within the AV groove subepicardial fat of the right and left free walls, the anteroseptal space, and the posteroseptal space. Accessory pathways insert directly into the atrial and basal ventricular myocardium, although they may course through the AV groove at a variable depth from subepicardial to subendocardial [5]. There are also vascular structures located in these regions. These include the circumflex coronary artery and coronary sinus in the left free wall space; the coronary sinus, middle cardiac vein, and posterior descending artery in the posteroseptal space; and the right coronary artery in the anteroseptal and right free wall spaces. AV accessory pathways may run in an oblique course rather than perpendicular to the transverse plane of the AV groove. As a result, the fibers may have an atrial insertion point that is transversely several centimeters removed from the point of ventricular attachment [15]. Finally, bypass tracts may occasionally exist as broad bands of tissue rather than discrete hair- like structures [5]. Associated structural cardiac abnormalities Accessory pathways are associated with structural heart abnormalities. Patients with hypertrophic cardiomyopathy appear to have a https://www.uptodate.com/contents/anatomy-pathophysiology-and-localization-of-accessory-pathways-in-the-preexcitation-syndrome/print 3/40 7/5/23, 10:45 AM Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome - UpToDate higher incidence of accessory pathways than the normal population. (See "Hypertrophic cardiomyopathy in adults: Supraventricular tachycardias including atrial fibrillation".) In one study, familial hypertrophic cardiomyopathy with Wolff-Parkinson-White syndrome was mapped to a locus on chromosome 7q3 [16]. Patients with Ebstein anomaly can have right sided accessory pathways associated with the abnormal tricuspid valve and often have multiple accessory pathways. (See "Clinical manifestations and diagnosis of Ebstein anomaly".) There is an association with a dilated cardiomyopathy and ventricular preexcitation that can have a genetic basis. In addition, there are patients with a dilated cardiomyopathy felt to be caused by the ventricular dyssynchrony introduced by the ventricular preexcitation. This can resolve after ablation of the accessory pathway analogous to the improvements in ventricular function seen after cardiac resynchronization pacing therapy in patients with left bundle branch block and ventricular dysfunction [17,18]. Posteroseptal accessory pathways may involve more than just the atrial and ventricular musculature, and include the musculature surrounding the coronary sinus [19]. In a study of 480 patients with posteroseptal or left posterior accessory pathways, 171 were found to involve the coronary sinus musculature [20]. The delta wave was negative in lead II in 70 percent of these patients. A coronary sinus diverticulum was found in 21 percent of these patients at this tertiary referral center, but in only 2 percent of the patients who had not had a prior ablation attempt. For this reason, it is important to perform venography of the proximal coronary sinus during an ablation procedure in a patient with a posteroseptal accessory pathway when elimination of the pathway proves to be difficult. ELECTROPHYSIOLOGY OF PREEXCITATION The normal temporal and spatial sequence of atrial and ventricular activation is altered in the Wolff-Parkinson-White (WPW) type of preexcitation because conduction between the atria and ventricles involves both an accessory pathway and the normal AV node-His Purkinje system. The vast majority of accessory pathways generate a fast action potential due to the rapid inward sodium current, similar to normal His-Purkinje tissue and atrial and ventricular myocardium (see "Cardiac excitability, mechanisms of arrhythmia, and action of antiarrhythmic drugs"). As a result, they have constant antegrade and retrograde conduction at all rates until the refractory period is reached, at which time conduction is completely blocked (nondecremental conduction). In contrast, the AV node, which depends on the slow inward calcium current for generation and propagation of its action potential, exhibits decremental conduction in which the conduction https://www.uptodate.com/contents/anatomy-pathophysiology-and-localization-of-accessory-pathways-in-the-preexcitation-syndrome/print 4/40 7/5/23, 10:45 AM Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome - UpToDate time of the impulse propagating through the AV node increases as the cycle length shortens (heart rate increased) [21]. Thus, AV