Figure 4.1.1

Questions

1. What is the rhythm?

2. Where is the accessory pathway located?

Discussion, Interpretation, and Answers

This ECG demonstrates a rhythm with normal narrow QRS morphology except the last QRS complex, which reveals preexcitation (Figure 4.1.2, asterisk). The preexcited complex has R>S in lead V₁ that localizes the accessory pathway on the free wall of the left atrioventricular annulus. The strongly positive delta wave in inferior leads (lead II, asterisk) makes a posterior location unlikely, suggesting a left lateral accessory pathway.¹ The reason for the accelerated junctional rhythm in this patient is unclear, but healthy young patients can have a robust junctional rhythm and also have marked variability in the sinus rate. An ECG during sinus rhythm at a slightly different time (Figure 4.1.3) shows consistent ventricular preexcitation over a left anterolateral accessory pathway.¹

Figure 4.1.2

Figure 4.1.3

Figure 4.1.2 begins with sinus P waves (black arrows). However, there are dissociated faster narrow QRS complexes reflecting an accelerated junctional rhythm (blue arrows). Activation originates from the AV node and directly proceeds to the His-Purkinje system without encountering the AV accessory pathway; therefore, the QRS complexes are normal without evidence of preexcitation. During this period of slowing of the spontaneous sinus node depolarizations and junctional escape rhythm, the P waves are hidden within the QRS complexes, and the atria are activated either from an isorhythmic sinus rhythm or retrogradely from the junctional rhythm.

Toward the end of the tracing, as the sinus rate accelerates, the sinus P waves are again seen ahead of the QRS complexes (black arrows). It is not until the last beat on the tracing that the P wave is well ahead of the expected junctional complex (red arrow) for antegrade conduction over the left sided accessory pathway to manifest in the form of preexcitation.

Preexcitation due to an AV accessory pathway is a variable fusion between ventricular excitation over the accessory pathway and the normal conduction system. Absence of preexcitation with junctional complexes confirms that the accessory pathway inserts to the atrium and ventricle across the atrioventricular annulus without involvement of the AV node or His-fascicular system. In contrast, a junctional rhythm in the presence of a fasciculoventricular pathway will continue to demonstrate delta waves. In fact, the degree of preexcitation in the fasciculoventricular tract is fixed.

Reference

1. Arruda MS, McClelland JH, Wang X, et al. Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolff-Parkinson-White syndrome. J. Cardiovasc. Electrophysiol. 1998;9(1):2–12.

Patient History

Twelve-lead electrocardiogram (ECG) recordings during electrophysiology studies in an 18-year-old female referred for evaluation of rapid palpitations.

Figure 4.2.1 Upper panel—Spontaneous ECG recording: a stable sinus rhythm (94/min) with normal PR (0.12 seconds) and normal QRS complexes is followed by an escape rhythm consisting of seven wide QRS complexes with a left bundle branch block (LBBB)-left axis pattern at a rate of 77/min. Note a fusion beat (*) on the next QRS complex before stable sinus rhythm (86/min) resumes. Lower panel—Fifteen seconds after intravenous administration of 10 mg adenosine triphosphate: after a short sinus rate slowing to 56/min, sinus rate increases and a succession of eight wide QRS conducted beats (94/min) is observed. The morphology of these wide QRS complexes is identical to the escape beats observed in the upper panel. Note the longer PR interval (150 ms) preceding the wide QRS complexes. Also note a fusion beat (*) on the next complexes before sinus rhythm with normal PR interval and QRS complexes resumes. Reproduced with permission from John Wiley and Sons; Belhassen B, Ilan M, Glick A. Wide QRS rhythm in a young woman with recurrent palpitations: What is the diagnosis? J Cardiovasc Electrophysiol. 2003;14:1376–1378.

Discussion

This patient showed the presence of an atrio-fascicular pathway with long conduction time (so-called Mahaim fiber) and attributed the LBBB-QRS complexes to antegradely preexcited beats (lower panel). An accessory pathway potential was found at the posterolateral area of the tricuspid annulus between A and V in sinus rhythm and preceding the QRS complexes during the escape beat. Therefore, the wide QRS complex escapes in the upper panel were actually an escape rhythm originating from the Mahaim fiber. The pathway was successfully ablated with radiofrequency ablation and the escape rhythm did not recur.

