The term “ventricular pre‐excitation” implies that the myocardium depolarizes earlier than expected if the stimulus follows the normal pathway through the specific conduction system (Wolff et al. 1930). In fact, this is not really what happens before excitation (pre‐excitation). Instead, it refers to ventricular excitation occurring earlier than expected. Three types of pre‐excitation have been defined: WPW‐type pre‐excitation occurs by means of the presence of accessory AV pathways (Kent bundle) (Figure 12.3). In general, only one accessory pathway (AP) exists (>90% of cases) and conduction is usually fast and in both directions (anterogradely and retrogradely) (≈2/3 of cases). On certain occasions (20%), the conduction of the AP occurs only retrogradely (concealed WPW). Other WPW‐type pre‐excitations are less frequent (Table 12.1). These APs can integrate a circuit (specific conduction system (SCS)–ventricle–AP–atrium–SCS) with anterograde or retrograde conduction, which constitutes the anatomic substrate of reentrant arrhythmias that are frequently observed in the presence of WPW‐type pre‐excitation (WPW syndrome). Table 12.1 shows the most characteristic ECG morphologies in sinus rhythm and during a tachycardia episode, according to the anatomic and functional properties of the different types of pre‐excitation (anterograde and/or retrograde conduction, and fast or slow conduction). The ECG changes in sinus rhythm are only observed when anterograde conduction exists. They consist mainly of a short PR interval and an abnormal QRS complex with initial slurring (delta wave) which is a manifestation of ventricular fusion, due to simultaneous activation through the accessory pathway and the AV node–His system. The short PR interval occurs because the sinus stimulus reaches the ventricles through the AP sooner than through the SCS. The presence of an abnormal QRS complex is the result of the ventricular activation taking place through two pathways: the normal AV conduction and the AP (a Kent bundle). These result in slightly early activation of the ventricles in subepicardial zones where there are very few Purkinje fibers. This explains not only the early QRS complex (short PR interval), but also the delta wave as the result of the slow activation of the myocardial tissue. The rest of the myocardial mass is activated through the normal pathway (SCS). The QRS complex is thus a genuine fusion complex. Table 12.1 Pre‐excitation types: (1) WPW‐type pre‐excitation; (2) atypical pre‐excitation; (3) short PR‐type pre‐excitation. Surface ECG rate and characteristics in sinus rhythm and during paroxysmal tachycardia episodes, according to the functional characteristics of the different types of pre‐excitation a Today, it is believed that the classical Mahaim fibers (nodoventricular and fasciculoventricular fibers) initiate paroxysmal tachycardias less frequently than the right atriofascicular tracts. Currently, it is considered that they are not involved in the circuit which triggers the tachycardia, which is usually due to a right atriofascicular tract, as previously mentioned. Figure 12.1 Right lateral view of the accessory pathways. Depending on what myocardial areas are activated through one pathway or the other, the QRS complex will show a greater or lesser degree of pre‐excitation. In the rare cases of type 2 pre‐excitation (Table 12.1), the baseline ECG may have morphologies varying from normal to subtle evidence of minimal pre‐excitation that looks like cases with left bundle branch block (LBBB) pattern (see Atypical pre‐excitation, below). In type 3 pre‐excitation, the only anomaly of the ECG is the short PR interval (see Short PR interval pre‐excitation, below). This generally ranges from 0.08–0.11 sec. Cases with normal PR interval are rare. They may occur due to the presence of a long left AV AP Kent bundle type with delayed atrial conduction. In this scenario, even though the ventricular activation is performed through a classical Kent bundle, the PR interval is usually at the lower limit of normality (0.12–0.13 sec), and therefore is not considered short. It is, however, shorter than when no pre‐excitation occurs, as conduction through the normal pathway would have a longer PR interval. Figure 12.2 Left top panel: Diagram of the P–QRS relationship in normal cases. AB: P wave; BC: PR segment; CD: QRS. Middle panel: WPW‐type pre‐excitation (the broken line represents the QRS complex if no pre‐excitation occurred). AD distance is the same as under normal conditions, with a wide QRS complex in detriment to the PR segment (BC distance), which partially or totally coincides with the delta wave. Lower panel: in cases of short PR segment, the QRS complex is shifted forward because the PR segment is shortened or