conduction is more rapid through the accessory pathway than through the AV node, a difference that is increased at fast heart rates. This difference has potentially great clinical importance. The progressive prolongation of AV nodal conduction time at faster atrial rates has a protective role, limiting the ventricular response to rapid atrial rates in atrial fibrillation or atrial flutter. This decreasing speed of conduction until some but not all beats are transmitted through the AV nodal tissue is called decremental conduction. Accessory pathways are dependent on the rapid inward sodium current for depolarization and characteristically do not demonstrate decremental conduction. As a result, arrhythmias that utilize accessory pathways can conduct frequently and rapidly, leading to very fast ventricular rates during atrial fibrillation that may degenerate into ventricular fibrillation. (See "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway".) Mahaim fibers may have somewhat different properties in that they may show slow and decremental anterograde conduction, proximal AV nodal-like electrophysiologic properties and distal bundle branch-like properties, conduction block in response to adenosine, and heat- induced automaticity during radiofrequency catheter ablation. Spontaneous automaticity may arise in Mahaim fibers, particularly during ablation procedures of the atrial insertion, and this may trigger antidromic circus movement tachycardias [22]. Accessory pathways that directly connect the atrium to the ventricle can occasionally show slow and decremental conduction in the retrograde direction. When these slowly conducting pathways serve as the retrograde limb during orthodromic AV reentrant tachycardia, the RP interval is usually longer than the PR interval. These accessory pathways can lead to the permanent form of junctional reciprocating tachycardia and are usually located in the posteroseptal space [23]. (See "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway", section on 'Permanent junctional reciprocating tachycardia'.) Rarely, accessory pathways that directly connect the atrium to the ventricle can also show decremental conduction in the antegrade direction. In these patients, preexcitation is not evident during sinus rhythm because conduction over the AV node is faster than over the accessory pathway, but the pathway can serve as the antegrade limb during antidromic AV reentrant tachycardia and give rise to a wide QRS tachycardia. These pathways are also usually in the posteroseptal location [24]. Ventricular activation Since an AV accessory pathway usually bypasses and conducts faster than the AV node, the onset of ventricular activation is earlier than expected if depolarization https://www.uptodate.com/contents/anatomy-pathophysiology-and-localization-of-accessory-pathways-in-the-preexcitation-syndrome/print 5/40 7/5/23, 10:45 AM Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome - UpToDate occurred via the AV node. Since the accessory pathway usually exhibits nondecremental conduction, early activation remains constant at all heart rates. Preexcited intraventricular conduction in WPW spreads from the insertion point of the AV bypass tract in the ventricular myocardium via direct muscle fiber-to-muscle fiber conduction. This process is inherently slower than ventricular depolarization resulting from rapid His-Purkinje system conduction. Thus, the net effect is earlier initial excitation of the ventricles (via the accessory pathway) but slower activation of the ventricular myocardium than occurs normally. The net effect is that the QRS complex consists of fusion between early ventricular activation caused by preexcitation with the later ventricular activation resulting from transmission through the AV node and the infranodal conduction system to the ventricles. The initial part of ventricular activation is slowed and the upstroke of the QRS complex is slurred because of slow muscle fiber-to-muscle fiber conduction; this is termed a delta wave ( figure 4A-B). The sooner conduction occurs over the accessory pathway in relation to the AV node, the greater the amount of myocardium depolarized via the accessory pathway, resulting in a more prominent or wider delta wave, and increasing prolongation of the QRS complex ( figure 5). Minimal preexcitation in WPW Preexcitation and delta waves may not be apparent in sinus rhythm in patients with WPW who have a left-lateral bypass tract as the antegrade route for conduction; in this setting, the time for the atrial impulse to travel from the