Electrophysiological Characteristics and Catheter Ablation of Para-Hisian Atrial Tachycardias

Brad S. Sutton, MD, MBA,
Saraswathy Manickavasagam, MD,
A. Gregory Deam, MD, and
Rakesh Gopinathannair, MD, MA

Division of Cardiovascular Medicine, University of Louisville Hospital
Louisville, Kentucky

Brad S. Sutton, MD, MBA,
Saraswathy Manickavasagam, MD,
A. Gregory Deam, MD, and
Rakesh Gopinathannair, MD, MA

Division of Cardiovascular Medicine, University of Louisville Hospital
Louisville, Kentucky

Focal atrial tachycardias (AT) originate from a circumscribed area with centrifugal spread to both atria. They can be due to enhanced automaticity, triggered activity, or microreentry. Sites of origin for focal AT tend to cluster at specific anatomical locations in the right and left atria, with crista terminalis being the most common location.1 Radiofrequency ablation has proven to be an effective long-term treatment strategy for focal AT, with high success rates and low risk of complications.2-5

Less commonly, symptomatic ATs can arise from the superoparaseptal or para-Hisian region. Mapping and ablation of these arrhythmias can pose unique challenges as sites of successful ablation may localize near the His bundle, the right or left side of the atrial septum, or the non-coronary cusp (NCC) of the aortic sinus of Valsalva, with small but significant risk of damage to the AV conduction system.

In this report, we discuss two cases of para-Hisian focal ATs, followed by a review of the unique anatomical and electrophysiological characteristics of this group of arrhythmias. An approach to mapping and ablation of para-Hisian ATs is also reviewed.

Case #1

A 63-year-old male, with a history of pacemaker placement for sick sinus syndrome, hypertension, and chronic obstructive pulmonary disease, was admitted to the hospital with syncope and episodes of chest discomfort associated with rapid palpitations. Patient complained of paroxysmal palpitations in the past. Pacemaker interrogation revealed recurrent episodes of supraventricular tachycardia (SVT) with a cycle length (CL) of 340–350 msec (171–177 beats/min) that corresponded to patient symptoms. While in the hospital, multiple episodes of narrow complex tachycardia resulting in chest discomfort and dizziness were noted, despite being on maximum tolerated doses of beta-blockers and diltiazem. Transthoracic echo showed no structural heart disease and normal left ventricular function, and a prior coronary angiogram showed no obstructive disease. Given recurrent symptoms despite AV blocking agents, as well as patient reluctance to antiarrhythmic therapy, electrophysiology study and catheter ablation was pursued.

Electrophysiologic Findings

Baseline rhythm was sinus with first-degree AV block and right bundle branch block. There was no evidence for antegrade preexcitation or dual AV node physiology. His-Purkinje function was intact with baseline HV interval of 47 msec.

Burst pacing from high right atrium (RA) at 300 msec easily induced a mid- to long-RP narrow complex tachycardia with a CL of 410 msec and 1:1 AV conduction (Figure 1). Tachycardia was also spontaneously present, with CL varying from 350–460 msec, and was fairly incessant. P-wave morphology during tachycardia showed isoelectric p-waves in lead V1 and across the precordium, positive p-waves in lead I, aVL and biphasic (neg-pos) p-waves in the inferior leads (Figure 2). Earliest atrial activation during tachycardia was noted in the distal His bundle electrogram and preceded the surface p-wave onset by 39 msec. Adenosine was not administered in this case secondary to significant reactive airway disease. Atrial tachycardia was diagnosed by the following findings:

  1. An AAV pattern of tachycardia initiation (Figure 1).
  2. Ventricular overdrive pacing dissociated SVT from the ventricle, ruling out AV reciprocating tachycardia. VAAV response could not be elicited due to lack of atrial entrainment. Septal VA interval >70 msec ruled out typical AV node reentry.
  3. During SVT CL changes, no consistent relationship between the HH and AA intervals was noted either in the antegrade or retrograde direction (Figure 3).

With tachycardia sustained by isoproterenol infusion, RA activation mapping was performed using a 4 mm tip ablation catheter (Safire, St. Jude Medical, St. Paul, MN) guided by 3D-electroanatomic mapping (Velocity, St. Jude Medical). Earliest atrial activation was noted superior to the region of the His bundle. Prominent His electrograms were noted at this location, and given the higher risk of damage to the AV conduction system, it was decided to map the aortic NCC.

The ablation catheter was advanced to the aortic root under fluoroscopic and intracardiac echo guidance (Figure 4, Panels A and B). At this location, low amplitude, multicomponent atrial electrograms with activation times earlier than those in the His bundle region were noted (Figure 5, Panel A). Ablation at this location terminated SVT in 2.6 sec (Figure 5, Panel B). Ablation catheter location at the successful site in NCC is shown in Figure 6 (Panels A and B). Two 60-second applications were delivered at this location (30 W, 55° C), and AT was no longer inducible despite aggressive testing. Patient remained arrhythmia-free at one-month follow up. There were no complications.