may even disappear. Top right: four examples of delta wave (arrow) by increasing order of relevance. (D) Atrial fibrillation patient in whom the first QRS is conducted over the normal pathway, while the second QRS is conducted over the accessory pathway with maximum pre‐excitation. Middle panel: example of four complexes with pre‐excitation, with an average‐sized delta wave. Lower panel: four complexes in a case of short PR pre‐excitation. A normal PR interval may also exist in the following cases: atypical long atriofascicular/atrioventricular anomalous tracts (currently termed “enhanced AV node conduction,” see above) with slow conduction or other atypical tracts, including the classical Mahaim fibers (very rare). These tracts may partially or completely prevent the slow intranodal conduction (Sternick and Wellens 2006) (see Atypical pre‐excitation, below). The QRS complexes show an abnormal morphology wider than the baseline QRS complex (frequently ≥ 0.11 sec) with characteristic initial slurring (delta wave) due to the activation being initiated at the working contractile myocardium in an area with few Purkinje fibers. The degree of abnormality of the QRS complex depends on the amount of ventricular myocardium that has been depolarized through the AP (Figure 12.1, arrow from A–D). The QRS complex morphology in the different surface ECG leads depends on which epicardial area is excited earliest. Studies correlating surface ECGs, vectorcardiography (VCG), and epicardial mapping performed during surgical ablation of APs by the Gallagher group (Tonkin et al. 1975) have shown the value of studying delta wave polarity to identify the site of earliest ventricular epicardial excitation. The first 20 ms vector in the ECG (first delta wave vector that can be measured on the ECG) is situated in different places on the frontal plane (in the horizontal plane it is always directed forward), depending on the site of earliest ventricular epicardial excitation. These studies precisely locate the AP according to the surface ECG findings, at 10 sites around the AV ring (Gallagher et al. 1978). There is an electrophysiological statement (Cosio et al. 1999) to standardize the terminology of APs around the AV junction. Milstein et al. (1987) (see Figure 12.6) described an algorithm that allows the correlation of the alterations found in the surface ECG with four ablation zones. From a practical point of view, the WPW‐type pre‐excitation may be classified into four types based on these findings: anteroseptal, right ventricular (RV) free wall, inferoseptal, and left ventricular (LV) free wall (Bayés de Luna and Baranchuk, 2017) (Figure 12.3). A complete electrophysiologic study (EPS) should be carried out to precisely identify the exact location of the AP before performing an ablation. Figure 12.3 WPW‐type pre‐excitation morphologies according to the different localization of the AV accessory pathway: (A) Right anteroseptal area (RAS); (B) right ventricular free wall (RFW); (C) inferoseptal area (IS); and (D) left ventricular free wall (LFW). In Figures 12.7–12.8, we can see examples of QRS morphologies in these four electrocardiographic modalities of WPW‐type pre‐excitation. Types I and II mimic a LBBB, with a more deviated left axis (ÂQRS beyond +30°) in type II, whereas in type I the ÂQRS is usually between +30° and +90°. In type III, the QRS is predominantly negative in inferior leads, especially in III and aVF, with R or RS morphology in V1 or V2, and the ÂQRS is between −30° and −90°. Type IV has a predominantly negative morphology in lateral leads (I, aVL) and a generally high R wave in leads V1 or V2, with a right axis deviation (ÂQRS beyond +90° up to +150°). Type IV is the most frequent (≈50% of cases) followed by inferoseptal (25%). The APs in close proximity to the bundle of His are located in the anteroseptal zone, close to the anteroseptal and midseptal tricuspid annulus (Arruda et al. 1998). The prevalence is low (1–2%), but it is important to localize them precisely by electrophysiologic studies (WPS) because they may present with AV block during the ablation procedure. Figure 12.4 (A) ECG–VCG of a patient with WPW type II (Ha: amplified horizontal plane). The arrows indicate the end of the delta wave. (B) Another ECG–VCG of a patient with WPW type II. Figure 12.5 A WPW patient with the accessory pathway located in the inferoseptal heart wall (type III WPW). This case may be mistaken for an inferior infarction, right ventricular hypertrophy, or right bundle branch block (RBBB). Other algorithms have been published (Lindsay et al. 1987; Chiang et al. 1995; Iturralde et al. 2006). Yuan et al. (1992) carried out a comparative study of eight algorithms, some of which allow for a better identification of the different