sinus node to reach the atrial insertion of the accessory pathway is longer than the time to reach the AV node. The presence of a septal Q wave in lead V6 of the surface ECG is useful to exclude minimal preexcitation with a high degree of reliability [25]. When there is uncertainty regarding the presence of ventricular preexcitation, vagal maneuvers can be performed or intravenous adenosine can be administered to cause transient AV nodal blockade. The P wave signal-averaged ECG may also be of help in identifying a concealed left-sided accessory pathway. In one series, such a bypass tract was associated with a more prolonged filtered P wave duration (132 versus 119 milliseconds in controls or patients with an AV nodal reentrant tachycardia) [26]. In addition, delta waves are not seen with non-WPW forms of preexcitation, such as Mahaim or James fibers, since these pathways terminate in the conducting system or in the ventricular myocardium close to the conducting system. Most Mahaim tachycardias, for example, are due to atriofascicular pathways. (See "Atriofascicular ("Mahaim") pathway tachycardia".) PR interval Since the impulse bypasses the AV node, the preexcited PR interval is often shorter than what would be considered normal; however, it may not be abnormally short in the https://www.uptodate.com/contents/anatomy-pathophysiology-and-localization-of-accessory-pathways-in-the-preexcitation-syndrome/print 6/40 7/5/23, 10:45 AM Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome - UpToDate absolute sense [27]. The degree of PR interval shortening and the amount of QRS interval widening depend upon several factors: The balance between the antegrade conduction time and refractory period of the accessory pathway and those of the normal AV node/His-Purkinje system; the conduction properties of both are variably influenced by the autonomic nervous system. The atrial insertion point of the AV bypass tract. The site of atrial impulse origin. Interatrial conduction time. Atrial refractoriness. Because of these factors, preexcitation may be less apparent during sinus tachycardia when AV node conduction time is short due to elevated sympathetic tone and decreased vagal tone. In addition, as mentioned above, an AV bypass tract that crosses the AV groove in the left lateral region may result in inapparent preexcitation and minimal PR interval shortening in sinus rhythm because of the greater interatrial distance required for impulse propagation from the sinus node to the left atrial insertion of the bypass tract. Intermittent preexcitation Intermittent preexcitation should be distinguished from day-to- day variability in preexcitation which results from changes in AV nodal conduction in relation to those of the accessory pathway usually due to changes in autonomic tone. True intermittent preexcitation is characterized by abrupt loss of the delta wave, normalization of the QRS duration, and an increase in the PR interval during a continuous ECG recording in the absence of any significant change in heart rate. This finding is generally a reliable sign that the AV bypass tract has a relatively long antegrade refractory period and is not capable of frequent impulse conduction, thus placing the patient at low risk for ventricular arrhythmias [27]. Preexcitation alternans In preexcitation alternans, a QRS complex manifesting a delta wave alternates with a normal QRS complex. This is also a marker for an accessory pathway with a relatively long antegrade refractory period. Concertina effect The amount of fusion of the QRS complex varies with the electrophysiologic properties of the accessory pathway, which are influenced by sympathetic and parasympathetic tone and their effect on the AV node. As a result, the appearance and width of the QRS complex depends upon the balance between preexcitation and normal excitation via the AV node. If AV nodal conduction is fast, the amount of myocardium activated via the accessory pathway is less, and hence there is a longer PR interval, less prominent delta https://www.uptodate.com/contents/anatomy-pathophysiology-and-localization-of-accessory-pathways-in-the-preexcitation-syndrome/print 7/40 7/5/23, 10:45 AM Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome - UpToDate wave, and narrower QRS complex. If AV nodal conduction is slow, more myocardium is activated via the accessory pathway, resulting in a shorter PR interval, more prominent delta wave, and wider QRS complex. Changing degrees of AV nodal conduction and hence fusion in some patients may cause the QRS duration and the PR interval