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Idiopathic ventricular arrhythmias (VAs), including ventricular tachycardia (VT) and premature ventricular contractions (PVCs), in patients with structurally normal hearts commonly arise from the right and left ventricular outflow tract (RVOT and LVOT). Most of these arrhythmias can be safely and effectively treated by catheter ablation, which has become a first-line therapy in symptomatic patients or in those with left ventricular (LV) dysfunction due to a high PVC burden.1 A particularly challenging subtype of arrhythmias are the VT/PVCs originating in the vicinity of the His bundle. They represent 3% to 9% of idiopathic VAs^2,3 and have distinct electrocardiographic features. Ablation at the parahisian region carries a risk of atrioventricular block, and a comprehensive approach is recommended to minimize risks.

Anatomy

The keystone for safe mapping and ablation of parahisian VAs is to understand the anatomy of the His region and neighbor structures, with special attention to the basal interventricular septum (IVS), the septal tricuspid valve, and the aortic cusp region (Figure 36.1).

The IVS consists of two parts: the membranous ventricular septum (MVS) and the muscular septum,⁴ which in turn can be divided into three zones based on anatomical landmarks: the inlet septum from the tricuspid annulus to the distal attachments of the tricuspid valve; the trabecular septum from the inlet to the apex and up to the crista supraventricularis; and the outlet or infundibular septum between the crista and the pulmonic valve. The most relevant from an ablation point of view is the MVS, a translucent portion of fibrous tissue located between the right and noncoronary cusps. From its upper insertion to the aortic annulus, the MVS extends obliquely down and left to the upper and posterior border of the muscular septum, where it becomes continuous with the subendocardium covering the right and left side of the ventricular septum.⁵ It measures 1 cm from the fibrous aortic annulus to the muscular ventricular septum; it is about 1 mm thick, and thus can be transilluminated ex vivo if a light is placed behind it in the LV. From the right side the MVS is covered by the septal leaflet of the tricuspid valve, which divides it into an interventricular component (between the right ventricle [RV] and LV) and an atrioventricular component (between the right atrium [RA] and LV). This relationship is important as some VAs can be ablated from the RA (see below).

The His bundle penetrates the MVS through the central fibrous body and then passes to the crest of the muscular ventricular septum, where it branches into the right and left bundle branches. The right bundle is a compact cord-like structure that runs superficially up to the level of the septal papillary muscle of the tricuspid valve, then it courses deeper in the IVS and finally becomes superficial again in its distal third to course within the ventricular trabeculations, usually traveling to the RV free wall in the moderator band, ending in the subendocardial plexus.6 The left bundle is a broad sheet-like structure and gives rise to a thin anterior fascicle and a broader posterior fascicle.⁵ The anterior fascicle crosses the LVOT to the anterolateral wall and the insertion of the anterolateral papillary muscle, while the posterior fascicle extends inferoposteriorly to the base of the posterior papillary muscle and the free wall. Also, in approximately 65% of individuals, a discrete third fascicle or left septal fascicle coursing to the midseptal area can be identified.⁷

As reflected in Figure 36.1, both the right coronary cusp (RCC) and left coronary cusp (NCC) are in close relationship with the His region. The RCC is immediately posterior to the infundibular portion of the RVOT and its posterior part is adjacent to the central fibrous body, which contains the penetrating portion of the His bundle. On the other side, the NCC is in contact with both atria and the interatrial septum, and therefore some ATs can be ablated from the NCC. However, the most anterior and rightward extension of the NCC may also be in contact with the RV, and occasionally, parahisian VAs can be cured by radiofrequency (RF) ablation within this cusp.⁸

Electrocardiographic Characteristics

Parahisian VAs share common electrocardiographic characteristics with RVOT VAs, including a left bundle branch block (LBBB) pattern and inferior axis. However, some particular features suggest an origin from the parahisian area (Figure 36.2).^2,3,7 These include:

♦ Positive deflection (R wave) in lead aVL, probably the most specific finding (60% vs. 9%; P < 0.05)⁹