types of septal pathways. They are difficult to memorize, and they are neither sensitive nor specific for all the cases. Later, Basiouny et al. (1999) reviewed 10 algorithms and found that the PPV was lower in those algorithms aimed at reaching a more precise localization (>6 sites), whereas PPV was found to be higher (>80%) when the AP was located on the left side. Because their reproducibility is not very high, it is advisable that each center become more familiar with the algorithm they consider best suited to their needs. A complete EPS should, therefore, be carried out to precisely identify the exact location of the AP before performing an ablation. Repolarization is altered except in those cases with minor pre‐excitation. These changes are secondary to depolarization alterations, and become more pathologic (more significant opposing polarity when compared with that of the R wave) as the degree of pre‐excitation increases (Figure 12.2). Figure 12.6 Algorithm used to localize the accessory pathway in one of the four ablation areas: right anteroseptal (RAS); right ventricular free wall (RFW); inferoseptal area (IS); and left ventricular free wall (LFW) (see text). Figure 12.7 Two examples of WPW type I pre‐excitation. (A) Important pre‐excitation in a 65‐year‐old patient with intermittent WPW. (B) Slight pre‐excitation in a 25‐year‐old patient with mitral stenosis. Observe in both cases the short PR and the positive delta wave in every lead except VR, where it is negative, and V1 where it is positive. The case on the left (A) can be confused with advanced LBBB and the case on the right (B) with not advanced LBBB. Figure 12.8 Two cases of WPW patient with the accessory pathway located in the left ventricular free wall (type IV WPW). These cases may be mistaken for a lateral infarction, right ventricular hypertrophy, or right bundle branch block. When pre‐excitation is intermittent, the complexes conducted without pre‐excitation may show repolarization alterations (negative T wave), which are explained by an electrical “electrical memory phenomenon” (Chatterjee et al. 1969; Nicolai et al. 1981; Rosenbaum et al. 1982). Approximately 5–10% of cases involve more than one AP. This may be clinically suspected when the patient suffers from syncope or malignant ventricular arrhythmia, or wide QRS complex paroxysmal tachycardia (antidromic tachycardia). Some ECG data are indicative of this association, both in sinus rhythm and during tachycardia. These are as follows: In general, this diagnosis suspicion should be confirmed with intracavitary electrophysiologic study (EPS). Some patients are referred with suspected WPW pre‐excitation when none exists and others have a genuine pre‐excitation and are considered normal. Using a selective AV node blocking agent, such as adenosine, may confirm or exclude the presence of pre‐excitation (Belhassen et al. 2000). Its rapid action, and fast degradation, makes Adenosine the best choice to confirm the presence of “hidden” accessory pathways in the EP lab. On the other hand, the presence of the septal Q wave in V6 is considered to be evidence that excludes minimal pre‐excitaton in doubtful cases (Bogun et al. 1999). Finally, Eisenberger et al. (2010) has shown a stepwise approach that is very sensitive and specific for excluding or confirming WPW pre‐excitation. Figure 12.9 Atrial fibrillation episode (A) and supraventricular paroxysmal tachycardia (B) in the same patient with WPW syndrome. See the typical ECG patterns in both cases. (C) Patient with WPW syndrome presenting with a very fast atrial fibrillation triggering a ventricular fibrillation (arrow). This was treated with electrical cardioversion. Figure 12.10 Intermittent pre‐excitation. In the first three complexes, the PR interval is short (80 ms) and the delta wave is observed. In the rest of the tracing, the delta wave disappears, but a short PR interval is still observed (100 ms). Thus, this surface ECG suggests the presence of two types of pre‐excitation, one of which short circuits the AV node (short PR, QRS with no delta wave), while the other is a pathway located in the ventricular myocardium (Kent bundle), since the PR interval is very short and a clear delta wave is seen. Figure 12.11 Intermittent type IV pre‐excitation: the pattern is similar to that observed in a lateral infarction (see aVL). It is important to recognize the different signs that allow us to suspect the presence of acute or chronic ischemia when pre‐excitation is present. However, this occurs very rarely because the presence of WPW pre‐excitation is less prevalent, especially in adults. In the acute phase, the repolarization changes, especially the ST segment elevation, may lead us to suspect acute coronary syndrome (ACS) with ST elevation. It