to periodically wax and wane, resulting in an appearance referred to as the "concertina effect" of preexcitation ( waveform 1 and waveform 2). In this phenomenon, PR intervals and QRS complex durations show a cyclic pattern, eg, preexcitation becomes progressively more prominent over a number of QRS complex cycles followed by a gradual diminution in the degree of preexcitation over several QRS cycles despite a fairly constant heart rate [28,29]. Accessory pathways exhibiting decremental conduction Approximately 10 percent of patients have accessory pathways in which conduction slows at faster rates of stimulation (decremental conduction), similar to the situation with the AV node. As noted above, the progressive prolongation of AV nodal conduction time at faster atrial rates has a protective role, limiting the ventricular response to rapid atrial rates in atrial fibrillation or atrial flutter. Accessory pathways which display decremental conduction in one direction may exhibit varied electrophysiologic properties in the other. As an example, one study examined the characteristics of the accessory pathway in 74 patients with decremental accessory pathways [30]. Among 64 patients with retrograde decremental conduction, anterograde conduction was not present in 64 percent, was intermittent in 8 percent, and was nondecremental in 28 percent. Five patients had anterograde but not retrograde conduction, and five had conduction in both directions. Another study examined 384 symptomatic patients with a single accessory pathway and found that retrograde decremental conduction over the accessory pathway was present in the posteroseptal (17 percent) and left free wall (3 percent), but absent in the other locations. Anterograde decremental conduction was only seen in the right free wall location (12 percent) [24]. Concealed accessory pathways Although AV accessory pathways usually conduct antegradely and retrogradely, some AV bypass tracts are capable of propagating impulses in only one direction [8,12,14,29-31]. Bypass tracts that conduct only in an antegrade direction are uncommon. They often cross the right AV groove, and frequently possess decremental conduction properties [8,27,31-33]. Bypass tracts that conduct only in the retrograde direction occur more frequently with an incidence reported as high as 16 percent [34]. Because they do not preexcite the ventricles, the surface ECG during sinus rhythm appears normal and therefore these pathways are called https://www.uptodate.com/contents/anatomy-pathophysiology-and-localization-of-accessory-pathways-in-the-preexcitation-syndrome/print 8/40 7/5/23, 10:45 AM Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome - UpToDate "concealed." Some concealed pathways may be able to conduct anterograde, but have such long refractory periods that they do not conduct during sinus rhythm and are concealed. Preexcitation can sometimes be seen in patients with this type of a concealed accessory pathway after a long sinus pause, such as immediately after termination of AV reciprocating tachycardia. Most concealed AV bypass tracts exhibit nondecremental conduction and, because they serve as conduit for retrograde ventriculoatrial conduction, they are associated with reentrant arrhythmias [34,35]. Concealed accessory pathways that have decremental properties are usually located in the posteroseptal region. However, these pathways also occur in nonseptal locations with an incidence as high as 25 percent in one series [36]. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Prevalence of concealed accessory pathways'.) RELATIONSHIP BETWEEN ACCESSORY PATHWAY SITE AND THE ELECTROCARDIOGRAPHIC PATTERN Many articles have attempted to correlate the site of the accessory pathway with the ECG pattern [13,37-41]. However, the ECG appearance of activation depends upon the extent of preexcitation and fusion; as a result, the same pathway may not always produce the identical ECG pattern. Furthermore, as many as 13 percent of individuals with preexcitation have more than one accessory pathway. