Basic and Bedside Electrocardiography, 1st Edition (2009)

Chapter 20. Wolff-Parkinson-White Syndrome

Anatomy of the Conduction System

·   Wolff-Parkinson-White (WPW) syndrome: WPW syndrome is a clinical entity characterized by preexcitation of the ventricles with symptoms of paroxysmal tachycardia.

o    Normal atrioventricular (AV) conduction: In normal individuals, the atria and ventricles are separated by a dense mass of fibrous tissues that prevent the spread of electrical impulses from atria to ventricles. The only pathway by which the atrial impulse can reach the ventricles is through the AV node and normal intraventricular conduction system (Fig. 20.1A).

o    WPW syndrome: In WPW syndrome, a bypass tract is present, which connects the atrium directly to the ventricle. The atrial impulse therefore is able to reach the ventricles not only through the AV node, but also through the bypass tract (Fig. 20.1B). This accessory pathway can cause premature activation of the ventricles. It can also serve as a pathway for reentry, which may result in clinical symptoms of paroxysmal tachycardia.

Figure 20.1: The Conduction System in Normal Individuals and in Patients with the WPW Syndrome. (A) The normal AV conduction system. The atrial impulse can enter the ventricles only through the AV node (arrow). (B) A bypass tract connecting the atrium directly to the ventricle across the AV groove. When a bypass tract is present, an atrial impulse can enter the ventricles not only through the AV node but also through the bypass tract (arrows). AV, atrioventricular.

Preexcitation of the Ventricles

·   Ventricular preexcitation: When a bypass tract is present, conduction of the sinus impulse to the ventricles is altered as shown in Figure 20.2.

o    Atrial activation: During normal sinus rhythm, activation of the atria is not altered. The sinus P wave remains normal.

o    Ventricular activation: When a bypass tract is present, the ventricles are activated through two separate pathways: the AV node and bypass tract. The QRS complex represents a fusion complex.

§  Bypass tract: Unlike in normal individuals in whom the sinus impulse can reach the ventricles only through the AV node, the presence of a bypass tract allows the atrial impulse to be conducted directly to the ventricles thus activating the ventricles prematurely. This causes the PR interval to be shorter than normal (Fig. 20.2B). The impulse spreads by muscle cell to muscle cell conduction causing the initial portion of the QRS complex to be inscribed slowly. This slow initial upstroke of the QRS complex is called the delta wave.

§  AV node: The sinus impulse is normally delayed at the AV node. As the impulse emerges from the AV node, it activates the ventricles rapidly through the normal conduction system causing the rest of the QRS complex to be inscribed normally (Fig. 20.2C).

Figure 20.2: Ventricular Preexcitation. (A) The sinus impulse activates the atria and a P wave is normally recorded. (B) The sinus impulse is normally delayed at the AV node but is conducted directly through the bypass tract causing the ventricles to be prematurely activated. This causes the PR interval to shorten and the initial portion of the QRS complex to be slurred. (C) The impulse finally emerges from the atrioventricular node and activates the rest of the ventricles normally.

Electrocardiogram Findings

·   Electrocardiogram (ECG) findings: The classical ECG findings in WPW syndrome include a short PR interval, a delta wave, and secondary ST and T wave abnormalities.

o    Short PR interval: The PR interval is short since the bypass tract conducts more rapidly than the AV node causing the ventricles to be excited prematurely. The PR interval is shorter than normal, but does not have to measure <0.12 seconds.

o    Delta wave: The delta wave is the initial portion of the QRS complex with a slow upstroke, as shown in Figure 20.3. It represents premature activation of the ventricles at the area of insertion of the bypass tract. Because conduction of the impulse is by direct muscle spread, which is slow and inefficient, this causes the initial portion of the QRS complex to be inscribed sluggishly. This initial portion with the slurred upstroke is called the delta wave.

o    ST and T wave abnormalities: The ST and T wave changes are secondary to the abnormal activation of the ventricles. The direction of the ST segment and T wave is opposite that of the delta wave.

The Bypass Tract

·   Bypass tract: Unlike the His-Purkinje system, the bypass tract consists of ordinary heart muscle and does not contain cells that are specialized for conduction.

o    The bypass tract may be left sided or right sided.

o    It may be single or multiple.

o    Conduction may be constant or intermittent (Figs. 20.4 and 20.5).

o    The bypass tracts may be active or inactive.

o    The bypass tract may conduct only anterogradely (from atrium to ventricle), only retrogradely (from ventricle to atrium) or both.

§  Manifest or overt bypass tract: The bypass tract is manifest or overt if it is capable of conducting anterogradely from atrium to ventricle resulting in the classical pattern of preexcitation.

§  Concealed bypass tract: The bypass tract is concealed if it is capable of conducting only retrogradely from ventricle to atrium. The baseline ECG will not show any evidence of preexcitation during normal sinus rhythm, but the presence of a bypass tract can potentially cause a reentrant tachycardia to occur.

Figure 20.3: Ventricular Preexcitation. A QRS complex is magnified from the rhythm strip to show the short PR interval measuring 0.11 seconds, delta wave, and ST-T abnormalities.

Figure 20.4: Intermittent Preexcitation. The rhythm strip is recorded in V1. The first three complexes show no evidence of preexcitation. The PR interval is prolonged and the QRS complexes are narrow. The last three complexes show ventricular preexcitation. The PR interval is short, the QRS complexes are wide and delta waves are present. The ST segments are also depressed with inverted T waves pointing away from the direction of the delta wave.

Figure 20.5: Intermittent Preexcitation. Intermittent preexcitation is shown by arrows #1-#4. The other complexes are conducted normally without preexcitation.

 

Figure 20.6: Size of the Delta Wave. (A) The delta wave is barely recognizable because of a smaller amount of myocardium activated from the bypass tract. This occurs when the bypass tract is left sided or conduction through the AV node is enhanced. (B) The delta wave is more prominent because a larger amount of myocardium is activated from the bypass tract. This is often seen in right sided bypass tracts or when there is delay in the conduction of the impulse at the AV node. AV, atrioventricular.

The Delta Wave

·   Size of the delta wave: The delta wave may be very conspicuous or it may be barely recognizable in the baseline ECG, depending on the amount of ventricular myocardium activated from the bypass tract.

o    Small delta wave: The delta wave may be barely recognizable if only a small amount of ventricular myocardium is activated from the bypass tract. This occurs if the bypass tract is left sided because a left-sided bypass tract is farther from the sinus node compared with a right-sided bypass tract. The farther the distance from the sinus node, the longer it takes for the sinus impulse to reach the bypass tract (Fig. 20.6A). This may result in normal or near normal PR interval. The delta wave is also small and inconspicuous if the atrial impulse is efficiently conducted through the AV node.

o    Large or prominent delta wave: The delta wave is prominent if a larger portion of the myocardium is activated from the bypass tract (Fig. 20.6B). This occurs when the bypass tract is right sided bringing it closer to the sinus node. The delta wave is also prominent if the sinus impulse is delayed at the AV node.

Localizing the Bypass Tract

·   An ECG is helpful in predicting the location of the bypass tract during normal sinus rhythm, during narrow complex tachycardia, and during wide complex tachycardia.