Case #2

A 57-year-old male with history of obstructive sleep apnea and paroxysmal palpitations presented to the emergency room with palpitations, dizziness, and chest discomfort and was noted to be in a mid- to long-RP narrow complex tachycardia at a rate of 148 beats/min with 1:1 AV conduction (Figure 7). P-wave morphology was biphasic with a slight negative predominance in V1, positive in I and aVL and isoelectric/biphasic in the inferior leads. He converted to sinus rhythm while receiving intravenous diltiazem in the emergency room. Transthoracic echocardiogram showed no significant structural heart disease. Given recurrent, highly symptomatic SVT despite AV blocking agents, the patient was referred for electrophysiology study and ablation. 

Electrophysiologic Findings

Baseline rhythm was sinus with normal sinus node, AV node, and His-Purkinje function. Sustained narrow complex tachycardia with a CL of 393 msec similar to the patient’s clinical tachycardia was easily induced with atrial burst pacing. The tachycardia appeared to be adenosine sensitive, and was easily induced and terminated by programmed stimulation. Tachycardia CL varied from 320–400 msec, and ventricular response to SVT ranged from 1:1 AV conduction to 2:1 AV block. Earliest atrial activation during SVT was noted in the His bundle region. Standard pacing maneuvers6 confirmed AT as the tachycardia mechanism.

Like in Case 1, RA activation mapping during AT showed earliest atrial activation (~10–15 msec earlier than the atrial electrogram in the His catheter) superior to the His bundle catheter location (Figure 8, Panel A). A test lesion here did not affect the tachycardia. The NCC was explored next, and activation time here was similar to the earliest activation times in the superoparaseptal RA (Figure 8 - Panel B, Figure 9). Ablation at this location resulted in suppression of AT during energy delivery; however, the tachycardia returned once ablation was stopped. This happened repeatedly despite reaching target temperatures. Transseptal catheterization was then performed and a steerable sheath was used to map the left side of the interatrial septum. However, all atrial electrogram timings in the left atrium (LA) were later than the His bundle electrograms.

Detailed mapping of the perinodal region was performed again from the RA and at a location slightly superior and septal to the mid-His bundle electrode (Figure 10), the atrial electrogram was ~15–20 msec earlier than the earliest atrial electrogram in the His bundle. Ablation at this location resulted in tachycardia termination. AV conduction remained intact, and AT was no longer inducible on follow-up electrophysiologic testing in the presence of isoproterenol. A 3D-electroanatomic map showing the successful ablation site is seen in Figure 11. The patient had complete resolution of symptoms and remained tachycardia-free at two-month follow up.

Discussion

Focal Atrial Tachycardias

Atrial tachycardias comprise ~5–15% of all SVTs presenting for ablation.6 Focal AT originates from a discrete atrial focus and spreads to both atria in a centrifugal pattern.7,8 As opposed to macroreentrant AT, which manifests continuous electrical activation, focal AT will generally have an isoelectric interval between P-waves.

Patient presentation in focal ATs can be quite variable in terms of age of onset and duration of symptoms, and may present variably even within an individual patient.9 While the clinical course tends to be benign in many, and may even be self-limited in children, those with incessant tachycardia are at risk for tachycardia-induced cardiomyopathy.10 Successful ablation of focal AT in these patients often restores normal left ventricular function. 

Para-Hisian Atrial Tachycardias

Focal ATs commonly arise from the crista terminalis, tricuspid and mitral annuli, and pulmonary veins.11 Uncommonly, they can arise in close proximity to the AV node and His bundle. This subset of ATs has been variously referred to as perinodal, para-Hisian, or paraseptal ATs.11,12 More recently, a small subset of focal ATs has been named as “arising from the NCC.”13-15 Elegant work by Liu et al,16 however, questions this nomenclature and shows that these ATs do not actually arise from the NCC; instead, they arise from the superoseptal RA or LA that abuts the NCC, and that the NCC just provides a suitable access point to successfully and safely ablate these AT foci that are otherwise difficult to reach from either the RA or LA (Figure 12).16

P-wave Morphology

Several studies support the use of surface p-wave morphology to localize the site of origin of focal AT.11 These algorithms are particularly useful in differentiating right- versus left-sided AT. However, in the case of septally located foci, these algorithms are imperfect, and 3D-electroanatomic mapping is usually required to effectively localize and ablate these rhythms. In both of our patients, p-wave morphology during AT was positive in lead I and aVL, and was biphasic in inferior leads. In Case 1, lead V1 was completely isoelectric, whereas in Case 2, it was biphasic with a negative predominance. Studies that looked at p-wave morphologies in septal ATs have failed to show a consistent electrocardiographic “signature” for ATs that arise from the para-Hisian region as well as adjacent to the NCC.12,13,16