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Accessory pathway location'.) The surface ECG does, however, provide important clues for the cardiologist to direct invasive mapping. It also serves as a guide for the electrophysiologist to anticipate the morbidity of the particular procedural approach required to treat a particular accessory pathway (eg, ablation of pathways near the AV node and bundle of His has a higher inherent risk of inducing AV block and requiring a permanent pacemaker). This information related to pathway location is helpful when counseling patients about the risks of ablation. The optimal time to use the surface ECG to estimate the location of the accessory pathway is in the electrophysiology laboratory during atrial pacing at a rate that results in maximal preexcitation. Localizing the accessory AV connection site based upon the ECG A useful approach to map the location of the common form of accessory pathway, the accessory AV connection (AAVC), combines the algorithms of Milstein ( figure 2 and algorithm 1) and Arruda ( figure 2 and algorithm 2) [13,39,41,42]. The Milstein approach accurately localizes the AAVC to general regions along the AV rings; the Arruda approach is more precise, as has been confirmed by https://www.uptodate.com/contents/anatomy-pathophysiology-and-localization-of-accessory-pathways-in-the-preexcitation-syndrome/print 9/40 7/5/23, 10:45 AM Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome - UpToDate endocardial mapping, and is helpful in further discriminating the septal areas of the AV rings. Distinctly classifying the posteroseptal/midseptal/anteroseptal areas also helps the clinician prepare the patient for different treatment options, including radiofrequency ablation, medical therapy, or monitoring. (See "Treatment of arrhythmias associated with the Wolff-Parkinson- White syndrome".) Vector of the delta wave The first step is to assess the vector of the delta wave: Is the delta wave vector directed away from or isoelectric to the leftward leads I, aVL, or V6? In other words, is the delta wave a Q wave or isoelectric in I, aVL, or V6? If yes and a left bundle branch block (LBBB)-type pattern is also present, (QRS 0.09 sec in lead I with an rS pattern in V1 or V2), a right anteroseptal pathway is suggested ( waveform 3). This connection initiates a generally rightward activation of the right ventricle (RV) in one of the leftward leads (leading to negative delta waves in aVL and/or V6). The asynchronous activation of the right and then the left ventricle (LV) produces the LBBB-like ECG pattern. The QRS axis is greater than +30 which helps distinguish the right anteroseptal from a right lateral pathway. If yes and a LBBB-type configuration is not present, a left lateral pathway is suggested ( waveform 4 and waveform 5). Preexcitation begins in the lateral portion of the left ventricle; as a result, initial activation is to the right as reflected by a negative delta wave in one or more of the leftward leads (ECG 2 shows isoelectric to negative polarity in I and aVL while ECG 3 shows a negative delta wave in aVL). The pattern may then resemble an atypical right bundle branch block, because preexcitation begins in the left ventricle. If the delta waves in leads I, aVL and V6 are other than a Q wave or isoelectric, examine the vector first in the frontal plane and then in the horizontal plane. Specifically, see if the delta wave vector in the frontal plane forms a Q wave or is isoelectric in two of leads II, III, or aVF. If yes, examine the horizontal plane. If there is an Rs or RS in V1, V2, or V3, a posteroseptal pathway is suggested ( waveform 6A-D). Preexcitation therefore begins in the posterior portion of the septum and sweeps anteriorly, giving the initial positive R complex in the anterior precordial leads. Further discrimination is discussed in the legends to the ECGs. If yes, and the pattern is other than an Rs or RS in V1, V2, or V3, a right lateral pathway is suggested ( waveform 7). Preexcitation begins in the lateral portion of the right ventricle, which is anatomically anterior and to the right; as a result, activation is posteriorly and to the left. A LBBB-type pattern results because the RV is activated before the LV. The axis is https://www.uptodate.com/contents/anatomy-pathophysiology-and-localization-of-accessory-pathways-in-the-preexcitation-syndrome/print 10/40 7/5/23, 10:45 AM Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome - UpToDate less than +30 (ECG 5 has a negative delta wave in III and is isoelectric in aVF), which distinguishes the right lateral from the anteroseptal pathway. If the pattern in leads II, III or aVF is not a Q or isoelectric delta wave, then: A left bundle branch type of pattern (QRS equal to or greater than 90 msec in I and rS in V1 or V2) with a QRS axis of more than +30 suggests a right anteroseptal pathway ( waveform 3). A left bundle branch type of pattern (QRS equal to or greater than 90 msec in I and rS in V1 or V2) with an axis that is +30 or less suggests a right lateral pathway ( waveform 7). An Rs or RS in