·   After preexcitation is diagnosed in the 12-lead ECG, the bypass tract can be localized during sinus rhythm by the following observations.

o    Left-sided bypass tract: When the bypass tract is left sided, the left ventricle is activated earlier than the right ventricle. The impulse will travel from left ventricle to right ventricle in the direction of V1, which is located on the right side of the sternum (Fig. 20.7). Thus, during normal sinus rhythm, a positive delta wave or tall R or Rs complex will be recorded in V1. This pattern of preexcitation is also called type A. Tall R waves in V1 can be mistaken for right bundle branch block, right ventricular hypertrophy or posterior infarction.

o    Right-sided bypass tract: When the bypass tract is right sided, the right ventricle is activated earlier than the left ventricle. The impulse spreads from right ventricle to left ventricle away from lead V1. This results in a negative delta wave with deep S or rS complex in V1 (Fig. 20.8). This pattern of preexcitation is also called type B. Because the S waves are deeper than the R waves in V1, the ECG may be mistaken for left bundle branch block, left ventricular hypertrophy, or anteroseptal myocardial infarction.

      

Figure 20.7: Left-Sided Bypass Tract. When the bypass tract is left sided, the initial impulse spreads from left ventricle to right ventricle during normal sinus rhythm as shown in the above diagram (arrows). This will result in tall R waves in V1. In this example, the bypass tract was localized at the posterior wall of the left ventricle and was successfully ablated.

·   Location: Approximately 50% to 60% of all bypass tracts are located at the free wall of the left ventricle, 20% to 30% at the posteroseptal area (left or right), 10% to 20% at the free wall of the right ventricle and the remaining 5% are located in the anteroseptal area (mostly right sided).

·   Left sided versus right sided: The morphology of the QRS complex in V1 is useful in differentiating a left-sided from a right-sided bypass tract.

o    Right-sided bypass tracts: As previously discussed, the bypass tract is right sided if the QRS complex is predominantly negative (QS or rS) in V1. Right-sided bypass tracts may be located at the posteroseptal area, right ventricular free wall or anteroseptal area (Figs. 20.9 and 20.10).

o    Left-sided bypass tracts: If the QRS complex is predominantly upright (tall R or Rs) in V1, the bypass tract is left sided. Left-sided bypass tracts may be located at the left ventricular free wall or the posteroseptal area. Anterior or anteroseptal bypass tracts rarely exist because the aortic annulus and mitral annulus are contiguous structures (Fig. 20.9).

·   Several methods of predicting the location of the bypass tract during normal sinus rhythm have been described. The bypass tract can be more accurately localized if the delta wave contributes significantly to the QRS complex. Although there are limitations in using the 12-lead ECG for localizing the bypass tract, the algorithm of Olgin and Zipes, shown below, is the simplest and most practical.

o    Step 1. Configuration of the QRS complex in V1:

§  A tall R wave in V1 indicates that the bypass tract is left sided.

§  A deep S wave in V1 indicates that the bypass tract is right sided.

o    Step 2A. Right-sided bypass tract: If the bypass tract is right sided, it may be posteroseptal, anteroseptal, or free wall in location.

§  Posteroseptal: QS complexes in the leads II, III, and aVF indicate that the bypass tract is posteroseptal in location.

Figure 20.8: Right-Sided Bypass Tract. When the bypass tract is right sided, the right ventricle is activated earlier than the left ventricle. This causes the initial impulse to spread from right ventricle to left ventricle away from lead V1 resulting in QS or rS complexes in V1. This electrocardiogram can be mistaken for left bundle branch block, left ventricular hypertrophy, or anteroseptal myocardial infarction.

Figure 20.9: Location of the Bypass Tract. The position of the bypass tract at the level of the AV grove is shown by the diagram. Right-sided bypass tracts are located at the right ventricular free wall, posteroseptal, or anteroseptal areas, whereas left-sided bypass tracts are located at the left ventricular free wall or posteroseptal area. The left anteroseptal area is occupied by the aortic root and the presence of a left sided anteroseptal bypass tract is rare. Ao, aorta; AV, atrioventricular; MA, mitral annulus; PA, pulmonary artery; TA, tricuspid annulus.

§  Anteroseptal: An inferior axis indicates that the bypass tract is anteroseptal in location.

§  Free wall: The presence of left axis indicates that the bypass tract is located at the right ventricular free wall.

o    Step 2B. Left-sided bypass tract: This may be posteroseptal or free wall.

§  Posteroseptal: QS complexes in leads II, III, and aVF indicate that the bypass tract is posteroseptal in location.

§  Left ventricular free wall: An isoelectric or negative delta wave in I, aVL, V5, and V6 indicates free wall bypass tract.

Figure 20.10: Localizing the Bypass Tract. Adapted from Olgin and Zipes.

Left-Sided Bypass Tract

·   Left ventricular free wall: Figure 20.11 is an example of a bypass tract at the free wall of the left ventricle. Tall R waves or Rs complexes in V1 suggest that the bypass tract is left sided. Negative delta waves or QS complexes in leads I and aVL suggest that the bypass tract is at the free wall since the impulse is traveling away from these leads.

·   Left-sided posteroseptal bypass tract: Example of left-sided posteroseptal bypass tract is shown in Figure 20.12. Tall R waves are present in V1 consistent with a left-sided bypass tract. Deep Q waves are present in II, III, and aVF suggest that the bypass tract is posteroseptal because the electrical impulse is traveling away from these leads.

Figure 20.11: Left Ventricular Free Wall. Tall R waves are present in V1 consistent with a left sided bypass tract. QS complexes are present in I and aVL resembling a lateral infarct. This suggests that the impulse is traveling away from the positive sides of leads I and aVL consistent with a bypass tract at the lateral free wall of the left ventricle.

Right-Sided Bypass Tract

·   Right-sided posteroseptal bypass tract: Example of a right-sided posteroseptal bypass tract is shown in Figure 20.13. V1 shows QS complexes consistent with a right-sided bypass tract. QS complexes are also present in leads II, III, and aVF, suggesting that the bypass tract is posteroseptal in location.

·   Anteroseptal bypass tract: Anteroseptal bypass tracts are usually right sided. Right-sided anteroseptal bypass tract has QS or rS in V1 with the axis directed inferiorly toward +30° to +120°. Q wave is present in aVL but not in V6 (Fig. 20.14).

·   Right ventricular free wall: Figure 20.15 shows a bypass tract at the right ventricular free wall. The QRS complex has a left bundle branch block pattern with left axis deviation. QS or rS complexes are present in V1 and the QRS complex in the frontal plane is usually directed to the left with an axis of +30° to -60°, resulting in tall R waves in I and aVL.

Figure 20.12: Left-Sided Posteroseptal Bypass Tract. Deep Q waves are present in leads II, III, and aVF resembling an inferior infarct. This is consistent with a posteroseptal bypass tract. The bypass tract is left sided because tall R waves are present in V1.

Figure 20.13: Right-Sided Posteroseptal Bypass Tract. QS complexes are present in leads II, III, and a VF consistent with a posteroseptal bypass tract. V1 shows a QS complex consistent with a right-sided posteroseptal bypass tract.

The WPW Syndrome

ECG Findings

·   Short PR interval

·   Delta wave

·   ST and T wave abnormalities

Mechanism

·   The main abnormality in WPW syndrome is the presence of a bypass tract that is separate from the normal AV conduction system. This anomalous pathway is also called accessory pathway or bundle of Kent. The bypass tract consists of ordinary myocardium that bridges the atrium directly to the ventricle across the AV groove.