Anatomical as well as electrophysiological complexity of the atrial septum and the para-Hisian region could account for this wide variability in p-wave morphology.13,16,18 The embryonic septum primum is usually thin and composed of layers of orthogonal myocytes and connective tissue, creating anisotropic conduction.19 What is, in fact, described as focal AT from the NCC seems to originate from epicardially-located paraseptal RA or LA tissue lying adjacent to the NCC.16 In a normal heart, the aortic root is centrally located with the NCC abutting the superior paraseptal region between the RA and LA (Figure 13).17 Local electrograms in the NCC therefore typically yield a large atrial signal and show atrial capture with pacing. Complex anatomy as well as anisotropy creating preferential conduction channels for impulse transmission could therefore contribute to variability in p-wave morphology in these tachycardias.18

Mechanisms

Mechanistically, focal ATs can be automatic, triggered, or microreentrant. The behavior of the tachycardia in the EP lab can provide clues to the mechanism. For example, automatic ATs exhibit “warm-up” and “cool-down,” are typically not initiated or terminated by pacing, and can be brought out by isoproterenol infusion.7 In contrast, triggered AT can be induced or terminated by programmed stimulation as well as atrial burst pacing, and typically cannot be entrained. Adenosine sensitivity has been reported as a signature of triggered-activity mediated focal ATs.12 However, the reported sensitivity of ATs to adenosine has been variable and may not be a reliable predictor of mechanism or location.20 In our cases, focal origin with centrifugal activation pattern, inducibility by programmed stimulation as well as burst pacing, amenability to pace termination, and response to isoproterenol and adenosine, all pointed to the mechanism being triggered activity.

Approach to Mapping and Ablation

As our cases demonstrate, activation mapping from the RA alone may be insufficient to distinguish between a right and left para-Hisian AT. Earliest atrial activation in the right septum can result from a right para-Hisian AT, AT adjacent to the NCC, or from rapid left-to-right conduction via Bachmann’s bundle of a left-sided AT. Liu et al have described the atrial activation pattern in AT arising adjacent to the NCC and outline the close anatomic relationship of the NCC to the paraseptal region. They found that atrial activation starts in the RA para-Hisian area followed by almost simultaneous activation of the LA anteroseptal area, and that pacemapping can reproduce this pattern and help confirm the presence of a NCC AT.16 Diffuse initial activation in the para-Hisian RA highly favors mapping in the NCC.

In the second patient in our series, although the atrial electrogram timing was similar in the NCC to that of the superoparaseptal RA, ablation in the NCC was unsuccessful. While we were able to achieve transient suppression of SVT during ablation in NCC, the tachycardia recurred upon stopping energy delivery, suggesting the AT focus was not in direct contact with the ablation catheter. It is possible that maneuvering the ablation catheter to the different location within the NCC might have had a better result but this proved to be technically difficult in this case. This further emphasizes the importance of detailed mapping of RA, LA as well as NCC for safely and effectively ablating these arrhythmias.

Radiofrequency ablation in the NCC has been shown to be safe and effective when local atrial activation in the NCC precedes that of the para-Hisian region, and the surface p-wave by ≥20 ms.21 Caution should be exercised whenever radiofrequency energy is applied in the para-Hisian region due to its proximity to the native conduction system. Cryoablation has played a significant role in the arrhythmias of such high-risk situations such as the pediatric patient or slow pathway modification near the AV node.22-24 However, its use in para-Hisian AT has been limited, but seems promising.23,24 Careful multimodality imaging with aortic root angiography, intracardiac echocardiography, 3D-electroanatomic mapping (often coupled with MRI or CT) and fluoroscopy can help to identify and avoid the AV node and His bundle. Pacemapping can help separate the NCC from the right coronary cusp; NCC pacing will result in atrial capture, whereas right coronary cusp pacing results in ventricular capture due to proximity to the left ventricular myocardium. When mapping the NCC, intracardiac echocardiography can be a valuable tool to assess proper catheter positioning. An aortic root angiogram and/or coronary angiogram should be performed prior to ablation if there is concern about proximity of the arrhythmia focus to the coronary ostia.

Radiofrequency energy can generally be administered via a non-irrigated ablation catheter (4 mm tip) at a starting power of 15W (with titration up to 30–50W) with a target temperature of 50–55° C. Usually, AT terminates within <10 seconds and a 60-second lesion is sufficient.12,13,15 Success rates have been excellent and have ranged from 87–100%, although long-term follow up is lacking.12,13 Given complex anatomic relationships of the structures in this area, we feel that it is important to wait at least 45 minutes post-ablation and re-test with isoproterenol infusion since delivery of high-energy or broader ‘insurance’ burns are not typically feasible.

Conclusion

In summary, para-Hisian ATs represent a subset of focal ATs arising from the superoparaseptal RA and LA with earliest atrial activation localized to the para-Hisian area. Triggered activity appears to be the most common mechanism underlying these focal arrhythmias. These ATs can be incessant and highly symptomatic, and can be extremely challenging to map and ablate, owing to unique anatomic and electrophysiological complexities of the para-Hisian location and close proximity to the AV conduction system. Detailed activation mapping of the RA and LA septum as well as the NCC of the aortic sinus is required and safe, and highly effective catheter ablation can be achieved in the vast majority of patients. Meticulous attention to catheter position and titration of energy delivery is key in ensuring a good outcome.

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