V1 or V2, but a pattern not that of a left bundle branch type as defined above, suggests a left lateral pathway ( waveform 4 and waveform 5). If other than an Rs or RS, the pathway may be difficult to localize and probably represents a left anterior lateral pathway ( waveform 8). Another algorithm is based upon a stepwise discriminant analysis of 18 variables in patients who had undergone successful catheter ablation [13]: Right-sided pathways were distinguished from left-sided pathways by the QRS transition in V1 to V3. Anterior-posterior, septal, and lateral pathways were localized by an analysis of delta wave and QRS polarities. The algorithm was quite successful in identifying right- and left-sided accessory pathways, right free wall from right septal, right anterolateral from posterolateral, and anteroseptal from other right septal pathways ( waveform 9). Left anterolateral pathways were also distinguished from left posterior pathways, and right posterolateral pathways were distinguished from left posteroseptal pathways. The reader who wishes to pursue the ECG patterns further should consult the sophisticated and complex scheme based upon delta wave polarity, which has been described in detail elsewhere [9]. Mahaim fibers may be suggested by a narrow QRS with an rS pattern in lead III. During tachycardia, these individuals usually have a LBBB-like QRS complex with left axis deviation [43]. A more detailed discussion for the specialist is available elsewhere [44]. SUMMARY https://www.uptodate.com/contents/anatomy-pathophysiology-and-localization-of-accessory-pathways-in-the-preexcitation-syndrome/print 11/40 7/5/23, 10:45 AM Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome - UpToDate Patients with a preexcitation syndrome have an additional or alternative pathway, known as an accessory pathway, which directly connects the atria and ventricle and bypasses the atrioventricular (AV) node. During sinus rhythm, AV conduction through an accessory pathway (most commonly a direct AV connection) results in the earlier activation of the ventricles than if the impulse had traveled through the AV node, resulting in ventricular preexcitation. (See 'Introduction' above.) Some accessory pathways are associated with structural heart abnormalities. (See 'Anatomic considerations' above.) The classic accessory pathway is the AV bypass tract in patients with the Wolff-Parkinson- White (WPW) pattern. This pathway directly connects atrial and ventricular myocardium, bypassing the AV node/His-Purkinje system. (See 'Anatomic considerations' above.) Delta waves may not be apparent in sinus rhythm in patients with WPW who have a left- lateral bypass tract as the antegrade route for conduction. (See 'Minimal preexcitation in WPW' above.) Although AV accessory pathways usually conduct antegrade and retrograde, some AV bypass tracts are capable of propagating impulses in only one direction. (See 'Concealed accessory pathways' above.) The electrocardiographic (ECG) appearance of activation depends upon the extent of preexcitation and fusion; as a result, the same pathway may not always produce the identical ECG pattern. (See 'Relationship between accessory pathway site and the electrocardiographic pattern' above.) Use of UpToDate is subject to the Terms of Use. REFERENCES 1. Wolff, L, Parkinson, et al. Bundle branch block with a short P-R interval in healthy young people prone to paroxysmal tachycardia. Am Heart J 1930; 5:685. 2. Definition of terms related to cardiac rhythm. Am Heart J 1978; 95:796. 3. Waller BF. Clinicopathological correlations of the human cardiac conduction system. In: Card iac Electrophysiology, Zipes DP, Jalife J (Eds), WB Saunders, Philadelphia 1990. p.249. 4. Anderson RH, Becker AE, Brechenmacher C, et al. Ventricular preexcitation. A proposed nomenclature for its substrates. Eur J Cardiol 1975; 3:27. https://www.uptodate.com/contents/anatomy-pathophysiology-and-localization-of-accessory-pathways-in-the-preexcitation-syndrome/print 12/40 7/5/23, 10:45 AM Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome - UpToDate 5. Ferguson TB, Cox JL. Surgical treatment for the Wolff-Parkinson-White syndrome: the endoc ardial approach. In: Cardiac Electrophysiology, Zipes DP, Jalife J (Eds), WB Saunders, Philadel phia 1990. p.897. 6. Cox JL, Gallagher JJ, Cain ME. Experience with 118 consecutive patients undergoing operation for the Wolff-Parkinson-White syndrome. J Thorac Cardiovasc Surg 1985; 90:490. 7. Cain ME, Cox JL. Surgical treatment of supraventricular arrhythmias. In: Management of car diac arrhythmias: the nonpharmacologic approach, Platia E (Ed), JB Lippincott, Philadelphia 1987. p.304. 