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Narrow QRS-complex extrasystoles inducing a varying degree of AV block – what is the mechanism?

 

Iskra Bayraktarova, Milko Stoyanov, Tchavdar Shalganov

Cardiology Department

National Heart Hospital – Sofia

 

Address for correspondence:

Assoc. prof. Tchavdar Shalganov, MD, PhD

Cardiology Department

National Heart Hospital

65, Koniovitsa Str

1309 Sofia

Tel: +359-2-9211-411

Fax: +359-2-9211-402

This e-mail address is being protected from spambots. You need JavaScript enabled to view it

Abstract:

Extrasystolic arrhythmia is a common clinical finding. Treatment is indicated in case of limiting symptoms and/or large proportion of the ectopy. The possible treatment options as well as the long-term prognosis depend on the precise type of the extrasystoles. Standard surface electrocardiogram does not always provide sufficient information for a differential diagnosis. We present a case of rare extrasystolic arrhythmia with ECG features typical of both supraventricular and ventricular ectopy. The precise diagnosis was established through an electrophysiological study.

Key words: extrasystoles; atrioventricular block; electrocardiogram; electrophysiological study; radiofrequency ablation.

Introduction

Supraventricular premature beats are commonly identified in clinical practice. Despite the possibility of sometimes identifying a precipitating factor for their occurrence (inflammation, ischaemia, hormonal imbalance, emotional or physical stress, alcohol usage, caffeine and nicotine-product consumption or other types of stimulants), it is not uncommon for extrasystoles to appear completely unprovoked. Their incidence rises with age, and the prognosis is in general favourable, except in cases where they trigger another type of supraventricular arrhythmia, for instance atrial flutter or atrial fibrillation. [3, 5] Therapy is indicated in cases of arrhythmia of a different type induced by the ectopic beats, or in the presence of disabling symptoms.

 

Case Presentation

We present the case of 54-year-old male with no prior history of cardiovascular or other type of chronic disease, with a 10-year history of competitive rowing in the past and current regular recreational fitness usage. About a year ago the patient first presented with frequent, extremely unpleasant extrasystoles. Because of these, a therapy of bisoprolol and magnesium was initiated in ambulatory care, which fully resolved the complaints within a few days. A month later the patient stopped the prescribed medication, and remained asymptomatic for several months. After an episode of intensive physical exertion the complaints recurred. The diagnostic tests suggested by the EHRA diagnostic algorithm for establishing the etiology of an extrasystolic arrhythmia were performed in out-patient clinic. [14] The patient was found to have a structurally normal heart, with only a mild left ventricular hypertrophy noted in the echocardiogram. No thyroid pathology was established. On the out-patient Holter-ECG monitoring extremely frequent (almost 4600) supraventricular extrasystoles were noted, described as having a negative P-wave in leads II, III and aVF, and positive P-wave in aVR. The previous therapy of bisoprolol and magnesium was restarted, with no effect on the symptoms. Following an unsuccessful treatment with propafenone, the patient took amiodarone with effect but soon after reaching the loading dose stopped taking the medication. Currently, the patient takes 120 mg slow release verapamil a day and has no complaints. Due to the strong desire of the patient to be medication-free, he is referred for an electrophysiological study (EPS) and possible radiofrequency ablation therapy.

During the hospital stay the standard 12-lead surface ECGs showed a stable sinus rhythm with permanent left anterior fascicular block, no signs of ventricular preexcitation, frequent monomorphic narrow QRS-complex extrasystoles in bi- and trigeminal pattern, with the extrasystolic QRS-complex being very similar to the QRS-complex of the sinus beats, and the regular sinus P-wave falling at different intervals relative to the ectopic beats (Fig. 1, A and B).

A repeat Holter-ECG monitoring for 37 hours was performed during a medication-free period. There were about 36 300 (23%) supraventricular extrasystoles recorded, mostly with a narrow QRS-complex, and a minor proportion had a varying degree of a right bundle branch block (RBBB) aberration (Fig. 2C). The pre-planned EPS was performed 7 days after the cessation of all antiarrhythmic medication. The following diagnostic catheters were used – a 20-pole halo catheter in the right atrium deployed near the tricuspid valve ring and a 6-pole catheter in the coronary sinus (Fig. 3). Sinus rhythm was registered, with frequent single extrasystoles with a QRS-complex similar in duration and form to the usual sinus complex, and an atrial potential that coincided with the ventricular complex or fell after it. The activation sequence of the P-wave was overwhelmingly identical to that in sinus rhythm and very few of the ectopic beats triggered a retrograde P-wave. A 4-mm tipped ablation catheter was introduced and point-by-point mapping was performed, after an initial placement of the catheter in the His bundle region for measurement of baseline conduction intervals (Fig. 3A). A His bundle potential from the distal electrode pair of the catheter was registered in sinus rhythm, and QRS 2 on Fig. 3A represents the recording during an extrasystole. During the course of the EPS the catheter from the coronary sinus was prepositioned in the His bundle region (Fig. 3C).

