Figure 2.1.1

Figure 2.1.2

Discussion, Interpretation, and Answer

Levo-looping of the embryonic bulboventricle from the developing heart tube results in morphologic ventricular inversion—morphologic right ventricle positioned on the left side and the morphologic left ventricle and the left bundle branches on the right. L-looping frequently occurs with double switch—atrioventricular and ventriculoarterial—in context of normally positioned atria (situs solitus) and transposition of great arteries, and is often referred to as CC-TGA. CC-TGA can be associated with membranous ventricular septal defect (VSD), pulmonary stenosis, and Ebstein’s anomaly of the morphologic tricuspid valve.

With situs solitus, the sinus node anatomy and atrial activation may be normal with a normal P-wave axis and morphology, as is seen in this case. L-looping can, however, occur in patients with situs inversus or situs ambiguus (heterotaxy syndromes with asplenia or polysplenia) that might impact the location of the sinus node and P-wave axis. The ventricular septal activation in CC-TGA occurs from the morphologic left bundle branch from right to left. As seen in the junctional escape complexes in Figure 2.1.3, conducted QRS complexes in CC-TGA are characterized by Q waves in leads V₁–V₂ and inferior leads (red arrows), and absence of “septal Q waves” in the left lateral leads (blue arrows).

Figure 2.1.3

One-third of patients with CC-TGA develop complete AV block. The AV conduction system in CC-TGA (and double-inlet left ventricle) is characterized by an anteriorly displaced AV node outside the triangle of Koch at the base of the right atrial appendage.^1,2 This gives rise to an anteriorly displaced AV bundle (bundle of His) that goes around the lateral/superior aspect of the valve of the transposed pulmonary artery that arises in juxtaposition to the mitral valve of the morphologic left ventricle (subpulmonary). This AV bundle continues and splits into the left and right bundle branches along the superior aspect of a membranous VSD that is often present. The normally located AV node in the triangle of Koch typically does not connect to the ventricle on account of malalignment of the atrial and ventricular septae. However, in certain patients this can function as the second AV nodal connection to a separate distinct bundle of His that courses along the inferior margin of the VSD.^1,3

Figure 2.1.1 shows sinus rhythm (Figure 2.1.3, vertical black arrows) with complete AV nodal conduction block. There is escape junctional rhythm with narrow complexes (black horizontal arrows, ~1900 ms or 32 bpm). The junctional rhythm is intermittently interrupted by wide QRS complexes (asterisks). The wide QRS complexes have a slurred onset and suggesting an “extra-fascicular” myocardial origin. The positive precordial concordance (upright QRS in leads V₁ and V₄–V₆) and the left frontal place axis localize the wide complexes to the posterior paraseptal region along the left-side AV annulus. As both wide QRS complexes in this tracing have a short, fixed preceding PR interval, it is quite likely these ventricular activations occur over a left posterior paraseptal accessory AV pathway. Only two P waves conduct over this accessory pathway (asterisks), and the others are blocked. The accessory pathway has weak antegrade conduction properties and is low risk for sudden death from rapid conduction of atrial fibrillation. Another observation in this ECG is the ventriculophasic sinus arrhythmia shown by the changing PP interval (orange double-headed arrows, L—long, S—short).

The level of AV block is thought to most commonly occur at the level of the AV bundle. The narrow escape complexes, albeit with a left axis (rS in lead II) would suggest either AV block at the level of the anterior AV node with junctional escape complexes with a left axis on account of variant ventricular anatomy, remodeling, or intraventricular conduction abnormalities, or alternatively block at the anterior AV bundle but escape complexes from a preserved posterior AV conduction system (expected to have left superior axis due to the relatively posterior location).

All the junctional escape complexes in Figure 2.1.1 time coincidentally with or immediately after sinus P waves. This precludes any assessment of retrograde VA conduction, as the atrial tissue is refractory and unexcitable after sinus activation. The first QRS complex in Figure 2.1.2, however, allows assessment of retrograde conduction. This QRS complex is followed by a retrograde P wave with a short RP interval (Figure 2.1.4, arrow). This P wave is negative in inferior leads (II > III), isoelectric in lead I, positive in lead V₁, and would localize to the left posteroseptal region, consistent with the location of the atrioventricular accessory pathway. The subsequent QRS complex is followed by P-wave fusion between sinus rhythm and retrograde atrial activation (asterisk). Following pacemaker implantation, the brisk retrograde conduction can lead to pacemaker syndrome or pacemaker-mediated tachycardia.

