Ablation of PVCs Originating Within the His Vicinity

Introduction

We report a case of incessant monomorphic premature ventricular contractions (PVCs) of an unusual location ablated near the His bundle. Anatomical considerations, electrocardiographic features, and pearls for successful catheter ablation are discussed. Other forms of idiopathic PVCs of similar electrocardiographic appearance are briefly reviewed as part of the differential diagnosis.

Case Description

A 33-year-old female without past medical history was referred for symptoms of fatigue, shortness of breath, and palpitations for the last nine months that prevented her from exercising, doing mild house chores, and playing with her children. A cardiac monitor showed incessant bigeminy. An echocardiogram showed an ejection fraction of 40%. Twelve-lead ECG showed frequent PVCs with a morphology of LBBB, inferior axis, and late R wave transition suggestive of a right ventricular origin (Figure 1).

She failed beta-blockers, diltiazem and flecainide. After discussion of the risks and benefits of ablation, she opted for catheter ablation.

After written informed consent was obtained, an electrophysiology study was performed in the post-absorptive state with mild sedation. Catheters were placed percutaneously in the right atrium, His bundle, and right ventricular apex. A 4 mm tip standard ablation catheter was used for mapping and ablation.

Her AV node-His-Purkinje system was normal. AH and HV intervals during sinus rhythm were 61 and 47 msec, respectively, and the effective ventricular refractory period at 600 ms was 230 msec. There was retrograde ventriculo-atrial conduction exclusively through the AV node.

An activation map was built during spontaneous PVCs with conventional mapping and using the EnSite Velocity NavX (St. Jude Medical). The earliest site was shown to be at the RV anterior-septum beneath the tricuspid valve, where a small His electrogram was recorded on the ablation catheter (Figure 2). 

Pace mapping was 12/12 from the His bundle location. The ventricular electrogram at the ablation site was abnormal with some fractionation and preceded the PVC by 24 ms, and the unipolar electrograms (ablation tip to Wilson central terminal) showed a QS pattern (Figure 2). 

A long SRO sheath was used to provide stability. Ablation was started with 5, 7, 10, 15, 20 and 30 Watts, while increasing the energy of each of those steps at 10 s intervals over 40 s. No junctional beats were observed during radiofrequency (RF) delivery. Spontaneous PVC stopped within seconds of RF delivery. 

The patient is symptom free on no medications at nine-month follow-up, and two cardiac event monitors did not shown any PVCs. Her ejection fraction has also normalized. 

Discussion

Most idiopathic non-reentrant ventricular tachycardia (VT) and premature ventricular contractions (PVCs) arise from the right (80%) or the aortic root within the sinus of Valsalva (10–15%).¹ The majority of right ventricular outflow tract (RVOT) PVCs originate from the posterior lateral aspect just inferior to the pulmonic valve, the so-called “septum” (Figure 3). RVOT VTs are more frequent in women, while men exhibit left ventricular outflow tachycardias (LVOT) more often.¹ The mechanism of these arrhythmias is trigger mediated. 

Less frequently, non-reentrant VT or PVCs can arise from the tricuspid valve including the His bundle, above the pulmonic valve, the aorta-mitral continuity, around the mitral annulus, right and left papillary muscles, and from an epicardial location accessible through the anterior interventricular vein (AIV) or via subxiphoidal percutaneous access.

Anatomical Considerations

The ventricular outflows, aortic sinus cusps (ASC), left ventricular summit (the highest portion of the basal left ventricle), the great cardiac vein, and AIV vein represent a complex anatomical region which has been described by some as the “Bermuda triangle.” It requires a thorough understanding of its anatomy to avoid catastrophic collateral damage, i.e., injury of the AV conduction system and the coronary arteries that are within this space.

The compact AV node is inferior to the central fibrous body and lies in front of the coronary sinus (Figure 3). The anatomical landmark for localization of the AV node is recognized as the triangle of Koch, formed by the His bundle, the coronary sinus, and the tendon of Todaro. The His bundle penetrates the central fibrous body (CFB), surrounded by fibrous tissue. The superior extension of the central fibrous body is the membranous septum, divided into an atrial and ventricular portion by the insertion of the septal leaflet of the tricuspid valve. This location is of great interest for ablation of supero-septal accessory pathways and PVCs near the His bundle. The common His bundle (after penetrating the CFB), becomes the right bundle and emerges as the LBBB by crossing the membranous septum just below the noncoronary (NCC) and right coronary cusp (RCC).