What is the narrow QRS-complex extrasystolic arrhythmia presented in the figures?

Discussion

In the presented ECG recordings a few different arrhythmic phenomena are recorded that raise the possibility of the final diagnosis, subsequently confirmed by the performed EPS.

Fig. 2A presents ECG in sinus rhythm at a rate of 70 beats per minute (R-R and P-P intervals of about 870 ms, PQ interval of ~160 ms), and frequent extrasystoles (QRS-complexes 2, 5, 7, 9) which share some of the characteristics of both supraventricular and ventricular origin: on the one hand, the QRS-complexes are narrow and have an almost identical to the sinus rhythm morphology, on the other hand, there is no preceding ectopic P-wave and the compensatory pause after the ectopic beats is full. Clearly visible as well are the sinus P-waves that fall at random intervals compared to the extrasystolic QRS-complexes – in QRS 9 the P-wave in situated very close to the following ectopic QRS-complex and gives the impression of a shortened PQ-interval; QRS 2 falls in the middle of the sinus P-wave; QRS 7 comes before the P-wave, which falls in the ST-segment of the extrasystolic QRS-complex and is subsequently blocked; and in QRS 5 the P- and T-waves coincide.

In fig. 2B QRS 2 is also an extrasystole, the following sinus P-wave falls in the ST-segment and is blocked, thereby imitating type 2 second-degree AV block.

In fig. 2C there are even earlier ectopic complexes registered, to the point they are interpolated – another demonstration that the extrasystoles do not affect the baseline P-P cycle. Also displayed is the interesting mutual effect between the ectopic and sinus complexes that depends on their temporal relationship. On the one hand, the distance from the ectopic QRS to the preceding sinus QRS-complex obviously influences the ectopic QRS morphology – while most of the ectopic complexes are morphologically quite similar to the sinus complex with only a very discreet resemblance to RBBB shape in lead V1, with the shortening of the coupling interval the ectopic beat aberrates with a typical RBBB morphology (QRS 12, fig. 2C), a phenomenon based on the longer refractory period of the right bundle branch of the conduction system. [8]

On the other hand, the time from the extrasystole to the following sinus impulse determines the fate of that following impulse. If the extrasystole is too late, the ectopic impulse is conducted to the ventricles and the immediately following impulse from the regularly occurring sinus P-wave meets with parts of the conduction system that are still refractory and is subsequently partially or fully blocked (the already described complexes in fig. 2A, also P- at the end of the T-wave in QRS 2 in fig. 2B). If the extrasystole is early enough (and the baseline P-P cycle – long enough) for the local conduction to return to normal, the next P-wave is conducted, but a varying degree of AV-block is noted and the PQ-interval is visibly affected by the time from the extrasystolic beat. In fig. 2C QRS 8, 9, 10 (where QRS 8 and 10 are sinus beats, and QRS 9 is an interpolated extrasystole) PQ 8 is 160 ms, the post-extrasystolic R9-R10 interval is 674 ms and the following PQ 10 interval is prolonged to 200 ms in comparison to the previous one. Even more markedly, in fig. 2B, QRS 3, 4, 5 (where QRS 3 and 5 are sinus beats, and QRS 4 – an interpolated extrasystole), the baseline PQ 3 interval is 160 ms, the post-extrasystolic R4-R5 interval is even shorter – only 580 ms, and the following PQ 5 interval, despite being hard to precisely measure due to the P- and T-wave fusion, is well beyond 200 ms.

In fact, based on the so far discussed elements of the surface ECG, the following conclusions can be drawn – the presented extrasystoles share a few of the characteristics of atrial extrasystoles, but are not atrial. In other ways they resemble ventricular extrasystoles, but are not ventricular.

