Basic Evaluation of Accessory Pathways
Introduction
The typical accessory pathway (AP) (bundle of Kent) is a muscle fiber bridging the atrio-ventricular (AV) groove and providing electrical continuity between the atrium and ventricle in parallel to the AV node-His-Purkinje axis.1 It can conduct antegradely, retrogradely, or bidirectionally. Antegradely conducting APs show ventricular preexcitation on the 12-lead ECG and are therefore “manifest.” If they conduct exclusively in the antegrade direction, they are “manifest only.” If they conduct only in the retrograde direction, they do not cause preexcitation and are therefore called “concealed.” Factors limiting antegrade conduction of concealed APs almost always occur at its ventricular insertion site (AP-ventricle [V] interface) and include 1) “impedance mismatch” (small AP fiber incapable of generating sufficient current to activate the large mass of ventricular muscle) and 2) retrograde concealment from sinus-driven AV node-His-Purkinje conduction into the AP with a prolonged anterograde refractory period (which can be unmasked if AV block occurs).2,3,4 The Wolff-Parkinson-White (WPW) pattern refers to ventricular preexcitation on the ECG, while the WPW syndrome is the association of symptoms with the WPW pattern.
The purpose of this chapter is to:
Describe the 12-lead ECG and electrophysiologic hallmarks of manifest preexcitation.
Localize APs by the 12-lead ECG and intracardiac recordings.
Define the electrophysiologic properties of APs.
Discuss sudden death risk stratification of APs.
HALLMARKS OF MANIFEST PREEXCITATION
12-LEAD ECG
During sinus rhythm, the ECG signs of ventricular preexcitation are 1) short PR interval (≤120 ms), 2) delta wave (slurring of the initial forces of the QRS complex), and 3) secondary ST-T wave abnormalities.5,6 The PR interval is short because the AP “bypasses” the AV node-His-Purkinje system to prematurely activate the ventricle (“preexcite”). The PJ interval, however, is normal because the time required to complete ventricular activation is unchanged.6 The QRS complex is a fusion between His-Purkinje and AP conduction, and the delta wave reflects the initial activation of the ventricle by the AP. During sinus rhythm, the degree of preexcitation is therefore primarily determined by 1) AP location relative to the sinus node and 2) status of AV nodal conduction. Preexcitation is greatest with right-sided APs near the sinus node because of the short conduction time to the AP relative to the AV node-His-Purkinje axis. Inapparent or minimal preexcitation can occur with left free wall APs because the large distance between the sinus node and AP causes minimal activation of the ventricle by the AP. Inapparent preexcitation can be unmasked by adenosine/coronary sinus (CS) pacing or excluded by the presence of a septal q wave in lead V6 (unobscured normal left to right septal activation by the His-Purkinje system) (Figs. 9-1 and 9-2).7,8,9,10 Latent preexcitation refers to preexcitation that is absent during sinus rhythm but becomes manifest only with atrial pacing and occurs with slow, decrementally conducting APs (e.g., atrio-fascicular AP). Intermittent preexcitation refers to abrupt loss of preexcitation during sinus rhythm that identifies a poorly conducting AP with a long antegrade refractory period and generally a low risk for sudden death (especially if present during catecholamine provocation (e.g., isoproterenol) (Fig. 9-3). Fixed preexcitation refers to constant preexcitation during sinus rhythm. Enhancing AV nodal conduction (exercise, isoproterenol) reduces the degree of preexcitation.
ELECTROPHYSIOLOGIC STUDY
The intracardiac hallmark of preexcitation is a short (<35 ms) or negative HV interval (Fig. 9-3).11 It corresponds inversely
to the size of the delta wave on the surface ECG. Because AV APs originate above the His bundle, His extrasystoles conduct to the ventricle without preexcitation. A preexcited His bundle extrasystole identifies a fasciculo-ventricular AP that originates below the His bundle.
to the size of the delta wave on the surface ECG. Because AV APs originate above the His bundle, His extrasystoles conduct to the ventricle without preexcitation. A preexcited His bundle extrasystole identifies a fasciculo-ventricular AP that originates below the His bundle.