·   During normal sinus rhythm, the only pathway by which the sinus impulse can reach the ventricles is through the AV node. The impulse is normally delayed at the AV node, resulting in a PR interval of 0.12 to 0.20 seconds. If a bypass tract is present, a second pathway is created by which the ventricles can be activated. Thus, during normal sinus rhythm, the impulse is normally delayed at the AV node but is conducted directly to the ventricle through the bypass tract. This causes the ventricle to be prematurely activated resulting in a shorter than normal PR interval usually measuring <0.12 seconds. As the impulse finally emerges from the AV node, it is conducted rapidly through the His-Purkinje system allowing the rest of the ventricles to be activated normally and more efficiently.

·   Preexcitation of the ventricle is seen in the ECG as a short PR interval with a delta wave.

o    Shortened PR interval: The PR interval is short because the atrial impulse reaches the ventricle faster through the bypass tract than through the AV node. The PR interval usually measures <0.12 seconds when there is preexcitation. However, the PR interval does not always have to be <0.12 seconds for preexcitation to occur. A normal PR interval ≥0.12 seconds is seen in approximately 25% of patients with preexcitation.

o    Delta wave: The delta wave is the slow, slurred initial deflection of the QRS complex. It represents myocardial conduction of the impulse through the ventricle at the area of insertion of the bypass tract. The delta wave is inscribed sluggishly because the impulse is propagated by direct myocardial spread. This causes the QRS complex to be inscribed slowly and is widened.

o    ST-T changes: The ST and T wave abnormalities are secondary to the abnormal activation of the ventricles and are directed away from the delta wave.

·   The size of the delta wave depends on the amount of myocardium activated by the accessory pathway. If there is significant delay of the impulse at the AV node, a larger portion of myocardium will be activated through the bypass tract resulting in a longer, larger, and more conspicuous delta wave. This causes a more bizarre and wider QRS complex. If the impulse is quickly and efficiently conducted across the AV node, the amount of myocardium activated by the bypass tract will be small and the delta wave may be barely noticeable because most of the ventricles will be activated through the normal His-Purkinje system. The size of the delta wave also depends on the location of the bypass tract. A right-sided bypass tract is closer to the sinus node than a left-sided bypass tract causing the ventricles to be activated earlier. A right-sided bypass tract therefore is expected to have a shorter PR interval and a more prominent delta wave than a left-sided bypass tract.

·   When there is preexcitation, the QRS complex is actually a fusion complex. The initial portion of the QRS complex is due to activation of the ventricles from the accessory pathway. The delta wave therefore represents the impulse that is contributed by the bypass tract. The remaining QRS complex represents activation of the ventricles through the normal AV conduction system.

Figure 20.14: Right-Sided Anteroseptal Bypass Tract. QS complexes are present in V1 and V2 consistent with a right sided bypass tract. The axis of the QRS complex in the frontal plane is inferior (>+60°). This is consistent with an anteroseptal bypass tract.

Figure 20.15: Right Ventricular Free Wall. QS complexes are present in V1 consistent with a right-sided bypass tract. There is also left axis deviation of the QRS complexes of approximately -30° consistent with a bypass tract at the right ventricular free wall.

Clinical Significance

·   Preexcitation of the ventricles is an electrocardiographic diagnosis characterized by the presence of a short PR interval and a delta wave. This specific pattern of preexcitation is also called the WPW ECG. Not all patients with the WPW ECG will develop symptoms of tachycardia. When preexcitation of the ventricles is associated with symptoms of tachycardia, the clinical entity is called WPW syndrome.

·   The bypass tract can be right sided (connecting the right atrium to the right ventricle anywhere within the tricuspid ring) or left sided (connecting the left atrium to the left ventricle anywhere within the mitral ring). It may be located anteroseptally, posteroseptally, or laterally at the free wall of the left or right ventricle. More than half of bypass tracts are located at the left lateral free wall connecting the left atrium to the left ventricle, about 20% to 30% are posteroseptal in location, 10% to 20% are at the right lateral wall connecting the right atrium to the right ventricle, and the remaining 5% are anteroseptal in location. Anteroseptal bypass tracts are mainly right sided.

·   The bypass tract may be single or multiple. Conduction may be fixed or intermittent and may be anterograde only (atrium to ventricle), retrograde only (ventricle to atrium) or both. Ventricular preexcitation therefore can manifest in different patterns and can be mistaken for other abnormalities not only during normal sinus rhythm, but also during tachycardia. Accordingly, preexcitation of the ventricle can be mistaken for left or right bundle branch block; left or right ventricular hypertrophy; posterior, inferior, anterior, and lateral Q wave myocardial infarction; non-Q wave myocardial infarction; myocardial ischemia; or other repolarization abnormalities. It can also be mistaken for ectopic beats or intermittent bundle branch block. The WPW ECG therefore is a great masquerader of several ECG abnormalities.

·   The 12-lead ECG is helpful in localizing the bypass tract during normal sinus rhythm. The more prominent the delta wave (or the greater the ventricular preexcitation), the more accurate is the localization. The location of the bypass tract during normal sinus rhythm should be compared with the location of the bypass tract during tachycardia. This may help identify if more than one bypass tract is present.

·   Approximately 10% to 20% of patients with Ebstein's anomaly has WPW syndrome with more than one bypass tract commonly present. In Ebstein's anomaly, the right ventricle is atrialized because of a downward displacement of the tricuspid leaflets into the right ventricle; thus, Ebstein's anomaly should always be suspected when a bypass tract is right sided. Other cardiac diseases associated with preexcitation include hypertrophic cardiomyopathies and mitral valve prolapse.

·   The presence of preexcitation can cause auscultatory changes in the heart.

o    Right-sided bypass tract: If the bypass tract is right sided, the right ventricle is activated earlier than the left ventricle. Delay in activation of the left ventricle will cause a softer first heart sound. Earlier activation of the right ventricle will cause earlier closure of the pulmonic component of the second sound, which can result in a single or paradoxically split second heart sound.

o    Left-sided bypass tract: If the bypass tract is left sided, the left ventricle is activated earlier than the right ventricle. This can cause the first heart sound to be accentuated. Delay in activation of the right ventricle will cause the pulmonic second sound to be further delayed resulting in wide splitting of the second heart sound. These auscultatory findings become audible only when a significant portion of the QRS complex is contributed by the bypass tract.

Treatment and Prognosis

·   Asymptomatic patients: The presence of preexcitation in the baseline ECG may not be associated with symptoms and may be discovered unexpectedly during a routine ECG for reasons unrelated to symptoms of tachycardia.

o    Among asymptomatic patients with intermittent preexcitation, without structural or congenital heart disease who continue to remain completely asymptomatic, the preexcitation may disappear, with a good prognosis. Routine electrophysiologic testing is not recommended.

o    Among asymptomatic patients with ECG pattern of preexcitation that is fixed or constant, the prognosis will depend on the physiologic characteristics and refractory period of the accessory pathway. The American College of Cardiology/American Heart Association (ACC/AHA) Task Force on Practice Guidelines for Clinical Intracardiac Electrophysiologic and Catheter Ablation Procedures does not recommend routine electrophysiologic testing in asymptomatic patients with preexcitation except those with a family history of sudden death or patients who are engaged in high-risk occupations or activities.

