8: Ventricular Preexcitation

Ventricular Preexcitation


8.1.  Concepts and Types



  • Ventricular preexcitation occurs when the electrical stimulus reaches the ventricles before the normal activation through the specific conduction system (SCS). In fact, this phenomenon is not really a preexcitation, but rather early ventricular excitation. [A]
  • Early ventricular excitation, mistakenly known as preexcitation, was described by Wolff, Parkinson, and White in young persons presenting paroxysmal arrhythmias, and is known as Wolff–Parkinson–White (WPW) syndrome. Early excitation occurs because of the existence of short muscular bundles with accelerated conduction (accessory pathway), known as Kent bundles, that connect the atria to the ventricles. These bundles may involve conduction that is anterograde, retrograde, or both. The degree of anomalous activation is variable (Fig. 8.1).
  • Rarely, early excitation takes place through long bundles that connect the right atrium with the fascicles or muscular mass of the right ventricle and present anterograde decremental conduction only. This is known as atypical preexcitation and includes the phenomenon previously known as Mahaim preexcitation.
  • Also the preexcitation may be due to the existence of an atrial-hisian bundle, which carries the stimulus from the atrium to the ventricle faster, or may be due simply to accelerated AV conduction. This is known as short PR-type preexcitation, or Lown–Gannon–Levine syndrome.
  • The presence of preexcitation, especially WPW syndrome, favors the appearance of potentially dangerous supraventricular arrhythmias (see later).
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Figure 8.1  The accessory bundle is indicated with an arrow. Ventricular depolarization is realized by two routes: normal (through the SCS and abnormal (through the accessory bundle). The zone depolarized by the abnormal route is shaded in B and C; the resulting complex is a fusion complex, since part of the ventricles are depolarized by the normal route (unshaded area) and part by the abnormal route (shaded area). In A, the complete depolarization is effected in the normal route and in D, entirely by the abnormal route (maximum preexcitation).

8.2.  WPW-Type Preexcitation


8.2.1.  Electrocardiographic Characteristics (Fig. 8.2) [B]


(A)  Short PR Interval


This is due to early ventricular excitation through an accessory pathway, that occurs before the normal excitation arrives through the SCS.

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Figure 8.2  Left top panel: Diagram of the P–QRS relationship in normal cases. (AB) P wave; (BC) PR segment; (CD) QRS. Middle panel: WPW-type preexcitation (the broken line represents the QRS complex if no preexcitation 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 preexcitation. Middle panel: example of four complexes with preexcitation, with an average-sized delta wave. Lower panel: four complexes in a case of short PR preexcitation.

(B)  QRS Morphology


The QRS is usually wide (≥0.11 s) and its morphology depends on the location of the accessory pathway. However, in all the cases as the location in the ventricular muscle of the accessory pathway takes place in an area with few Purkinje fibers, some initial slurrings in the QRS complex, known as delta wave, are present. Later, the stimulus arrives through the normal pathway, and the ventricles are activated through two fronts, configuring a true fusion complex that presents a greater or lesser degree of preexcitation depending on the quantity of preexcited ventricular mass (Fig. 8.1).


Figure 8.2 shows various degrees of WPW-type preexcitation (above right). See how from A to C an increasing degree of delta wave. D is a case of atrial fibrillation with a second complex presenting the maximum degree of preexcitation. In the middle part of the figure, four successive complexes are seen in a case of moderate preexcitation. With a clear short PR and an exclusive short PR-type preexcitation below. On the upper left, normal ventricular activation is shown. In the middle, WPW preexcitation shows short PR and a delta wave with an earlier QRS complex seen in points, but with the same final QRS resembling that found in normal patients. This is because ventricular activation is a fusion complex between the first preexcited part and the second part activated by a normal pathway.


8.2.2.  Types of WPW-type Preexcitation [C]


WPW-type preexcitation may be classified into four types according to the accessory pathway location. Figure 8.3 shows this organization and the repercussions of the anomalous pathway location on ECG morphology. We must always remember that in WPW preexcitation ventricular activation is shared by the accessory pathway and the normal pathway (Figs 8.1–8.3). Figures 8.4 and 8.5 show examples of the four types of preexcitation with evident delta waves.

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Figure 8.3  WPW-type preexcitation 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). ES = early stimulation.
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Figure 8.4  Left: ECG of WPW preexcitation type I in a 28-year-old patient. Right: ECG of WPW preexcitation type II. The most important difference is the ÂQRS direction; in type I around +50° and type II around +15°: see Fig. 8.3). These cases mimic LBBB pattern, case A with a less advanced pattern.
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Figure 8.5  Left: 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). Right: One case of a WPW patient with the accessory pathway located in the left ventricular free wall (type IV WPW). This case may be mistaken for a lateral infarction, right ventricular hypertrophy, or right bundle branch block.

Many algorithms have been described based on the location of the delta wave in certain leads. These algorithms can be used to locate the accessory pathway quite precisely (Bayés de Luna, 2012a). However, the predicted location must always be confirmed before performing ablation of the pathway.