The EPS pinpoints the final diagnosis. In the presented electrophysiological recordings it is clear that in sinus complexes distinct A, H and V potentials are registered, with AH and HV intervals well within the normal range (Fig. 3A). In the ectopic complexes the ventricular excitation follows at a fixed distance behind a His bundle potential that is not preceded by an atrial depolarisation. There are complexes where the atrial depolarisation with the characteristic sinus sequence happens during or a varying interval after the described HV sequence. Actually the recordings from fig. 3A, QRS 2, fig. 3B, QRS 2 and fig. 3C, QRS 1 explain the described interplays between the sinus P-waves and the ectopic QRS 9 and 2 in fig. 2A and QRS 2 in fig. 2B.

The contemporary concepts of the automaticity of the specialised conduction system of the heart contribute the automatic properties of the AV junction to cells of the His-Purkinje system. [6, 10, 12] The so called “nodal” rhythms probably originate from the coronary sinus area low in the atria or from the bundle of His, and not from the AV node itself. [1, 15] The lack of registered retrograde atrial depolarisation mostly clears the ectopic focus as part of the bundle of His.

The His bundle ectopy is considered a rare arrhythmia [9], although some authors consider that the localisation of the ectopy makes it multifaced and hard to differentiate on standard surface ECG, and subsequently – a frequently missed or otherwise classified phenomenon. [1, 2, 13]

The characteristics of the extrasystolic arrhythmia we present, clearly discernible on surface ECG, cover the criteria for the “extrasystoles from the bundle of His” diagnosis, postulated by Fletcher in 1953 [9] and refined by Marriott in 1957 [13], and namely: 1. premature beats that have the same morphology as the sinus beats; 2. the sequence of the sinus P-waves remains undisturbed in time and form; and 3. the extrasystoles are followed by a full compensatory pause.

Despite interpolated His bundle extrasystoles (and those described as “nodal” due to the abovementioned reasoning) being a relatively rare finding [1], we find that in the third criterion it is justified to add “or are interpolated”. This phenomenon is observed when the baseline sinus rate is low enough that it allows for a full recovery of the conduction system after the extrasystole, and subsequently no compensatory pause is necessary.

The AV block of the first and second degree with a short coupling interval between the extrasystoles and the closely following sinus P-waves is actually one of the typical forms of expression of His bundle extrasystoles in the standard surface ECG [2, 15]. This phenomenon is explained by the concealed retrograde conduction of the premature His depolarisation towards the AV node. Even blocked by the AV node and not conducted to the atria (no recorded retrograde P-wave), this premature impulse modifies the conduction of the following sinus impulse.The too closely following sinus P-wave is blocked by the fully refractory AV node (QRS 2 in fig. 2B).

A comparatively later post-extrasystolic P-wave is conducted forward with a varying degree of delay through the partially refractory AV node (the sinus complexes after the interpolated extrasystoles in fig. 2B and C). Because there is no real disturbance of the conduction (normal conduction AH and HV intervals are recorded during conducted sinus complexes), this finding is described as pseudo-AV block in the literature. Depending on the exact features of the conduction system in the particular patient and the precise characteristics of the extrasystoles, the pseudo-AV block can be of a higher degree and can subsequently necessitate additional antibradycardia therapy in the form of a permanent pacemaker implant [2, 11].

In the presented case no need for antibradycardia treatment is found. However, bearing in mind the low tolerance of the symptoms and also the desire of the patient to be medication-free, in the context of the diagnostic EPS that led to the final diagnosis, radiofrequency ablation of the ectopic focus was attempted. Detailed mapping was performed in the anterior and anteroseptal area, and also around and above the coronary sinus ostium. Several radiofrequency pulses of a very low starting energy and with slow up-titration of the power were made at the points of clearly registered His bundle potential and shortened HV interval. During some of the applications a “warm-up phenomenon” was induced, with the ectopic beats becoming more frequent and no subsequent suppression of the ectopy. Due to the high risk of inducing damage to the normal conduction system, the procedure was terminated. There are two reports in the specialised literature of successful His bundle extrasystoles ablation – by Choi et al [4] using radiofrequency, and by Eizmendi et al [7] using cryoenergy.

Theoretically, owing to the structural characteristics of the bundle of His (relatively thin for its length) any attempts for ablation of an ectopic focus that is part of the bundle proper carry the significant risk of causing loss of physiological function of this critical part of the conduction system of the heart. Additionally, it is very difficult to estimate in advance the relative size of the ectopic focus in comparison to the size of the His bundle itself. All of this makes the balance successful ablation/preserved conduction quite delicate. As far as the cryoablation provides a smoother and to some degree reversible control over the applied lesion, it could theoretically be the method of choice [17]. In any ablation attempt, however, the balance gain/risk should be a major factor. Due to the electivity of the procedure in our patient and the resolved symptoms under verapamil treatment in the past, we decided not to persevere unnecessarily in our desire to ablate to pinpointed ectopic focus in the bundle of His proper.