·   Symptomatic patients: In patients with classical preexcitation manifested by short PR interval and delta wave associated with clinical symptoms of tachycardia, the overall prognosis remains good except that there is an approximate 0.15% to 0.39% chance of sudden cardiac death occurring over a 3- to 10-year follow-up. The ACC/AHA/European Society of Cardiology (ESC) guidelines for the management of patients with supraventricular arrhythmias consider ablation therapy as Class I indication for patients with accessory pathways that are symptomatic. Antiarrhythmic therapy in these patients receives a Class IIa recommendation.

Figure 20.16: Conduction across the Bypass Tract. (A) The bypass tract can conduct only anterogradely from atrium to ventricle (dotted arrow); (B) only retrogradely, from ventricle to atrium; and (C), both anterogradely and retrogradely, from atrium to ventricle and from ventricle to atrium.

Arrhythmias Associated with the WPW Syndrome

·   One of the clinical features of the WPW syndrome is its predisposition to develop arrhythmias. The following are the most important arrhythmias associated with the WPW syndrome:

o    AV reciprocating tachycardia or AVRT

§  Orthodromic or narrow complex AVRT

§  Antidromic or wide complex AVRT

o    Atrial fibrillation

·   The electrophysiologic characteristics of the bypass tracts are highly variable. Some bypass tracts can conduct only anterogradely from atrium to ventricle (Fig. 20.16A), some only retrogradely from ventricle to atrium (Fig. 20.16B), and others can conduct both anterogradely from atrium to ventricle and retrogradely from ventricle to atrium (Fig. 20.16C). This may influence the type of arrhythmia associated with the WPW syndrome.

Narrow Complex and Wide Complex AV Reciprocating Tachycardia

·   AV reciprocating tachycardia (AVRT): AVRT is the most common arrhythmia associated with the WPW syndrome. AVRT is a supraventricular tachycardia that may have narrow or wide QRS complexes. The QRS complexes may be narrow or wide depending on how the ventricles are activated during the tachycardia.

o    Narrow complex AVRT: This type of AVRT has narrow QRS complexes because the atrial impulse enters the ventricles anterogradely through the AV node during tachycardia (Fig. 20.17A). The impulse follows the intraventricular conduction system and activates the ventricles, normally resulting in QRS complexes that are identical to that during normal sinus rhythm. This type of AVRT is also called orthodromic or narrow complex AVRT and was discussed in Chapter 16, Supraventricular Tachycardia due to Reentry.

o    Wide Complex AVRT: This type of AVRT has wide QRS complexes because the atrial impulse enters the ventricles through the bypass tract during the tachycardia (Fig. 20.17B). The impulse activates the ventricles outside the normal conduction system resulting in wide QRS complexes, which can be mistaken for ventricular tachycardia. Wide complex AVRT is also called antidromic AVRT and is further discussed in this chapter.

Figure 20.17: Orthodromic and Antidromic AVRT. (A) Orthodromic AVRT. During tachycardia, the impulse is conducted from atrium to ventricle across the AV node resulting in narrow QRS complexes. (B) Antidromic AVRT. During tachycardia, the atrial impulse is conducted from atrium to ventricle across the bypass tract resulting in wide QRS complexes, which can be mistaken for ventricular tachycardia. AVRT, atrioventricular reciprocating tachycardia.

Narrow Complex or Orthodromic AVRT

·   Mechanism of narrow complex AVRT. Narrow complex AVRT is discussed in more detail in Chapter 16. The tachycardia is triggered by a premature atrial or ventricular impulse.Figure 20.18 illustrates how a premature atrial impulse can precipitate a narrow complex AVRT.

o    The premature atrial impulse should be perfectly timed to occur when the AV node has fully recovered from the previous impulse while the bypass tract is still refractory. Because the AV node has a shorter refractory period, the premature atrial impulse is able to conduct through the AV node, but is blocked at the bypass tract (Fig. 20.18A).

o    The ventricles are activated through the normal AV conduction system, resulting in a narrow QRS complex (Fig. 20.18B). After the ventricles are activated, the impulse is conducted retrogradely from ventricle to atrium across the bypass tract. After the atria are activated, the impulse can reenter the AV node resulting in a narrow complex tachycardia called orthodromic AVRT (Fig. 20.18C). Delta waves are not present during tachycardia because activation of the ventricles occurs exclusively through the AV node.

Figure 20.18: Orthodromic or Narrow Complex AVRT. (A) A premature atrial complex (PAC) is conducted through the AV node but not through the bypass tract. (B) The ventricles are activated exclusively through the normal conduction system causing the QRS complex to be narrow. (C) The impulse is conducted from ventricles to atria across the bypass tract. The atria are activated retrogradely allowing the impulse to be conducted back to the ventricles through the AV node. Note that delta waves are present only during normal sinus rhythm but not during tachycardia. AV, atrioventricular; AVRT, atrioventricular reciprocating tachycardia.

Figure 20.19: Antidromic or Wide Complex AVRT. (A) A premature atrial complex (PAC) is conducted through the bypass tract but not through the AV node. (B) The QRS complex is wide because the ventricles are activated outside the normal conduction system. (C) The impulse is conducted retrogradely from ventricles to atria through the atrioventricular conduction system. The atria are activated retrogradely allowing the impulse to be conducted back to the bypass tract. AVRT, atrioventricular reciprocating tachycardia.

Wide Complex or Antidromic AVRT

·   Mechanism of wide complex AVRT: Antidromic or wide complex AVRT is triggered by a premature impulse originating from the atria or ventricles. The diagram illustrates how the tachycardia is initiated (Fig. 20.19).

o    The premature atrial impulse should be perfectly timed to occur when the bypass tract has fully recovered from the previous impulse while the AV node is still refractory. Because the bypass tract has a shorter refractory period, the premature atrial impulse will enter the bypass tract but is blocked at the AV node (Fig. 20.19A).

o    The atrial impulse activates the ventricles through the bypass tract (Fig. 20.19B). The impulse spreads from one ventricle to the other by muscle cell to muscle cell conduction, causing a wide QRS complex. The impulse is conducted retrogradely to the atria across the AV conduction system. The atria are activated retrogradely, thus completing the circuit. The atrial impulse can again reenter the bypass tract and the circuit starts all over again (Fig. 20.19C).

Conduction Pathways in Antidromic AVRT

·   Wide complex AVRT: There are two types of wide complex AVRT:

o    Ventriculoatrial conduction across the AV node: In wide complex AVRT, anterograde conduction of the atrial impulse to the ventricles occurs through the bypass tract and retrograde conduction of the impulse from ventricles to atria occurs through the AV node (Fig. 20.20A). This wide complex AVRT is called type I antidromic AVRT. This type of wide complex tachycardia may be terminated by vagal maneuvers and AV nodal blockers because the AV node is part of the reentrant circuit.

o    Ventriculoatrial conduction across another bypass tract: Retrograde conduction of the ventricular impulse to the atria may occur through a second bypass tract instead of the AV node, although this is extremely rare (Fig. 20.20B). This wide complex AVRT is called type II. Type II wide complex AVRT can not be terminated by vagal maneuvers or AV nodal blockers because the AV node is not part of the reentrant circuit. The ECG of type I and type II wide complex AVRT are identical showing wide QRS complexes.