Patient History

A 28-year-old male with recurrent palpitations and ventricular preexcitation.

Figure 4.3.1

Discussion

Electrophysiology testing demonstrated a baseline HV interval of 20 ms. Bypass tract conduction was anterograde only, and the pattern of preexcitation did not change with incremental atrial pacing, the delivery of atrial premature beats, or with spontaneous junctional beats. These observations, as well as the morphology of preexcitation, are consistent with a fasciculoventricular pathway, which was incidental. His palpitations were secondary to AV nodal tachycardia, which was treated with slow pathway modification.

Patient History

A 30-year-old female patient complaining of recurrent attacks of rapid palpitations. Her basic ECG showed no evidence of manifest preexcitation, while her ECG during tachycardia is shown in Figure 4.4.1. She was admitted to the cardiac electrophysiology laboratory for diagnosis and ablation of her tachycardia.

Figure 4.4.1 Surface ECG during tachycardia. Twelve-lead ECG of the patient during tachycardia at a rate of 210 bpm showing wide complex tachycardia having RBBB morphology. Though it has a monophasic R in V₁, yet the terminal delay typical of RBBB is not evident.

From the beginning of the procedure, the tachycardia was incessant, and proved to be AVNRT, for which the slow pathway was successfully ablated. ECG after ablation of the slow pathway intermittently showed the following (Figure 4.4.2):

Figure 4.4.2 Surface ECG after slow pathway ablation. After slow pathway ablation, there was intermittent development of RBBB morphology. Atrial pacing reproduces the same morphology as that which occurs spontaneously. As shown with atrial pacing, the surface ECG shows RBBB morphology that returns to normal with cessation of pacing.

Questions

1. What does the ECG intermittently show?

2. What does this tracing suggest?

Answers

1. Intermittent conduction over a bystander pathway antegradely conducting with atriofascicular accessory pathway decremental properties, resulting in RBBB-like morphology.

2. This tracing differs from the regular Mahaim fibers in the site of insertion, which is probably in the proximal left bundle.

Discussion and Interpretation

The intracardiac recording excludes actual right bundle branch block (RBBB), which has a relatively long HV interval, with antegrade activation of the His. The presence of prolonged AH with short HV, and distal to proximal activation of the His with a wide complex morphology with ventriculoatrial dissociation, indicates an antegradely conducting accessory pathway with decremental conduction properties. Interestingly, the common insertion site of Mahaim fibers produces a left bundle branch block (LBBB) morphology with delayed transition to after V₄. Thus, the apical activation precedes the basal, and distal to proximal activation of the His. In this case, it seems that the bystander pathway passing the His bundle is inserted in the conduction system on the left side rather than the right, probably at the proximal left bundle. This is because the basal right ventricle is still activated early, and the cause for terminal delay is due to activation of the lateral left ventricle (LV). However, there was no LV catheter inserted to confirm the later finding. Latent left-sided decremental atriofascicular accessory pathway has been previously described, but contrary to our case, it was involved in the tachycardia.¹

Figure 4.4.3 Intracardiac recordings after ablation. Surface ECG and intracardiac recording after ablation, where the ablation catheter (MAP) is placed in the high right atrium (HRA). After the second beat, there is an atrial premature contraction (earliest in the MAP/HRA catheter) that was non-conducted. This is followed by a normally conducted beat, with incomplete RBBB. The following beat is aberrantly conducted with RBBB pattern on the surface ECG. At the HBE, the AH/AV is prolonged, and HV shortens with the distal His preceding the proximal His, which disappears or is delayed just before the V. Note that despite the RBBB morphology, the LV (in distal CS) lead still appears more delayed than the RV (see text for explanation).

Figure 4.4.4 Intracardiac recording during change from narrow to wide complex. Surface ECG and intracardiac recording after ablation, where the ablation catheter (MAP) is placed in the high right atrium (HRA). The first two beats are narrow, while the following two beats are wide with RBBB morphology. The patient has sinus tachycardia and similar P wave on surface ECG (upright in I and aVF) and the earliest atrial activation in the MAPp (H/LRA). There is autonomic modulation of the sinus rate with gradual increase in HR over the four beats (520/500/495/490 ms). The first beat is normally conducted with normal AH/HV and proximal to distal activation of the His. In the second beat with slight acceleration of the sinus rate, there is more AH prolongation, and is still proximal to distal activation of the His; however, the HBEd shows double H activation, indicating intra-Hisian conduction delay. This is followed by conduction over the atriofasicular pathway in the third and fourth beat, with AH prolongation, HV shortening, and distal-to-proximal activation of the His.