is more difficult to make the correct diagnosis in ACS without ST elevation. In the chronic phase of Q wave myocardial infarction, the association may sometimes be suspected when repolarization shows more symmetrical T waves (Fiol‐Sala et al. 2020). Sometimes, echocardiography imaging is required to establish the presence of localized wall motion abnormalities. In any case, the presence of a short PR interval and/or a delta wave, always keeping in mind the possibility of WPW‐type pre‐excitation, are key ECG data for the correct diagnosis of this condition. The presence of short PR and delta wave indicates pre‐excitation. Therefore, in practice the association is usually only diagnosed when pre‐excitation is transient. However, there are cases with borderline PR interval or pseudo‐delta wave such as in cardiomyopathy or distal bundle branch block in which the association may be suspected if the bundle branch block is contralateral to the pre‐excited ventricle (Pick and Fisch 1958, Denes et al. 1975). This results in QRS complexes that may show an early pre‐excitation delta wave and also a terminal slurring due to BBB (i.e. left anomalous pathway + RBBB). On the contrary, the presence of BBB with ipsilateral pre‐excitation results in masking the BBB due to premature depolarization of the blocked ventricle by the anomalous pathway. Patients with Ebstein disease present frequently right anomalous bundle and RBBB. Iturralde et al. (1996) demonstrated that RBBB pattern is usually masked by pre‐excitation. After ablation and pathway removal, a clear pattern of RBBB may be seen. Figure 12.12 “Concertina” effect. The five first complexes are identical and show short PR and pre‐excitation. In the next four complexes, pre‐excitation decreases with a shorter PR = 0.12 sec. The three last complexes do not show any pre‐excitation and the PR = 0.16 sec. Figure 12.13 Conduction occurs via both the normal and the accessory pathway. When the stimulus is conducted over the accessory pathway, the PR interval is shorter than when the stimulus is conducted over the normal pathway (0.15 sec). Pre‐excitation may be intermittent (Figures 12.10, 12.11, and 12.13). Sometimes the degree of pre‐excitation changes progressively (“concertina” effect) (Figure 12.12). Pre‐excitation may increase if stimulus conduction through the AV node is depressed (vagal maneuvers, some drugs such as digitalis, beta blockers, calcium antagonists, adenosine, etc.) and vice versa (full “pre‐excitation is obtained when the stimulus travels predominantly through the accessory pathway”). It may decrease when the AV node conduction is facilitated (i.e. through exercise etc.) (Figure 12.13). Historically, intermittent pre‐excitation was associated with “benign” pathways, but this concept is currently under revision (Jastrzębski et al. 2017). We have already commented on how the presence of sudden changes in the QRS complex morphology with the delta wave remaining present, or changes from the typical WPW pattern to short PR interval alone, suggests that two pathways of pre‐excitation could coexist (Figure 12.10). Patients with WPW pre‐excitation can present paroxysmal reentrant tachycardia using an AP (AVRT) (slow–fast type), accounting for 50% of all supraventricular paroxysmal tachycardias (see Figures 15.11–15.13). In this case, during tachycardia, ventricular depolarization usually occurs through the normal pathway (AV node–His), and the AP serves as the retrograde limb of the macro‐reentrant circuit. For this reason, the QRS complex does not show pre‐excitation at this time (orthodromic tachycardia). In fewer than 10% of cases of paroxysmal tachycardia, antegrade ventricular depolarization takes place over the AP, depicting a very wide QRS complex (antidromic tachycardia) (see Figure 15.16). Antidromic tachycardia can also occur through two accessory WPW‐type pathways, one with anterograde conduction and the other with retrograde conduction. When antidromic tachycardia is the result of an atypical pre‐excitation (long atriofascicular pathway with decremental conduction) (type 2 pre‐excitation in Table 12.1), the QRS complex morphology of the tachycardia presents some differences with respect to the QRS morphology in cases of typical AV (Kent bundle) antidromic tachycardia. The differences particularly concern the R/S transition in precordial leads, which is delayed beyond V3 in atypical pre‐excitation (compare Figures 15.16 and 16.18). The rare cases of incessant reentrant AV junctional tachycardias are explained by a circuit involving an accessory pathway with slow retrograde conduction (fast‐slow type) (Farré et al. 1979; Critelli et al. 1984) (see Figure 15.15). Patients with WPW‐type pre‐excitation can present with atrial fibrillation and flutter