·   Localizing the bypass tract during wide complex AVRT: The ventricular insertion of the bypass tract can be localized during a wide complex tachycardia.

o    Right bundle branch block configuration: If the wide complex AVRT has a right bundle branch block configuration (R waves are taller than S waves in V1), the bypass tract is left sided. During tachycardia, the left ventricle is activated earlier than the right ventricle. Thus, the impulse spreads from left ventricle to right ventricle causing a tall QRS complex in V1 (Fig. 20.21A).

o    Left bundle branch block configuration: If the wide complex AVRT has a left bundle branch block configuration (S waves are deeper than the R waves in V1), the bypass tract is right sided. During wide complex AVRT, the right ventricle is activated earlier that the left ventricle. Thus, the ventricular impulse spreads from right ventricle to left ventricle causing a negative complex in V1 (Fig. 20.21B).

·   Figure 20.22 is from a patient with right-sided bypass tract. During wide complex AVRT (Fig. 20.22B), the QRS complexes have a left bundle branch block configuration consistent with a right-sided bypass tract. During narrow complex AVRT (Fig. 20.22C,D), the retrograde P waves are upright in leads I and aVL, which is also consistent with a right-sided bypass tract. The location of the bypass tract during narrow complex AVRT matches the location of the bypass tract during wide complex AVRT and during normal sinus rhythm. If the location of the bypass tract during tachycardia and during normal sinus rhythm does not match, more than one bypass tract may be present.

·   Figures 20.22C,D are from the same patient as Figures 20.22A, B. Retrograde P waves (arrows) are upright in leads I and aVL during narrow complex AVRT consistent with right-sided bypass tract.

Figure 20.20: VA Conduction in Antidromic AVRT. (A) In type I antidromic AVRT, the atrial impulse enters the ventricles through the bypass tract and returns to the atria through the AV node. This type of antidromic AVRT can be terminated by AV nodal blockers. (B) In type II antidromic AVRT, the impulse enters the ventricles through the bypass tract and returns to the atria through a second bypass tract. This type of antidromic AVRT cannot be terminated by AV nodal blockers. Both wide complex tachycardia look identical and can be mistaken for ventricular tachycardia. AV, atrioventricular; VA, ventriculoatrial; AVRT, atrioventricular reciprocating tachycardia.

Figure 20.21: Localizing the Bypass Tract during Wide Complex AVRT. (A) When the bypass tract is left sided (bypass tract connects left atrium to left ventricle), tall R waves are recorded in V1 during wide complex tachycardia. Because the left ventricle is activated first, the impulse will travel from left ventricle to right ventricle toward V1. (B) If the bypass tract is right sided, the right ventricle is activated first and the impulse is conducted from right ventricle to left ventricle causing deep S waves in V1. AVRT, atrioventricular reciprocating tachycardia.

Antidromic or Wide Complex AVRT

·   Another example of wide complex AVRT is shown in Fig. 20.23. The QRS complexes are tall in V1 consistent with a left-sided bypass tract.

Wide Complex AVRT

·   Treatment: The reentrant pathway during wide complex AVRT generally involves the same structures as that during narrow complex AVRT. Thus, vagal maneuvers and AV nodal blockers are usually effective in terminating the tachycardia (Fig. 20.24A). Before AV nodal blocking agents are given, it should be ascertained that the wide complex tachycardia is not ventricular tachycardia because catastrophic results may occur if the tachycardia turns out to be ventricular rather than supraventricular. Furthermore, adenosine, which is a very effective agent in converting AVRT to normal sinus rhythm, can cause atrial fibrillation in up to 10% of patients. This may be catastrophic if the patient has preexcitation. Additionally, if the wide complex AVRT uses a second bypass tract for ventriculoatrial conduction (type II wide complex AVRT), AV nodal blockers will not be effective in terminating the tachycardia because the AV node is not part of the reentrant pathway. Thus, ibutilide, procainamide, or flecainide, which are capable of blocking the reentrant circuit at the level of the bypass tract (Fig. 20.24B), are the preferred agents according to the ACC/AHA/ESC guidelines in the management of patients with supraventricular arrhythmias.

ECG Findings of Antidromic or Wide Complex AVRT

·   The QRS complexes are wide measuring _120 milliseconds. The tachycardia is difficult to distinguish from ventricular tachycardia.

·   The tachycardia is very regular because the tachycardia uses a fixed reentrant circuit.

·   AV block is not possible because the atria and ventricles are part of the reentrant pathway.

·   Although retrograde P waves are present, similar to orthodromic AVRT, the P waves can not be identified because they are obscured by the ST segment.

Mechanism

·   AVRT is possible only when a bypass tract is present. For tachycardia to occur, the AV node and bypass tract should have different electrophysiologic properties. The tachycardia can be triggered by a premature atrial or ventricular impulse and can be narrow complex (orthodromic) or wide complex (antidromic).

o    Orthodromic or narrow complex AVRT: If the bypass tract has a longer refractory period than the AV node, a perfectly timed premature atrial impulse is blocked at the bypass tract, but is conducted to the AV node and His-Purkinje system, resulting in a narrow complex or orthodromic AVRT. Unlike the baseline ECG in which delta waves are present due to preexcitation, there are no delta waves during the tachycardia because the ventricles are activated exclusively from the AV node. This tachycardia was already discussed in Chapter 16, Supraventricular Tachycardia due to Reentry.

o    Antidromic or wide complex AVRT: If the AV node has a longer refractory period than the bypass tract, a premature atrial impulse can enter the bypass tract but not the AV node, resulting in wide complex or antidromic AVRT. In antidromic AVRT, the premature atrial impulse is conducted through the bypass tract and activates the ventricles by direct myocardial spread resulting in a wide QRS complex. The ventricular impulse is conducted retrogradely to the atria across the AV node and reenters the ventricles through the bypass tract. The reentrant tachycardia involves a large circuit consisting of the bypass tract, ventricles, bundle branches, bundle of His, AV node, and atria before circling back to the bypass tract to activate the ventricles. Because the ventricles are activated exclusively from the bypass tract, the whole QRS complex is not a fusion complex and is essentially a delta wave.

Figure 20.22: (A) Baseline Electrocardiogram (ECG) Showing Preexcitation. Delta waves with short PR intervals are present in leads I, aVL, V2, and V3 consistent with preexcitation. The QRS complex is negative in V1 with deep S waves consistent with a right sided bypass tract. (B) Wide Complex AVRT. The 12-lead ECG is from the same patient as (A). It shows a wide complex tachycardia with deep S wave in V1 suggesting that the bypass tract is right sided. This wide complex tachycardia can be mistaken for VT. (C) Narrow complex tachycardia. The ECG shows narrow complex AVRT. The frontal leads are magnified in (D) to show that the retrograde P waves (arrows) are upright in I and aVL consistent with a right-sided bypass tract.

 

Figure 20.22: (Continued) (D) Narrow complex AVRT. The ECG is from (C). Only the frontal leads are magnified to show that the P waves are upright in leads I and aVL during SVT. AVRT, atrioventricular reciprocating tachycardia; SVT, supraventricular tachycardia.

Clinical Significance

·   Narrow complex AVRT is the most common arrhythmia in patients with the WPW syndrome occurring in approximately 85% to 95% of patients who have symptoms of tachycardia. Wide complex AVRT is rare, occurring only in 5% to 10% of patients with WPW syndrome. Antidromic or wide complex AVRT is a classic example of wide complex tachycardia of supraventricular origin.