Figure 2.1.4

This patient had CC-TGA without evidence of VSD or pulmonary stenosis. The systemic ventricle (morphologic right ventricle) was hypertrophied and had reduction in systolic function (ejection fraction 30%). He received an atrial-biventricular cardiac resynchronization therapy pacemaker (he declined defibrillator implantation). On electrophysiology study, he had a left-sided posteroseptal accessory pathway with good retrograde conduction properties (effective refractory period 270 ms) that was successfully ablated.

References

1. Anderson RH, Becker AE, Arnold R, et al. The conducting tissues in congenitally corrected transposition. Circulation. 1974;50(5):911–923.

2. Anderson RH, Arnold R, Thapar MK, et al. Cardiac specialized tissue in hearts with an apparently single ventricular chamber (double inlet left ventricle). Am. J. Cardiol. 1974;33(1):95–106.

3. Hosseinpour AR, McCarthy KP, Griselli M, et al. Congenitally corrected transposition: Size of the pulmonary trunk and septal malalignment. Ann. Thorac. Surg. 2004;77(6):2163–2166.

Patient History

A 65-year-old patient with chronic obstructive pulmonary disease (COPD) that present in a long strip recording of lead II evident brusque changes of P wave (Figure 2.2.1).

Figure 2.2.1 Continuous lead II. Observe the abrupt and repeated change in P-wave morphology and polarity not related to the respiration in a patient with chronic obstructive pulmonary disease (COPD). Two types of P-wave morphology are observed: peaked P wave and flat P wave.

Question

How might these changes be explained?

These ECG changes of P wave may be due to:

1. Changes with respiration

2. Fusion beats between sinus and ectopic rhythm

3. Artifacts

4. Sinus rhythm with atrial aberrancy

Discussion, Interpretation, and Answer

The correct answer is 4.

These changes are due to atrial aberrancy. This concept was coined more than 40 years ago by Chung in 1972¹ as “the bizarre configuration of the P wave of a sinus beat immediately after an atrial, AV, or ventricular premature complexes, and is equivalent in the atria to the concept of ventricular aberrancy”.

The concept of atrial aberrancy also encompasses brusque changes of P-wave morphology that may appear in either the same or separate ECG strip, and may or may not be related to the changes in heart rate.^2,3 These changes in morphology (aberrancy) are due to transient changes in the way of transmission of the sinus impulses in the atria. This can sometimes be due to transient interatrial block; however, in this case where there is no ECG pattern of interatrial block,^4–7 it may be due to changes in the transmission of stimulus probably through right atrium. These changes may appear in the same recording, (Figure 2.2.1), in different days (Figure 2.2.2), or immediately after an atrial or ventricular premature beat (Figures 2.2.3–2.2.5). In the setting of Chung,¹ aberrant atrial conduction is an infrequent ECG finding that usually occurs in the elderly with organic heart disease, especially ischemic heart disease. It can also be in chronic cor pulmonale.² The clinical significance is uncertain, but usually occurs in patients with heart disease and atrial involvement.

The current case has the following characteristics:

The P-wave changes are not an artifact, are not related with respiration, and are not fusion beats.

1. The recording starts with 3 flat P wave followed by 13-peaked P wave, 17-flat P wave, and finally 3 peaked waves. This is not a respiratory cycle.

2. The changes from one morphology to another are sudden or with only one complex (the third of second strip) that may correspond to a minor degree of aberrancy. Therefore, there are no fusion beats.

The type of aberrancy of Figure 2.2.2 may explain that patients with important subacute cor pulmonale and pathological P wave of right atrium enlargement (Figure 2.2.2A) may present transient or permanent disappearance of the ECG criteria of the right atrial enlargement (Figure 2.2.2A, 2.2.2B, and 2.2.2C).

Figure 2.2.2 A. A 45-year-old patient with subacute cor pulmonale. Note the right axis of P wave (ÂP) around + 80º (right) few days later (B), the ÂP was left, returning to the right in a third ECG (C) recorded at 15 days. This example shows that criteria of right atrial enlargement may be concealed due to atrial aberrancy.

Finally, in Figures 2.2.3 to 2.2.5, we can see different changes of the P wave that appear after an premature atrial complex (PAC) or an premature ventricular complex (PVC). These bizarre P waves are not an artifact or an escape beat. They most likely correspond to atrial aberrancy due to them being recorded at different times with the same morphology. Figure 2.2.3 shows that after a PAC there is a change in the refractory period of the atria, and the next impulse (x) is partially blocked in the same part of the right atrium and presents a very different pattern (more peaked) than the other ones.