episodes more frequently than the general population (Figures 15.31 and 15.41). This happens because patients with WPW often present with a shorter atrial refractory period and higher atrial vulnerability (Hamada et al. 2002). All these properties favor the triggering of atrial fibrillation (AF). Occasionally, a fast retrograde conduction of a premature ventricular complex over the AP falls in the atrial vulnerable period (AVP), or a paroxysmal reentrant tachycardia triggers atrial fibrillation (Peinado et al. 2005). In the presence of rapid atrial fibrillation, more stimuli are conducted to the ventricles through the AP than through the normal pathway. If one of them falls in the vulnerable ventricular period, it may trigger ventricular fibrillation (VF) and sudden death (Figure 12.9C) (Castellanos et al. 1983). This phenomenon accounts for some cases of sudden death, especially in young people, although this is fortunately rare. Figure 15.41 shows a patient with WPW syndrome and an atrial fibrillation (top) and atrial flutter (bottom) episodes. In both cases, the differential diagnosis with ventricular tachycardia (VT) is difficult, even more in cases of atrial flutter because the heart rate is regular (see Chapter 15, Atrial fibrillation: ECG findings). In cases of atrial fibrillation, the diagnosis is based on the irregularity of the rhythm and the presence of narrow QRS complexes, sometimes premature and sometimes late, whereas in VT the rhythm is regular and, if narrow QRS complexes are present, they are always premature (captures) (see Figure 16.15). However, in a 2:1 atrial flutter with pre‐excitation, these key points for differential diagnosis do not exist. We have to take into consideration other clinical and ECG data (history taking, AV dissociation, etc.). Figure 12.9A,B shows a patient with both a paroxysmal tachycardia and an atrial fibrillation episode.
Chapter 12
Ventricular Pre‐excitation
Concept and types of pre‐excitation
WPW‐type pre‐excitation (type 1)
Concept and mechanism
ECG characteristics
Accessory pathway
Frequency
ECG in sinus rhythm
ECG during tachycardia
Type 1
(a) Fast conduction in both ways: AV accessory pathway (classical Kent bundle) (see Figures 9.1–9.7)
60–65%
Short PR
δ wave
No 8 wave
RP′ < P′R
(b) Fast conduction in the AV accessory pathway (only in retrograde direction) (concealed pre‐excitation)
20–30%
Normal PR
No δ wave
No δ wave
RP′ < P′R
(c) Fast conduction in the AV accessory pathway (only in anterograde direction) (frequently two or more bundles involved)
5–10%
Short PR
δ wave
Wide QRS due to an anterograde conduction of the stimuli through the accessory pathway (antidromic tachycardia)
(d) Only retrograde and slow conduction through AV accessory pathway
≈ 5%
Normal PR
No δ wave
Frequently incessant tachycardia with RP′ > P′R
(e) Presence of >1 accessory pathway
5–10%
May switch from one to another QRS morphology qrs or qRs in V1
This diagnosis is generally difficult based only on a surface ECG
Antidromic tachycardia or alternating antidromic/orthodromic tachycardia
Alternation of short and long PR Morphology changes in ectopic P wave Electrophysiological studies confirm this diagnosis
Type 2
Slow anterograde conduction, generally through a long atriofascicular tract (distal right branch), without retrograde conduction (including classical Mahaima fibers–node ventricular or fascicle ventricular‐)
Rare
Non‐existent or slight pre‐excitation (i.e. no Q in V5–V6, with borderline PR and uncertain 8 wave, and rS in III) This is due to the slow conduction through the abnormal tract.
Globally the ECG is normal or presents different grades of LBB pattern
Antidromic tachycardia with anterograde conduction through the right atriofascicular tract and retrograde conduction through the RBB. Therefore, it features a LBBB morphology. Compared with the antidromic tachycardias (generated due to anterograde conduction through a right AV accessory pathway—Type C in this table), features a narrower QRS complex and a delayed transition to RS in precordial leads (compare Figures 15.16 and 16.18)
Type 3
AV node accelerated conduction, sometimes due to an atriohisian tract (short PR pre‐excitation)
Rare
Short PR interval
No δ wave
Normal QRS complex
No δ wave
PR interval
Ventriculogram alterations (Figures 12.4 and 12.5)
Repolarization alterations
ECG diagnosis of more than one accessory pathway (Wellens et al. 1990)
How to confirm or exclude the presence of pre‐excitation
Differential diagnosis of WPW‐type pre‐excitation
Associated ischemic heart disease
Associated with bundle branch block
Spontaneous or induced changes of the abnormal morphology
Arrhythmias and WPW–type pre‐excitation: Wolff–Parkinson–White syndrome (Figure 12.9)
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