Reference

1 Goldberger JJ, Pederson DN, Damle RS, et al. Antidromic tachycardia utilizing decremental, latent accessory atrioventricular fibers: Differentiation from adenosine-sensitive ventricular tachycardia. J. Am. Coll. Cardiol. 1994;24(3):732–738.

Patient History

A 55-year-old female had brief episodes of tachycardia for many years. Her baseline ECG was normal. However, a prolonged episode allowed her to arrive in the emergency department where a 12-lead ECG was recorded (Figure 4.5.1 and Figure 4.5.2).

Question 1

What is the tachycardia mechanism?

Figure 4.5.1

Figure 4.5.2

Answer 1

This is a regular 170 bpm tachycardia with wide QRS and typical left bundle branch block (LBBB) morphology. P waves can be seen in V₁ as notches at the T-wave onset, 130 ms after the QRS onset (Figure 4.5.2). This can be a ventricular tachycardia with 1/1 retrograde conduction, or a supraventricular tachycardia with a functional LBBB, as sinus rhythm ECG was always normal. The markedly superior axis and late transition is also compatible with an atriofascicular tachycardia. The tachycardia was abruptly interrupted by IV adenosine (Figure 4.5.3).

Figure 4.5.3

Question 2

What is the tachycardia mechanism?

Answer 2

VT interruption by adenosine is unusual, but adenosine may interrupt a triggered focus, usually found in the ventricle from the outflow tract, which is not suggested by the frontal plane QRS orientation. As the adenosine blocks the AV node, a reentrant tachycardia using the AV node should be suspected.

Fortunately, tachycardia resumed later and was recorded by the monitoring system (Figure 4.5.4).

Figure 4.5.4

Question 3

What is the mechanism?

Answer 3

The tachycardia is triggered by an atrial extrasystole. It is followed by an AV prolongation and a LBBB QRS. Retrograde P wave can be seen in the V₁ precordial lead, after a long ventriculoatrial conduction time, suggesting an accessory pathway.

A later EP study confirmed a posteroseptal accessory pathway with predominant retrograde conduction. Reinspection of Figure 4.5.4 shows evidence of antegrade preexcitation just after the adenosine interrupted tachycardia.

Comment: The identification of a tachycardia is easier when a 12-lead ECG can record its onset and its interruption.

References

1. Coumel P, Attuel P. Reciprocating tachycardia in overt and latent preexcitation. Influence of functional bundle branch block on the rate of the tachycardia. Eur. J. Cardiol. 1974;1(4):423–436.

2 Sung RJ, Castellanos A, Gelband H, et al. Mechanism of reciprocating tachycardia initiated during sinus rhythm in concealed Wolff-Parkinson-White syndrome: Report of a case. Circulation. 1976;54(2):338–344.

Patient History

A 36-year-old female presented for treatment of daily palpitations and syncope. Her baseline ECG is shown in Figure 4.6.1. Where is the pathway located, and what is the likely successful site of ablation?

Figure 4.6.1 Baseline electrocardiogram.

Discussion

The baseline ECG reveals the presence of preexcitation with a negative delta wave in leads V₁, V₃–V₆, as well as leads I, III, and aVF. There is a positive delta wave in leads V₂ and I. The negative component of the delta wave in lead II (Figure 4.6.2, green arrow) and the positive component in V₂ (Figure 4.6.2, green arrow) is consistent with an inferior paraseptal epicardial accessory pathway, likely from the coronary sinus.¹ A unique feature of this ECG is the negative component of the delta wave in leads V₅–V₆ (Figure 4.6.2, red arrow), although in some beats there is a small r wave in lead V₆. This suggests that the pathway has an apical ventricular insertion as opposed to a typical basal ventricular insertion of the accessory pathway.

Figure 4.6.2 Baseline electrocardiogram analysis.