AP LOCALIZATION
APs can be found anywhere along the tricuspid or mitral annuli except classically at the fibrous aorto-mitral continuity (left anteroseptal region), although rare cases have been reported.12 In decreasing order of frequency, AP sites include left free wall, posteroseptal, right free wall, and anteroseptal.11 Rarely, APs are located in the atrial appendages, CS diverticulum, ligament of Marshall, and noncoronary cusp of the aortic valve.13,14,15,16,17
12-LEAD ECG
The ECG clues to identify the approximate location of an AP are its 1) delta-wave axis during manifest preexcitation and 2) P-wave axis during orthodromic reciprocating tachycardia (ORT).11,18,19,20,21,22,23
Delta-Wave Axis
The horizontal delta-wave transition in the anterior precordium (V1-V3) differentiates left-sided, septal, and right-sided APs, while the vertical delta-wave axis determines its anterior or posterior location along the annulus (Fig. 9-4).11,18,19,20,21,22 Early delta-wave transition (at or before V1) indicates a left-sided AP because initial ventricular forces are directed anteriorly toward the right ventricle. Negative delta waves in the lateral (I, aVL) or inferior leads identify a left free wall or left posterior AP, respectively. Transition at V2 (overlying the interventricular septum) indicates a right postero- or midseptal AP. Posteroseptal APs show a sum of delta-wave polarities in the inferior leads (II, III, aVF) ≤ −2, while midseptal APs show a sum of −1, 0, or +1. In the absence of incomplete right bundle branch block (RBBB) or infundibular pattern, a terminal r wave in V1 raises the possibility of a left-sided septal AP (possibly due to early activation of the proximal left bundle by the left-sided AP with late activation of the right ventricle) (Fig. 9-5).24,25 A negative delta wave in II, steep (≥45 degrees) positive delta wave in aVR, and deep S wave (R ≤ S) in V6 suggest an epicardial posteroseptal AP within the CS or its branches.26 Late transition (at or beyond V3) indicates a right-sided AP. Anteroseptal APs show a “left bundle branch block” (“LBBB”) type pattern with a small narrow positive delta wave transitioning at V3, sum of delta-wave polarities in the inferior leads (II, III, aVF) ≥ + 2, and a frontal axis +30 to +120 degrees. Classic true parahisian APs, however, show negative delta waves in V1 and V2 or sum of initial r wave (V1 + V2) <0.5 mV (because initial forces are directed away from V1 and V2—both of which are
equidistant from the midline sternum that overlies the membranous septum).21 Right free wall APs generally transition later beyond V3 indicating that initial ventricular forces are directed posteriorly toward the left ventricle and demonstrate a frontal axis +30 to −60 degrees.
equidistant from the midline sternum that overlies the membranous septum).21 Right free wall APs generally transition later beyond V3 indicating that initial ventricular forces are directed posteriorly toward the left ventricle and demonstrate a frontal axis +30 to −60 degrees.
P-Wave Axis
P-wave polarities during ORT also differentiate left-sided, septal, and right-sided APs. A rightward axis (aVR [+], aVL [−]) indicates eccentric atrial activation arising from a left-sided AP, while a leftward axis (aVR [−], aVL [+]) identifies eccentric activation
from a right-sided AP. Postero- and midseptal APs generate a narrow P wave with a midline superior axis (aVR and aVL [+]), while anteroseptal APs can produce positive P waves inferiorly.12,23
from a right-sided AP. Postero- and midseptal APs generate a narrow P wave with a midline superior axis (aVR and aVL [+]), while anteroseptal APs can produce positive P waves inferiorly.12,23
FIGURE 9-3 Intermittent (2:1) preexcitation over a right (top) and left (bottom) free wall AP. During preexcitation, the HV is short (negative). |
ELECTROPHYSIOLOGIC STUDY
Location of the AP is determined by the 1) earliest site of ventricular activation during manifest preexcitation; 2) earliest site of atrial activation during retrograde AP conduction; and, if present, 3) AP potentials.11,20 A less commonly used method for AP localization is differential atrial pacing, which identifies the AP atrial insertion site by identifying the atrial pacing site yielding the shortest stimulus-delta interval.27 During the electrophysiologic study, multiple annular sites are mapped using catheters positioned at the His bundle region (anteroseptum) and within the CS (posteroseptum and left AV sulcus). While a venous equivalent to the CS is absent for the tricuspid annulus, its endocardium can be mapped using a multipolar “Halo” catheter.
Earliest Site of Ventricular Activation
Because the AP preexcites the ventricle, its ventricular insertion site is identified by locating the earliest ventricular electrogram relative to delta-wave onset (“pre-delta”).
Earliest Site of Atrial Activation
Two patterns of retrograde AP conduction are 1) concentric (midline) or 2) eccentric. Septal APs generate concentric patterns earliest near the CS os (posteroseptal AP) or His bundle region (anteroseptal AP). Right and left free wall APs create eccentric patterns with earliest atrial sites away from the septum. During retrograde AP conduction (ventricular pacing, ORT), the earliest site of atrial activation identifies its atrial insertion site.