Sometimes preexcitation is intermittent and occasionally may appear progressively (concertina effect). Figure 8.6 shows a case of sudden intermittent preexcitation and Figure 8.7 shows how preexcitation disappears progressively (concertina effect).

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Figure 8.6  Intermittent type IV preexcitation: the pattern with preexcitation is similar to Q wave MI (see VL).
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Figure 8.7  Concertina effect. The five first complexes are identical and show short PR and preexcitation. In the next four complexes, preexcitation decreases with a shorter PR = 0.12 s. The three last complexes do not show any preexcitation and the PR = 0.16 s.

8.2.3.  Confirming or Ruling Out Preexcitation



  • The injection of adenosine, a selective blocker of the AV node, can confirm (if the ECG pattern appears clearly), or rule out (if the ECG pattern does not modify) the preexcitation. [D]
  • The presence of q in V6 practically rules out preexcitation.

8.2.4.  WPW-Type Preexcitation and Arrhythmias


WPW preexcitation may be related to certain types of arrhythmia.


A.  Reentrant Paroxysmal Tachycardias of the AV Junction with an Accessory Pathway [E]


(JRT-AP; also named AVRT, see Chapter 11.)



  • The accessory bundle may participate in the reentrant circuit of a paroxysmal tachycardia of the AV junction, with retrograde conduction through the accessory pathway and anterograde conduction through the SCS. The atria are activated through the accessory pathway after anterograde activation of the ventricles through the normal pathway, and thus P’ is located after a narrow QRS. This differentiates these tachycardias from those in which the re-entrant circuit is found exclusively in the AV junction (JRT-E) (see Chapter 10).
  • Figure 8.8 shows in the first two complexes (A) the activation through the accessory pathway (c8-fig-5001) and later (B), after an atrial extrasystole (P’), the activation blocked in the accessory pathway and carried anterograde in through the AV junction of the SCS with a narrow QRS (1), originating a re-entrant tachycardia with retrograde atrial activation through the accessory pathway (P’ located after QRS) (P’R > RP’). The subsequent QRS complexes are also narrow (3) (orthodromic tachycardia) (see Chapter 11).
  • In rare cases of reentrant tachycardia, the anterograde conduction to the ventricles is made through one accessory pathway (Kent bundle or a long anomalous pathway in atypical preexcitation with retrograde conduction (see Fig. 8.3). This is known as antidromic tachycardia.
  • ECGs can generally be used to identify these two types of antidromic tachycardias that present a similar morphology to that of LBBB (QS in V1 and R in V6). Antidromic tachycardia through the Kent bundle presents a LBBB-like morphology with transition to R in precordial leads before V4 and the antidromic tachycardia through a long atriofascicular pathway of atypical preexcitation presents a LBBB-like morphology with a transition to R in precordial leads in V4 or later (see Bayés de Luna, 2011 and 2012a). For the differential diagnosis of antidromic tachycardia with ventricular tachycardia. See Section 12.2.3.2 in Chapter 12 (Steurer et al., 1994).
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Figure 8.8  Scheme of a heart with a right accessory AV pathway, which leads to faster than normal AV conduction (short PR) and early activation of part of the ventricles and appearance of abnormal QRS morphology (delta wave) (A). All this may be observed in the first two P-QRS complexes of the scheme. The QRS is a fusion complex due to initial depolarization through the accessory AV pathway (curved tracing) and the rest of depolarization through the normal AV pathway (rectilinear tracing). The third P wave is premature (atrial ectopic P’) that finds the accessory AV pathway in the refractory period. Due to this, the impulse is only conducted by normal AV conduction (rectilinear tracing in AV node) usually with a longer than normal P’R interval, because the AV node is in a relative refractory period. This stimulus produces a normal QRS complex (1), due to the fact that the accessory AV pathway is already out of the refractory period. Then it is conducted retrogradely to the atria, through the accessory pathway generating an evident P’ after the QRS complex (RP’ < P’R). In the case of junctional reciprocal tachycardia with circuit exclusively in the AV junction (JRT-E), the P’ is within the QRS complex or can be seen in its final part, modifying the QRS morphology (Fig. 11.7). After that the impulse re-enters and is conducted down to the ventricles via normal AV conduction (2). Due to this macroreentry circuit, the reciprocating tachycardia is maintained. The conduction in this circuit is retrograde via accessory AV pathway (curved tracing) and anterograde via the normal AV conduction (rectilinear tracing). The RP’ interval is smaller than the P’R interval, which is typical of junctional reciprocating tachycardia that involves an accessory AV pathway (WPW). (See Plate 8.8.)