A subsequent electrophysiology study mapped the earliest Kent potential (Kp), localizing the pathway location to the basal inferior paraseptal location 5 mm inside the coronary sinus; Figure 4.6.3 shows the Kp during 2:1 retrograde ventriculoatrial block in the accessory pathway and Figure 4.6.4 shows the retrograde Kp after induction of orthodromic atrioventricular reentrant tachycardia with ventricular programmed stimulation at an interval of 600/350 ms. Mapping within the middle cardiac vein from an apical to a basal location failed to identify a Kp. Ablation at the Kp within the coronary sinus eliminated both anterograde and retrograde pathway conduction (Figure 4.6.5). The unique negative delta wave in leads V₅–V₆ is consistent with the accessory pathway insertion into an apical ventricular location. The proximal portion of the accessory pathway was successfully mapped to the proximal coronary sinus. The work of Sun et al. has shown that posteroseptal accessory pathways contain muscle sleeves that course within the cardiac veins.² In this patient, the ventricular insertion of the accessory pathway produces a QRS morphology consistent with a ventricular tachycardia exiting from the apical crux.³

Figure 4.6.3 Intracardiac electrograms with Kent potential during ventricular pacing.

Figure 4.6.4 Intracardiac electrograms with Kent potential during supraventricular tachycardia.

Figure 4.6.5 Right anterior oblique and left anterior oblique views of accessory pathway location.

This pathway most likely coursed from the atrium through the coronary sinus en route to the apical ventricular crux. If this pathway could not be localized with endocardial mapping, epicardial mapping and ablation has been reported to eliminate epicardial pathway conduction successfully.^4–6

Ventricular pacing from the right ventricular outflow tract was associated with 2:1 retrograde block (cycle length 580 ms). The green arrow identifies the Kent potential mapped to a location 5 mm within the coronary sinus. CS 17,18 was located at the coronary sinus ostium. The coronary sinus catheter is a 20 pole catheter with 2-mm spacing. The RVa catheter was in the right ventricular outflow tract.

Orthodromic atrioventricular reentrant tachycardia induced with ventricular programmed extrastimulus testing at interval of 600/350 ms. The green arrow identifies the Kent potential mapped to a location 5 mm within the coronary sinus. CS 17,18 was located at the coronary sinus ostium. The coronary sinus catheter is a 20-pole catheter with 2-mm spacing. The RVa catheter was in the right ventricular apex.

Kent potential at the site of successful ablation was mapped to a location 5 mm within the coronary sinus (in the left anterior oblique [LAO] view) and the anterior aspect of the coronary sinus (in the right anterior oblique [RAO] view).

References

1. Arruda MS, McClelland JH, Wang X, et al. Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolff-Parkinson-White syndrome. J. Cardiovasc. Electrophysiol. 1998;9:2–12.

2. Sun Y, Arruda M, Otomo K, et al. Coronary sinus-ventricular accessory connections producing posteroseptal and left posterior accessory pathways: Incidence and electrophysiological identification. Circulation. 2002;106:1362–1367.

3. Kawamura M, Gerstenfeld EP, Vedantham V, et al. Idiopathic ventricular arrhythmia originating from the cardiac crux or inferior septum: Epicardial idiopathic ventricular arrhythmia. Circ. Arrhythm. Electrophysiol. 2014;7: 1152–1158.

4. de Paola AA, Leite LR, Mesas CE. Nonsurgical transthoracic epicardial ablation for the treatment of a resistant posteroseptal accessory pathway. Pacing Clin. Electrophysiol. 2004;27:259–261.

5. Sapp J, Soejima K, Couper GS, et al. Electrophysiology and anatomic characterization of an epicardial accessory pathway. J. Cardiovasc. Electrophysiol. 2001;12:1411–1414.

6. Scanavacca MI, Sternick EB, Pisani C, et al. Accessory atrioventricular pathways refractory to catheter ablation: Role of percutaneous epicardial approach. Circ. Arrhythm. Electrophysiol. 2015;8:128–136.

Patient History

An 18-year-old male, without medical history, was admitted to the intensive care unit for aborted sudden cardiac death after a night of binge drinking and cannabis use. The initial cardiac rhythm was ventricular fibrillation, and five shocks were later delivered by an automated external defibrillator. Blood alcohol level was 1.8 g/L. Coronary angiography was normal.

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