Conclusion

We present a first in Bulgaria case of extrasystolic arrhythmia from an ectopic focus in the bundle of His. This type of electrocardiographic and electrophysiological finding seems to be more insufficiently diagnosed than objectively quite rare. The symptoms of the patient largely depend on the concrete manifestation of the arrhythmia and the corresponding wide spectrum of possible surface ECGs. The therapeutic approach should be appropriately chosen for the subjective tolerance of the symptoms and the objective findings from the complete cardio-vascular status. At this point of time, however, the definitive ablation treatment remains a practical rarity.

 

References

1. Abedin,Z., R.P.Sapru. His bundle ectopic beats: His bundle electrocardiographic study. – JAMA, 227, 1974, 5, 549-551.

2. Ameen, A. et al. His bundle extrasystoles revisited: the great electrocardiographic masquerader. Pacing Clin Electrophysiol, 34, 2011, 6, 56-59.

3. Binici, Z. et al. Excessive supraventricular ectopic activity and increased risk of atrial fibrillation and stroke. – Circulation, 121, 2010, 17, 1904-1911.

4. Choi, K.J. et al. Successful ablation of Hisian ectopy identified by a reversed His bundle activation sequence. – J Interv Card Electrophysiol, 6, 2002, 2, 183-186.

5. Chong, B.H. et al. Frequent premature atrial complexes predict new occurrence of atrial fibrillation and adverse cardiovascular events. – Europace, 14, 2012, 7, 942-947.

6. Damato, A.N., S.H. Lau. His bundle rhythm. – Circulation, 40, 1969, 4, 527-534.

7. Eizmendi, I. et al. Successful catheter cryoablation of Hisian ectopy using 2 new diagnostic criteria based on unipolar and bipolar recordings of the His electrogram. – J Cardiovasc Electrophysiol, 23, 2012, 3, 325-329.

8. Fisch, C. Abberration: seventy five years after Sir Thomas Lewis. – Br Heart J, 50, 1983, 4, 297-302.

9. Fletcher, E. Extrasystoles arising from the main bundle of His. – Br Heart J, 17, 1955, 4, 566-568.

10. Hoffman, B.F., P.F. Cranefield. The physiological basis of cardiac arrhythmias. – Am J Med, 37, 1964, 5, 670-684.

11. Jimenez-Diaz, J. et al. Mobitz type II second-degree AV block with narrow QRS and junctional extrasystoles: what is the mechanism? – J Cardiovasc Electrophysiol, 25, 2014, 4, 447-449.

12. Kurian, T. et al. Anatomy and physiology of the human AV node. – Pacing Clin Electrophysiol,33, 2010, №6, 754–762.

13. Marriot H.J.L., S.M. Bradley. Main-stem extrasystoles. – Circulation, 16, 1957, 4, 544-547.

14. Raviele A. et al. Management of patients with palpitations: a position paper from the European Heart Rhythm Association. – Europace, 13, 2011, 7, 920–934.

15. Rosen K.M. et al. Pseudo A-V block secondary to premature nonpropagated His bundle depolarizations: documentation by His bundle electrocardiography. Circulation, 42, 1970, 3, 367-373.

Legend to the figures

Fig. 1. ECG recordings of the two consecutive days (only lead II is shown). The extrasystolic beats are marked with an asterisk (*), and the neighbouring sinus P-waves are marked with a vertical line (|). The speed of the recordings is 25mm/sec.

Fig. 2. Holter-ECG, peripheral leads and V1. The ectopic QRS complexes are marked with an asterisk (*), and the neighbouring sinus P-waves are marked with a vertical line (|). The speed of the recordings is 25mm/sec.

Fig. 3. EP study recordings. The ectopic QRS complexes are marked with an asterisk (*). In panels A and B the ablation catheter is positioned at the bundle of His. In panel C the catheter from the coronary sinus is moved to the bundle of His and accordingly, the His potential is recorded in the lowermost channel. H – His-bundle potential; A – atrial potential; V – ventricular potential; Hal – 20-pole “halo” type catheter; Abl – ablation catheter; CS – catheter in the coronary sinus. Uppermost in the recordings is an ECG with leads I, aVF and V1. The speed of the recordings is 150mm/sec.

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