♦ Tall monophasic R wave in lead I

♦ Smaller R wave in lead III than in lead II

♦ QS pattern in V₁

♦ Relatively narrow QRS duration in the inferior leads

Of note, these characteristics make them seem somewhat similar to conducted sinus beats. Precordial transition is variable, with 80% of cases showing R/S transition in leads V₂ and V₃.^3,9 A left superior axis has also been described in VAs in which successful ablation site is below the His bundle area in the RV or LV.² In addition, Ito et al. found that an RSR or RR pattern in lead aVL was relatively specific of parahisian VAs.¹⁰

The distinctive ECG characteristics are explained by the anatomic situation of the His bundle region, which is located at the most posterior and rightward portion of the RVOT. This produces a leftward shift of the depolarization vector, leading to R waves in lead I and aVL and lower R-wave amplitude in lead III than lead II (vector forces directed preferentially to lead II rather than lead III). In addition, the depolarization of the His-Purkinje network explains the narrower QRS duration compared to most RVOT VAs.

When a parahisian origin is suggested by ECG characteristics and early activation at the His catheter (a catheter recording a His potential in sinus rhythm), the next step is to perform a detailed mapping of all the structures adjacent to the His bundle region. These are: (1) the RV septum, including the area behind the septal leaflet of the tricuspid valve; (2) the RCC and NCC; (3) the LV septum below the aortic valve; and (4) the contiguous RA (Figure 36.1B). As with any VA, individualization of the patient’s anatomy is essential. We routinely use intracardiac echocardiography (ICE) and CARTOSOUND™ (Biosense Webster, Diamond Bar, CA) to create a 3D anatomic map of both ventricles. Multiple tomographic images are obtained from the RA and the RV and reconstructed using the CARTOSOUND module. The right and left His are tagged in the 3D map. The aortic cusps are identified and delineated, including the ostium of the coronary arteries.

Any attempt of RF delivery should be preceded by a detailed activation mapping of all neighboring structures. Pace mapping can also be applied but is usually less reliable, as all the aforementioned structures are in close anatomical proximity and pace maps may be similar. Thus, it is important that the patient presents to the laboratory with the clinical arrhythmia. In case of infrequent PVCs, induction of VT or PVCs is attempted with isoproterenol infusion and ventricular or atrial burst pacing.

We usually use irrigated ablation catheters with contact force capacity to monitor real-time contact with the tissue and vector direction at the catheter tip, which is essential for arrhythmia elimination. Targets for RF delivery include earliest local activation preceding the QRS and the presence of a QS pattern in the unipolar electrogram of the ablation catheter, usually associated with good pace mapping. If the earliest ventricular activation is observed close to the His bundle region in the RV, a distance of at least 5 mm away from the site recording the largest His potential is desired.⁷ If the site with earliest ventricular activation also exhibits a His potential, initial ablation from adjacent structures such as the NCC or RCC is reasonable, even if the activation in those structures is simultaneous or slightly later. If VT/PVC suppression occurs in the first 10 seconds, RF delivery is continued for an additional 30 to 60 seconds. If no effect is observed after 10 to 15 seconds, RF delivery is terminated and the catheter repositioned. RF should be immediately stopped in case of AH prolongation, junctional rhythms, or transient heart block. Eventually, ablation from more than one structure may be necessary. Sometimes, an initial burn may result in a slight change of the QRS morphology, which suggests a change in the exit site and indicates that the first lesion was not delivered at the optimal site.

Some practical considerations for mapping and ablation in different parahisian structures are described below.

Mapping of the parahisian region of the RV is mainly hindered by 2 anatomical obstacles; the Eustachian ridge and the tricuspid valve, both of which may prevent good contact and stable catheter position at this location. These obstacles can be overcome with the use of a long, steerable sheath (Agilis, St. Jude Medical, Minneapolis, MN) to displace the Eustachian ridge down and achieve appropriate support to enter the RV. It is important to also map behind the septal leaflet of the tricuspid valve, for which is necessary to apply a second curve to the ablation catheter (see Figures 36.3 and 36.4).

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