8. Gallagher JJ, Sealy WC, Kasell J. Intraoperative mapping studies in the Wolff-Parkinson-White syndrome. Pacing Clin Electrophysiol 1979; 2:523. 9. Gallagher JJ, Pritchett EL, Sealy WC, et al. The preexcitation syndromes. Prog Cardiovasc Dis 1978; 20:285. 10. Reddy GV, Schamroth L. The localization of bypass tracts in the Wolff-Parkinson-White syndrome from the surface electrocardiogram. Am Heart J 1987; 113:984. 11. Fananapazir L, German LD, Gallagher JJ, et al. Importance of preexcited QRS morphology during induced atrial fibrillation to the diagnosis and localization of multiple accessory pathways. Circulation 1990; 81:578. 12. Lindsay BD, Crossen KJ, Cain ME. Concordance of distinguishing electrocardiographic features during sinus rhythm with the location of accessory pathways in the Wolff- Parkinson-White syndrome. Am J Cardiol 1987; 59:1093. 13. Milstein S, Sharma AD, Guiraudon GM, Klein GJ. An algorithm for the electrocardiographic localization of accessory pathways in the Wolff-Parkinson-White syndrome. Pacing Clin Electrophysiol 1987; 10:555. 14. Cain ME, Luke RA, Lindsay BD. Diagnosis and localization of accessory pathways. Pacing Clin Electrophysiol 1992; 15:801. 15. Otomo K, Gonzalez MD, Beckman KJ, et al. Reversing the direction of paced ventricular and atrial wavefronts reveals an oblique course in accessory AV pathways and improves localization for catheter ablation. Circulation 2001; 104:550. 16. MacRae CA, Ghaisas N, Kass S, et al. Familial Hypertrophic cardiomyopathy with Wolff- Parkinson-White syndrome maps to a locus on chromosome 7q3. J Clin Invest 1995; 96:1216. 17. Dai CC, Guo BJ, Li WX, et al. Dyssynchronous ventricular contraction in Wolff-Parkinson- White syndrome: a risk factor for the development of dilated cardiomyopathy. Eur J Pediatr 2013; 172:1491. https://www.uptodate.com/contents/anatomy-pathophysiology-and-localization-of-accessory-pathways-in-the-preexcitation-syndrome/print 13/40 7/5/23, 10:45 AM Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome - UpToDate 18. Chiu SN, Chang CW, Lu CW, Wu MH. Restored cardiac function after successful resynchronization by right anterior and anteroseptal accessory pathway ablation in Wolff- Parkinson-White syndrome associated dilated cardiomyopathy. Int J Cardiol 2013; 163:e19. 19. Chauvin M, Shah DC, Ha ssaguerre M, et al. The anatomic basis of connections between the coronary sinus musculature and the left atrium in humans. Circulation 2000; 101:647. 20. Sun Y, Arruda M, Otomo K, et al. Coronary sinus-ventricular accessory connections producing posteroseptal and left posterior accessory pathways: incidence and electrophysiological identification. Circulation 2002; 106:1362. 21. Prystowsky EN, Page RL. Electrophysiology and autonomic influences of the human atrioven tricular node. In: Electrophysiology of the Sinoatrial and Atrioventricular Nodes, Mazgalev T, Dreifus L, Michelson EL (Eds). 22. Sternick EB, Timmermans C, Sosa E, et al. The electrocardiogram during sinus rhythm and tachycardia in patients with Mahaim fibers: the importance of an "rS" pattern in lead III. J Am Coll Cardiol 2004; 44:1626. 23. Gaita F, Haissaguerre M, Giustetto C, et al. Catheter ablation of permanent junctional reciprocating tachycardia with radiofrequency current. J Am Coll Cardiol 1995; 25:648. 24. de Chillou C, Rodriguez LM, Schl pfer J, et al. Clinical characteristics and electrophysiologic properties of atrioventricular accessory pathways: importance of the accessory pathway location. J Am Coll Cardiol 1992; 20:666. 25. Bogun F, Kalusche D, Li YG, et al. Septal Q waves in surface electrocardiographic lead V6 exclude minimal ventricular preexcitation. Am J Cardiol 1999; 84:101. 26. Yoshida T, Ikeda H, Hiraki T, et al. Detection of concealed left sided accessory atrioventricular pathway by P wave signal averaged electrocardiogram. J Am Coll Cardiol 1999; 33:55. 27. Josephson ME. Preexcitation Syndromes. In: Clinical Cardiac Electrophysiology, Lea & Febige r, Philadelphia 1993. p.311. 28. German LD, Gallagher JJ. Functional properties of accessory atrioventricular pathways in Wolff-Parkinson-White syndrome. Clinical implications. Am J Med 1984; 76:1079. 29. Nalos, PC, Deng, et al. Intermittent preexcitation: Clinical recognition and management. Pract Cardiol 1985; 11:49. 30. Chen SA, Tai CT, Chiang CE, et al. Electrophysiologic characteristics, electropharmacologic responses and radiofrequency ablation in patients with decremental accessory pathway. J Am Coll Cardiol 1996; 28:732.