General Electrocardiographic Characteristics

Multiple ECG algorithms have been developed to help localize the PVC origin. Because of the close anatomical proximity of these structures, no ECG algorithm has proven to be perfect. The following discussion is predicated on standard ECG lead placement, i.e., precordial leads V1 and V2 at the fourth right and left intercostal space and shoulder placement of limb leads. Mild changes in ECG lead placement could significantly affect QRS transition and amplitude of the QRS signals. Of note, ECG leads are usually placed inferiorly and more medially to allow space for epicardial defibrillation patches and electroanatomical mapping, resulting in taller R waves in V1-V2 and reduced R waves in lead I.²

PVCs arising from these basal structures of the heart share an inferior axis, i.e., R waves in inferior leads and predominant S waves in V1, V2 (Table 1).

Because of a lack of structural heart disease, the 12-lead ECG is a very useful tool to regionalize the area of PVC origin. 

As a first step and also for preprocedural planning, right versus left ventricular origin can be inferred by an early R wave transition. Early QRS transition by V1-V2 and lack of S waves in V5-V6 are seen in the ASC origin (Figure 3).^1,3 PVCs from the RVOT feature a QRS transition by V4. Septal RVOT sites (left posteromedial) exhibit narrower and taller R waves in inferior leads, QRS without notching, and s wave in lead I.⁴ It is important to underscore that the RVOT is anterior and “leftward” to the aortic root (Figure 4).

Left coronary cusp PVCs frequently exhibit a W or M pattern shape in V1.⁵ A downward notch in V1 has been suggested for an origin at the right and left coronary commissure (Figures 4 and 5).⁶

PVCs from the mitral annulus and aortic-mitral continuity hardly present a challenge in the differential diagnosis (Figure 5). They tend to have broader R waves in V1 (like RBBB pattern) morphology. A qR pattern in lead V1 is seen in PVCs from the aortic-mitral continuity.⁷ PVCs from the epicardium (Figure 5) have a wider and slurred QRS because propagation of the impulse occurs slowly through the ventricular muscle instead of using the specialized conduction system.⁸  

His Bundle PVCs

Contrary to right outflow tract PVCs, Yamauchi et al⁹ described His PVC morphology to exhibit R waves in aVL (QS in RVOT) and shorter QRS duration in the inferior leads, which can be explained by a downward location of the His bundle.

Komatsu et al¹⁰ described two different kinds of His bundle PVCs. See Table 2 for differences. Our case falls within group 1 with the peculiarity of ventricular fractionation at the ablation site.

Ablation Considerations of PVCs Near the His Bundle

Ablation in patients with symptomatic monomorphic PVCs that are drug resistant or drug intolerant, or those who do not wish for long-term drug therapy, are considered a class IIa indication (level of evidence: C).¹¹

Ablation of asymptomatic and very frequent PVCs is also contemplated in the guidelines when there is associated left ventricular dysfunction (Class IIb, level of evidence: C).¹¹

Careful mapping is necessary to locate the target ablation site. If no ventricular site is found to precede the QRS by 25–30 ms or there is not a QS pattern in the unipolar recording, it is advisable to map the NCC and RCC. We usually try to start 5 mm far from the largest His bundle recording and use low power starting at 10 W up to 30 W. A long preformed sheath is recommended to provide stability during ablation.

Complications

Data about complications from ablation of PVCs near the His bundle can be extrapolated from ablation of Wolff-Parkinson-White syndrome and anteroseptal (superoparaseptal) pathways. 

The risk of AV block has been estimated to be 2%.¹² Note the risk of AV conduction injury is lower than expected, because the His bundle is insulated by a fibrous sheath when penetrating the central fibrous body. However, ablation of mid anterior-septal pathways, and thus, peri-nodal PVCs, carries a significantly higher risk of inadvertently damaging the AV conduction system. RBBB is described in 2–17% of ablation of anteroseptal pathways.¹²

Careful observation was performed for any successive junctional ectopic beats, which would act as a warning sign for subsequent atrioventricular block.

Di Biase et al¹³ also proved cryoablation to be a suitable form of energy, with less risk of damaging the AV conduction system but with a slightly higher recurrence.

In the presented case, PVCs were successfully eliminated using radiofrequency energy without impairing atrioventricular conduction. 

Disclosures: Dr. Navarrete reports consultancy with St. Jude Medical (modest). Dr. Iqtidar has no disclosures to report. 

References

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