·   Wide complex AVRT is difficult to differentiate from ventricular tachycardia because both arrhythmias have wide QRS complexes. Ventricular tachycardia usually occurs in patients with history of myocardial infarction or left ventricular systolic dysfunction. Wide complex AVRT occurs in patients who are younger with known preexcitation and generally preserved left ventricular systolic function. The ECG algorithm for diagnosing wide complex tachycardia of ventricular origin is further discussed in Chapter 22, Wide Complex Tachycardia.

·   The ventricular insertion of the bypass tract can be localized during wide complex tachycardia. The bypass tract is left sided if the QRS complexes have a right bundle branch block configuration (R waves are taller than S waves in V1). If the QRS complexes have a left bundle branch block configuration (S waves are deeper than the height of the R waves in V1), the bypass tract is right sided.

·   Although it can be assumed that patients with preexcitation who develop narrow complex tachycardia have AVRT as the cause of the tachycardia, in more than 5% of patients with preexcitation, the narrow complex tachycardia is due to AV nodal reentrant tachycardia rather than AVRT. The exact mechanism of the tachycardia is important if radiofrequency ablation is being considered.

·   Patients with Ebstein anomaly may have more than one bypass tract. These patients may not respond to AV nodal blockers during wide complex AVRT because the AV node may not be part of the reentrant pathway. Similarly, ablation therapy may not be as effective because several bypass tracts may be present.

·   Wide or narrow complex AVRT is paroxysmal with abrupt onset and sudden termination. During tachycardia, prominent jugular venous pulsations from cannon A waves are usually seen in the neck. These jugular pulsations are due to synchronous contraction of both atria and ventricles.

Treatment

·   Wide complex tachycardia of uncertain diagnosis: Wide complex AVRT may be difficult to differentiate from ventricular tachycardia. If the diagnosis of the wide complex tachycardia is uncertain and there is possibility that the tachycardia is ventricular rather than supraventricular, AV nodal blockers, especially verapamil, should be avoided. Verapamil is negatively inotropic and a potent vasodilator. If verapamil is inadvertently given to a patient with ventricular tachycardia, the patient may become hemodynamically unstable because most patients with ventricular tachycardia have left ventricular systolic dysfunction. Additionally, AV nodal blockers should not be given if there is irregularity in the R-R interval, which may indicate atrial fibrillation with preexcitation. Finally, patients with preexcitation who develop wide complex tachycardia may not be due to AVRT but may be due to focal atrial tachycardia or atrial flutter conducting across a bypass tract. This type of wide complex tachycardia will not respond to AV nodal blockers. Agents that will slow conduction across the bypass tract such as ibutilide, procainamide, or flecainide given intravenously are preferred agents according to the ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias.

Figure 20.23: (A) Antidromic or Wide Complex AVRT. The 12-lead ECG shows a wide complex tachycardia from antidromic AVRT. The QRS complexes show tall R waves in V1 consistent with a left-sided bypass tract. The tachycardia can be mistaken for ventricular tachycardia. (B) After Conversion to Normal Sinus Rhythm. The 12-lead ECG is from the same patient as (A). The rhythm is normal sinus. There are multiple leads showing short PR interval and delta waves (arrows) consistent with ventricular preexcitation. Negative delta waves are present in III and aVF with tall R waves in V1 consistent with a left-sided posteroseptal bypass tract. The location of the bypass tract during wide complex AVRT matches that during normal sinus rhythm. AVRT, atrioventricular reciprocating tachycardia; ECG, electrocardiogram.

 

Figure 20.24: Effect of AV Nodal Blockers in Wide Complex AVRT. If the retrograde pathway involves the AV node as shown in(A), vagal maneuvers and AV nodal blockers will be effective in terminating the tachycardia. However, if the AV node is not part of the reentrant pathway (B), AV nodal blockers will not be effective in terminating the tachycardia. Antiarrhythmic agents that can block the impulse at the bypass tract are the preferred agents for terminating the tachycardia. The asterisks indicate that the drugs are available as intravenous preparations. VA, ventriculoatrial; AV, atrioventricular.

·   Wide complex AVRT: Wide complex AVRT can be terminated by slowing conduction across the AV node or bypass tract. The most vulnerable arm of the tachycardia circuit is the AV node, which can be inhibited with vagotonic maneuvers such as Valsalva, carotid sinus pressure, immersion of the face in cold water (diving reflex), gagging, coughing, or straining. If vagotonic maneuvers are not effective, pharmacologic therapy should be considered among stable patients and electrical cardioversion among patients who are not stable. Electrical cardioversion is also an option even among stable patients, especially if the etiology or mechanism of the wide complex tachycardia is uncertain.

o    Pharmacologic agents: AV nodal blockers and antiarrhythmic agents that inhibit conduction across the bypass tract are both effective in terminating wide complex AVRT.

§  Adenosine: Although adenosine is effective in terminating AVRT, it is not the best agent when there is wide complex AVRT for the following reasons:

§  Adenosine can cause atrial fibrillation in up to 10% of patients, which may be catastrophic in patients with preexcitation. Thus, resuscitative equipment should be available if adenosine is being given to a patient with known WPW syndrome.

§  There is a subset of antidromic AVRT in which AV conduction of the impulse occurs through one bypass tract and ventriculoatrial conduction occurs through another bypass tract. AV nodal blockers such as adenosine will not be effective because this type of AVRT does not use the AV node as part of the reentrant circuit.

§  Finally, there are other supraventricular arrhythmias such as focal atrial tachycardia and atrial flutter that can result in wide complex tachycardia when a bypass tract is present. These arrhythmias will conduct to the ventricles across the bypass tract and will not respond to adenosine because the AV node is not involved with the tachycardia. Thus, antiarrhythmic agents that can slow the impulse at the bypass tract are preferred agents.

§  Antiarrhythmic agents: According to the ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias, antiarrhythmic agents that block the bypass tract are more effective and are preferred in the acute treatment of wide complex AVRT. This includes procainamide, ibutilide, or flecainide. Flecainide is not available intravenously in the United States.

§  Procainamide: Procainamide is the drug of choice and is given intravenously to a total dose of 10 to 12 mg/kg, not to exceed 1,000 mg. The dose is given within 30 minutes at the rate of 100 mg every 2 to 3 minutes followed by a maintenance infusion of 1 to 4 mg/minute.

§  Ibutilide: One mg is given intravenously over 10 minutes. The 10-mL solution can be injected slowly IV or diluted with D5W to a total volume of 100 mL and infused over 10 minutes. If the wide complex AVRT has not converted to normal sinus rhythm after 10 minutes, the same dose is repeated. Experience with ibutilide is not as extensive as that with procainamide although the drug may be as effective.