B.  WPW Preexcitation and Atrial Fibrillation or Flutter



  • Patients with WPW more frequently present episodes of atrial fibrillation (AF) or flutter (AFL). Usually this is explained because a ventricular extrasystole (VE) carried quickly and retrogradely through the accessory pathway encounters atria that are vulnerable because they are outside the refractory period, which is generally shorter, and may trigger AF or AFL.
  • Occasionally, a supraventricular paroxysmal tachycardia may also trigger AF or AFL for a similar reason.
  • The differential diagnosis between AF of WPW syndrome and ventricular tachycardia is relatively easy, even though QRS is wide in both scenarios. The diagnostic criteria are exposed in the legend of Figure 8.9. However, the differential diagnosis is more difficult when AFL, rather than AF, is present (Fig. 8.10). [F]
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Figure 8.9  Twelve-lead ECG of a Wolff–Parkinson–White (WPW) syndrome in atrial fibrillation. Note the great degree of aberrancy of the complexes, that makes necessitates differential diagnosis with ventricular tachycardia (VT); this may be very difficult especially in the presence of a regular ventricular conduction (atrial flutter) (see Fig. 8.10B). In this example the diagnosis of WPW syndrome with atrial fibrillation and not of VT is supported by: (i) the presence of delta waves in some leads (V2, V3) and the presence of different morphologies of QRS, with more or less degrees of aberrancy, as the expression of different degrees of conduction over the accessory pathway; (ii) irregular RR; (iii) narrow QRS, which may or may not be premature (see asterisk). In ventricular tachycardia, narrow QRS complexes are always premature (captures) (Fig. 12.11); and (iv) awareness of the existence of this arrhythmia.
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Figure 8.10  A 50-year-old patient with type IV Wolff–Parkinson–White (WPW) atrial fibrillation (top) and atrial flutter (bottom) episodes simulating a ventricular tachycardia (A). The isolated, wide R morphology, with a notch in the descending arm does not correspond to a right bundle branch block (RBBB) aberrancy. Furthermore, the following facts are in favor of a WPW syndrome with atrial fibrillation and not of ventricular tachycardia (in addition to other clinical features and the prior awareness of the WPW syndrome diagnosis): (i) The wide complexes show a very irregular rate and morphology (varying wideness) because of the presence of different degrees of preexcitation. (ii) The two narrow complexes – 6 and the last one in A – are late and premature, respectively. In sustained ventricular tachycardia, QRS are more regular and if captures occur (narrow complexes), they are always premature (see Fig. 12.11). (B) In the WPW syndrome with atrial flutter (in this case 2 × 1, 150 bpm) differential diagnosis with sustained ventricular tachycardia through the ECG is even more difficult. It is important to obtain the clinical history and to follow the criteria of differential diagnosis between VT and supraventricular tachycardia with aberrancy, especially those described by Steurer (Chapter 12).

C.  Atrial Fibrillation in WPW Syndrome and Sudden Death



  • Sudden death (SD) in WPW may appear in the presence of very fast AF when the RR is very short, allowing the supraventricular stimulus to fall into the vulnerable stage in the ventricles (Fig. 8.11). This usually does not occur if preexcitation disappears at high heart rate during a stress test, and if the refractory period of the accessory pathway is long. [G]
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Figure 8.11  Patient with WPW syndrome presenting with a very fast atrial fibrillation triggering a ventricular fibrillation (VF). See especially the short RR interval previous to PVC that triggers VF (see arrow). This was treated with electrical cardioversion.

8.2.5.  Differential Diagnosis in WPW-Type Preexcitation



  • WPW types I and II = LBBB. [H]
  • WPW type III = inferior infarction, right ventricular enlargement (VE), and RBBB.
  • WPW type IV = lateral infarction, right VE, and RBBB.

The key in every case is to measure the PR interval and to detect any delta waves.


8.3.  Atypical Preexcitation



  • The accessory bundle is long, with slow con­duction and goes from the right atrium to the right ventricle (atriofascicular or atrioventricular bundle). [I]
  • The ECG is often almost normal, or with only small degrees of preexcitation in the form of small initial slurrings of R wave in I and V6, and often with rS in lead III that mimick partial LBBB (accessory pathway in RV).
  • It may originate tachycardias with wide QRS usually of LBBB type, because the anterograde conduction is made through one long right accessory bundle (see Figure 8.2.4.A and Bayés de Luna 2011, and 2012a).

8.4. Short PR-Type Preexcitation



  • In this case early excitation is produced by an accelerated AV conduction, or by the existence of an atrial hisian bundle that avoids slow conduction through the AV node. [J]
  • Figure 8.2 (bottom) shows a case of short PR-type preexcitation in which the end of QRS complex occurs earlier because the entire activation, which starts early, occurs through the SCS.
  • Figure 8.12 shows a typical example of short PR-type preexcitation. It is important to remember that these patients are also at risk for potentially serious arrhythmias, especially in cases of rapid AF.
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Figure 8.12  Example of typical short PR interval preexcitation syndrome (PR interval = 0.10 sec).

Self-assessment




A.  What is ventricular preexcitation and how many types exist?

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  2. 5: Atrial Abnormalities
  3. 10: Concepts, Classification, and Mechanisms of Arrhythmias
  4. 9: Myocardial Ischemia and Necrosis

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Aug 29, 2016 | Posted by in CARDIOLOGY | Comments Off on 8: Ventricular Preexcitation

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