Figure 2.2.3 A P wave that appeared after a PAC that has different morphology from previous and successive ones. It is not an artifact or escape complex because it was recorded many times with the same PR, and is most likely explained by atrial aberrancy.

Figure 2.2.4 also shows a transient change of P wave after a PAC. The P wave changes from a pattern of advanced interatrial block (aIAB) to another of partial interatrial block (pIAB) (from ± to bimodal (x)) that occur is due to the refractory period of the upper part of atria being shortened due to PAC. The next P wave may be conducted with lower degree of interatrial block (IAB) (transient or second-degree A-IAB).

Figure 2.2.4 In the presence of an A-IAB pattern (first P ± in VF) after a PAC there is a pause followed by transient P-IAB pattern that is followed again by a pattern of A-IAB.

In other occasions (Figure 2.2.5) the presence of A-IAB (P ± in II) after one PVC appears as a pause followed by a peaked P wave that has a normal PR interval and is not an artifact. This presumably corresponds to an atrial aberrancy (right atrium).

Figure 2.2.5 In a case of A-IAB after two sinus beats with ± morphology of P wave, a PVC appears which is followed by a P wave with normal P-R conduction and different morphology, only positive (peaked P). This is due to atrial aberrancy.

Conclusion

• Carefully watching the P wave is a useful way to perform the correct diagnosis. Cases with atrial aberrancy that appears transiently explain that the diagnosis of RAE may be temporally masked⁶ (Figure 2.2.2).

• Cases of atrial aberrancy usually appear in the elderly with organic heart disease and atrial involvement.

References

1. Chung E. Aberrant atrial conduction. Unrecognized electrocardiographic entity. Br. Heart J. 1972;34:341–346.

2. Júlia J, Bayés de Luna A, Candell J, et al. Aberrancia auricular: A proposito de 21 casos. Rev. Esp. Cardiol. 1978;31(2):207.

3. Bayés de Luna A. Bloqueo a nivel auricular. Rev. Esp. Cardiol. 1979;32(1):5–10.

4. Bayés de Luna A, Fort de Ribot R, Trilla E, et al. Electrocardiographic and vectorcardiographic study of interatrial conduction disturbances with left atrial retrograde activation. J. Electrocardiol. 1985;18(1):1–13.

5. Bayés de Luna A, Platonov P, García-Cosio F, et al. Interatrial blocks. A separate entity from left atrial enlargement: A consensus report. J. Electrocardiol. 2012;45:445–451.

6. Bayés de Luna A. Clinical electrocardiography. Sussex, U.K.: Wiley-Blackwell. 2012;103.

7. Bayés de Luna A, Massó-van Roessel A, Escobar Robledo LA. The diagnosis and clinical implications of interatrial block. Eur. Cardiol. Rev. 2015;10(1):54–59.

Patient History

The following electrocardiogram (ECG) tracings were recorded during electrophysiology studies performed without sedation in a 71-year-old male with obstructive hypertrophic cardiomyopathy and recurrent syncope.

Discussion

Baseline ECG shows sinus rhythm with normal PR and QRS duration. The His potential has normal configuration; AH is prolonged at 150 ms and HV normal (50 ms). Incremental atrial pacing showed supra-Hissian block with Wenckebach sequence at 100/minute.

Catheter-induced atrial fibrillation (AF) then occurred. Heart rate initially ranged from 50 to 85/minute then atrioventricular (AV) block lasting 3 seconds occurred (Figure 2.3.1). This event was reproducibly documented and not related to any significant change in the patient’s respiratory status. After AF spontaneously converted after #5 minute, short bursts of rapid atrial pacing reproducibly induced transient AV block on very late sinus beats (Figure 2.3.2).

Figure 2.3.1

Figure 2.3.2

Despite the fact the His potential could not be recorded during AV block, the assumption was a phase 4 dependent block located at the proximal His area. A similar case was previously reported.¹

Reference

1. Belhassen B, Danon L, Shoshani D, et al. Paroxysmal atrioventricular block triggered by orthostatic hypotension. Am. Heart J. 1986;112:1107–1109.

Patient History

An 86-year-old female with history of hypertension and hypercholesterolemia is admitted for orthostatic syncope preceded by dizziness. The patient has left hemiparesis after an ischemic stroke. She is under treatment with perindopril, indapamide, rosuvastatin, and clopidogrel.

Questions

1. What is the underlying rhythm?

2. Could help this tracing in explaining the etiology of syncope?

Figure 2.4.1 Sinus rhythm with second-degree atrioventricular block with Luciani periods (standard leads).

Figure 2.4.2

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