§  Other antiarrhythmic agents: Other Class IA (quinidine and disopyramide) IC (propafenone) and Class III agents (sotalol) are not available as intravenous preparations, but are effective for long-term therapy by inhibiting the bypass tract. These agents are negatively inotropic and should not be given when there is left ventricular dysfunction or heart failure. If the patient has left ventricular systolic dysfunction, amiodarone is the preferred agent. Amiodarone, however, has not been shown to be more effective than other agents and has several long-term toxic effects and is reserved in the treatment of patients with structural cardiac disease.

o    Electrical cardioversion: Electrical cardioversion is reserved for patients who are hemodynamically unstable with hypotension, congestive heart failure, or with symptoms of ischemia from tachycardia. It is also an initial option to patients who are hemodynamically stable. It should also be considered if the patient does not respond to initial pharmacologic therapy or when the diagnosis of the wide complex tachycardia remains uncertain. In stable patients, a low energy setting is generally adequate in terminating the tachycardia (50 joules).

o    Intracardiac pacing: The tachycardia can also be terminated by a perfectly timed premature atrial complex or premature ventricular complex because the atria and ventricles are part of the reentrant circuit. Before the era of radiofrequency ablation, insertion of permanent pacemakers with antitachycardia properties has been used in the treatment of both antidromic and orthodromic AVRT. The device can detect the tachycardia and paces the atria or ventricles to interrupt the arrhythmia.

o    Radiofrequency ablation: Radiofrequency ablation of the bypass tract using catheter techniques is now the preferred therapy and receives a Class I recommendation in symptomatic patients with preexcitation especially in younger individuals to obviate the need for long-term antiarrhythmic therapy. The procedure is usually very effective with more than 95% chance of cure. If radiofrequency ablation is not technically feasible, ablation surgery should be considered.

Prognosis

·   Patients with preexcitation who develop symptoms from tachycardia, overall prognosis remains good. These patients should be referred to an electrophysiologist for further evaluation with a chance for complete cure.

Atrial Fibrillation

·   Atrial fibrillation is one of the most dreadful arrhythmias associated with WPW syndrome. This arrhythmia has the potential of degenerating to ventricular fibrillation, which can result in sudden cardiac death. The ECG findings of atrial fibrillation in the presence of preexcitation are:

o    Irregularly irregular R-R intervals.

o    Varying morphologies of the QRS complexes.

o    The ventricular rate is usually rapid.

·   During atrial fibrillation, the atrial impulses can reach the ventricles through both AV node and bypass tract resulting in varying degrees of ventricular fusion. Because the bypass tract consists of ordinary myocardium, it can allow atrial complexes to enter the ventricles resulting in very rapid ventricular rates (Fig. 20.25).

·   Atrial fibrillation degenerating to ventricular fibrillation is rare, even among symptomatic patients with WPW syndrome. Atrial fibrillation however carries the potential for sudden death. Patients with WPW syndrome with bypass tracts that are capable of conducting at rates >240 beats per minute (R-R interval between two preexcited complexes ≤250 milliseconds or ≤6 small blocks) are at risk for sudden death as shown in Figures 20.25 and 20.26.

Atrial Fibrillation in Patients with WPW Syndrome

·   Treatment: The standard treatment of atrial fibrillation is to slow the ventricular rate with AV nodal blocking agents such as calcium channel blockers, beta blockers, and digoxin. In patients with preexcitation, the use of these agents is not only contraindicated, but also may be catastrophic. AV nodal blockers slow down conduction and decrease the number of impulses entering the ventricles anterogradely through the AV node. This will reduce the number of impulses bombarding the ventricular end of the bypass tract, rendering the bypass tract less refractory (Fig. 20.27). Calcium channel blockers can also cause peripheral vasodilatation, which may result in reflex increase in sympathetic tone. This may increase conduction through the bypass tract. The use of digitalis is particularly dangerous because digitalis does not only block the AV node, but also enhances conduction through the bypass tract.

·   Electrical cardioversion is the treatment of choice in patients with atrial fibrillation who are unstable. In stable patients, procainamide is the pharmacologic agent of choice. Ibutilide, amiodarone, propafenone, and sotalol are also effective. These agents can slow the ventricular rate but can also convert atrial fibrillation to sinus rhythm.

Atrial Fibrillation and WPW Syndrome

ECG Findings of Atrial Fibrillation and WPW Syndrome

·   The R-R intervals are irregularly irregular.

·   The ventricular rate is unusually rapid.

·   The QRS complexes have different configurations, some narrow, some wide, and others in between.

Figure 20.25: Atrial Fibrillation and the WPW Syndrome. In patients with WPW syndrome with atrial fibrillation, atrial impulses can enter the ventricles through both bypass tract and AV node. Note that in the middle of the rhythm strip, narrow QRS complexes are present (bracket). These impulses are conducted through the AV node. The wide QRS complexes (arrows) are preexcited and are conducted through the bypass tract. Some QRS complexes are fusion complexes due to activation of the ventricles from both bypass tract and AV node. The R-R interval between two wide QRS complexes measure <250 milliseconds (distance between the two arrows) making the patient high risk for ventricular fibrillation.

Mechanism

·   When atrial fibrillation occurs in a patient without a bypass tract, atrial impulses can reach the ventricles only through the AV node because this is the only pathway that connects the atria to the ventricles. Accordingly, the ventricular rate is usually controlled because the capacity of the AV node to transmit atrial fibrillatory impulses to the ventricles is limited.

·   When atrial fibrillation occurs in a patient with WPW syndrome, the bypass tract serves as a second pathway, in addition to the AV node, for atrial impulses to reach the ventricles. Because the bypass tract consists of ordinary myocardium, it is capable of conducting atrial impulses more rapidly to the ventricles than the AV node, resulting in very rapid ventricular rates, which can degenerate to ventricular fibrillation and sudden death.

·   The QRS complexes have varying configurations because two separate pathways are involved in conducting atrial impulses to the ventricles. Wide QRS complexes occur when atrial impulses are conducted through the bypass tract and narrow complexes are present when the AV node and conduction system transmit atrial impulses to the ventricles. In addition, fusion complexes of varying configurations are present when the AV node and bypass tract simultaneously contribute to ventricular activation.

Clinical Implications

·   Atrial fibrillation is the most serious arrhythmia associated with WPW syndrome. The arrhythmia can result in very rapid ventricular responses, which can lead to hypotension, diminished coronary perfusion, and ventricular fibrillation. This may cause sudden death even in healthy individuals.

·   Approximately 30% to 40% of patients with preexcitation with symptoms of tachycardia will develop atrial fibrillation. The presence of AVRT increases the incidence or predisposition to develop atrial fibrillation, which (in the presence of preexcitation) may degenerate to ventricular fibrillation. Conversely, in patients with AVRT, successful ablation of the accessory pathway will diminish the incidence of atrial fibrillation.

·   It is possible that completely asymptomatic patients with preexcitation may suddenly develop atrial fibrillation as the initial symptom degenerating to ventricular fibrillation, although this is exceedingly rare. Electrophysiologic testing in patients who are asymptomatic is not necessary, as previously discussed.

·   Patients with preexcitation who are symptomatic have a higher chance of developing atrial fibrillation, although the chance that the atrial fibrillation can degenerate to ventricular fibrillation is also rare. Patients with preexcitation who are symptomatic should be risk stratified so that those who are high risk for cardiac sudden death can be identified.

o    The following markers suggest that the patient is low risk for sudden death.

§  Patients with preexcitation in the resting ECG, but are completely asymptomatic.

§  The preexcitation is noted only intermittently during routine ECG.

§  There is immediate disappearance of preexcitation during stress testing.

§  The delta waves disappear when procainamide is given intravenously.

o    The following are markers of a high-risk patient. These observations suggest that the bypass tract has a short refractory period and is capable of conducting atrial impulses rapidly.

§  The delta wave persists during stress testing.

§  The refractory period of the bypass tract is short measuring ≤250 milliseconds between preexcited complexes. This can be measured during spontaneously occurring atrial fibrillation or it can be induced in the electrophysiology lab during electrophysiologic testing.

§  History of cardiac arrest from ventricular fibrillation.

§  Presence of multiple accessory pathways.

§  Presence of Ebstein anomaly.

Figure 20.26: Atrial Fibrillation and WPW Syndrome. ECG (A) shows atrial fibrillation in a patient with known WPW syndrome. Note the irregularly irregular R-R intervals and the presence of bizarre QRS complexes of varying morphologies. The R-R interval between both preexcited complexes measures ≤250 milliseconds, making patient high risk for ventricular fibrillation. (B) From the same patient upon conversion to normal sinus rhythm. ECG (B) shows preexcitation. The patient underwent successful ablation of a left-sided posteroseptal bypass tract. ECG, electrocardiogram; WPW, Wolff-Parkinson-White.

Figure 20.27: Atrial Fibrillation and the WPW Syndrome. (A) During atrial fibrillation, atrial impulses can enter the ventricles through the AV node and bypass tract. Atrial impulses entering the AV node can activate the ventricles and at the same time depolarize the ventricular end of the bypass tract retrogradely (arrows). This can render the bypass tract refractory, thus slowing down the number of atrial impulses entering the ventricles through the bypass tract. (B) When AV nodal agents are given, the number of atrial impulses entering the AV node is decreased. This will also decrease the number of impulses depolarizing the ventricular end of the bypass tract. Because there is less inhibition of the ventricular end of the bypass tract, the bypass tract is less refractory and will allow more atrial impulses to enter the ventricles through the bypass tract anterogradely. AV, atrioventricular; WPW, Wolff-Parkinson-White.

Treatment

·   Treatment of atrial fibrillation in patients with WPW syndrome associated with wide QRS complexes includes direct current cardioversion, use of antiarrhythmic agents, and radiofrequency ablation.

·   Direct current cardioversion: In hemodynamically unstable patients associated with rapid ventricular rates, direct current cardioversion receives a Class I recommendation. It carries a Class II a recommendation among patients who are stable according to the 2006 ACC/AHA/ESC guidelines in the management of patients with atrial fibrillation.

·   Antiarrhythmic agents: In patients with atrial fibrillation who are not hemodynamically unstable and do not need to be cardioverted, pharmacologic agents that block the bypass tract can be given as initial therapy.

o    Procainamide: Procainamide is the drug of choice and is given intravenously at a dose of 10 to 12 mg/kg within 30 minutes at the rate of 100 mg every 2 to 3 minutes, not to exceed 1,000 mg. This is followed by a maintenance infusion of 1 to 4 mg/minute. This is effective not only in slowing the ventricular rate, but also in converting atrial fibrillation to normal sinus rhythm in more than 50% of patients with atrial fibrillation. This drug carries a Class I indication according to the 2006 ACC/AHA/ESC practice guidelines.

o    Ibutilide: One mg of ibutilide is given IV slowly over 10 minutes and repeated if needed after an interval of 10 minutes. Ibutilide can block both bypass tract and AV node. This is effective in converting atrial fibrillation to normal sinus rhythm and also carries a Class I recommendation.

o    Flecainide: Intravenous flecainide receives a Class IIa recommendation in stable patients with atrial fibrillation with rapid ventricular rates with wide QRS complexes. The intravenous dose is 1.5 to 3.0 mg/kg over 10 to 20 minutes. This agent is not available intravenously in the United States.

o    Other antiarrhythmic agents: Amiodarone, quinidine, and disopyramide can also inhibit the bypass tract and carry a Class IIb recommendation. Only amiodarone is available intravenously. The other agents are not available as IV preparations in the United States.

·   In patients with preexcitation, AV nodal blocking agents are contraindicated and may be fatal when there is atrial fibrillation. AV nodal blocking agents decrease the number of impulses entering the ventricles through the AV node, making the bypass tract less refractory. It can also enhance conduction across the bypass tract. This will allow more fibrillatory impulses to pass through the bypass tract from atrium to ventricle, thus increasing the ventricular rate during atrial fibrillation. Digoxin is particularly a dangerous pharmacologic agent to use in patients with WPW syndrome with atrial fibrillation. Digoxin not only blocks the AV node, but also enhances conduction through the bypass tract, further increasing the ventricular rate during atrial fibrillation. Verapamil also inhibits the AV node and is a potent vasodilator. It may enhance conduction through the bypass tract by reflex increase in sympathetic tone. These agents receive a Class III recommendation.

·   In patients with concealed bypass tracts (no evidence of preexcitation in baseline ECG) who develop atrial fibrillation, the treatment of atrial fibrillation is similar to a patient without a bypass tract. AV nodal blocking agents such as beta blockers, calcium channel blockers, and digitalis can be given safely in controlling the ventricular rate during atrial fibrillation. The use of digitalis as long-term maintenance therapy, however, should be discouraged unless other AV nodal blocking agents are ineffective or are poorly tolerated.

·   Some patients may be mistakenly identified as having concealed bypass tracts because they do not manifest any evidence of preexcitation in baseline ECG. These patients may not have any preexcitation because the bypass tract is not given the chance to become manifest—either from its distal location from the sinus node (left-sided bypass tracts) or efficient conduction of the sinus impulse across the AV node. Anterograde conduction of the atrial impulse to the ventricles may occur during atrial fibrillation. These patients are difficult to identify unless electrophysiologic testing is performed.

Figure 20.28: Other Causes of Preexcitation. (A) Preexcitation with a bypass tract connecting the atrium directly to the ventricles. This is associated with the classic ECG of WPW syndrome. (B) Mahaim fibers connecting the AV node directly to the ventricle (nodo-ventricular fiber), bundle of His directly to ventricle (Hisioventricular fiber) and bundle branches or fascicles directly to the ventricles (fasciculoventricular fiber). (C) A bypass tract connecting the atrium directly to the bundle of His. This is often associated with a Hisioventricular fiber resulting in a pattern similar to the WPW ECG (A). (D) A small AV node resulting in a short PR interval and a normal QRS complex. ECG, electrocardiogram; WPW, Wolff-Parkinson-White.

Prognosis

·   Prognosis is good even among patients with history of atrial fibrillation because electrical ablation is curative. If radiofrequency ablation is not feasible, surgical ablation should be considered.

Other Causes of Ventricular Preexcitation

·   Ventricular preexcitation may be due to pathways other than direct connection between the atrium and the ventricle. The following summarizes the different pathways that can cause preexcitation.

o    Bundle of Kent: The bypass tract connects the atrium directly to the ventricle (Fig. 20.28A). This is the most common cause of preexcitation.

o    Mahaim fibers: Mahaim fibers may have different connections:

§  Nodoventricular connection: A bypass tract connecting the AV node directly to the ventricle (Fig. 20.28B).

§  Hisioventricular connection: A bypass tract connecting the His bundle directly to the ventricle (Fig. 20.28B,C).

§  Fasciculoventricular connection: A bypass tract connecting the right bundle, left bundle, or fascicles directly to the ventricles (Fig. 20.28B)

§  Atrio-Hisian connection: Connects the atria directly to the His bundle, thus bypassing the AV node (Fig. 20.28C).

o    Superconducting AV node: Small AV node resulting in a short PR interval with normal QRS complex (Fig. 20.28D).

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