Ablation of Focal Atrial Tachycardias


Key Points

Anatomy

  • Atrial tachycardia (AT) foci exhibit a characteristic anatomic distribution in both atria.

  • The right atrium is the most common location with two-thirds of right sided focal AT arising from the crista terminalis.

Pathophysiology

  • Focal AT may be caused by microreentry, abnormal automaticity, or triggered activity.

  • This mechanistic distinction is less relevant in the current era of radiofrequency ablation.

Arrhythmia Diagnosis

  • Focal AT must be distinguished from other arrhythmias using both electrocardiographic clues and diagnostic approaches in the electrophysiology laboratory.

  • Differential diagnoses include macroreentrant AT, atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, and inappropriate sinus tachycardia.

Mapping

  • Initial evaluation of the P wave morphology of the 12-lead electrocardiogram can indicate the likely region of origin of the focal AT.

  • Detailed evaluation usually includes a 3-dimensional mapping system looking for the earliest activity relative to P wave onset.

  • Anatomic sites in close proximity should be independently mapped.

Ablation

  • Ablation end points include loss of all spontaneous AT activity and noninducibility

  • Ablation success rates in excess of 80% to 90% may be expected.

Funding sources / conflicts of interest:

Professor Kalman is supported by practitioner fellowships from the NHMRC.

Introduction

Focal atrial tachycardia (AT) is the least common form of supraventricular tachycardia (SVT). It accounts for approximately 5% to 15% of SVT cases undergoing catheter ablation. Focal AT is characterized by the presence of a discrete atrial focus with centrifugal spread of atrial activation away from that site. Focal ATs are usually paroxysmal and self-limited, although in some patients, focal AT may be incessant, which can lead to the development of tachycardia-mediated cardiomyopathy (TMC). Focal AT may result in the initiation of other atrial arrhythmias such as atrial macroreentry or atrial fibrillation (AF) if the rate of focal firing is particularly rapid along with the development of secondary atrial remodeling.

Focal AT is frequently unresponsive to pharmacologic therapy. With the advent of catheter ablation, this type of tachycardia can be treated with high long-term success rates. Importantly, mapping and ablation of focal AT are greatly facilitated by the characteristic anatomic distribution. In addition, the use of sophisticated 3-dimensional mapping technologies greatly facilitates accurate localization, but it is important to remember that P wave analysis and conventional multipolar mapping techniques remain important adjunctive tools.

Many different classical mechanisms of focal AT have been described including abnormal automaticity, triggered activity, and microreentry. However, the underlying mechanism seems less important in the ablation era because these diverse mechanisms manifest similarly on activation mapping. This chapter will discuss the anatomic distribution, pathophysiology, mapping and ablation techniques of this uncommon arrhythmia.

Anatomy

AT foci do not originate in random locations throughout the atria but instead cluster in characteristic anatomic sites ( Fig. 10.1 A and B ). The right atrium (RA) is the most common location with approximately 55% to 63% of foci originating in this chamber. Within the RA, two-thirds of foci arise from along the crista terminalis (CT) with the superior and mid CT more common than the inferior CT. Other common sites include the tricuspid annulus (TA), the coronary sinus (CS) ostium, the perinodal (parahissian) region, RA appendage (RAA), and RA septum. In the left atrium (LA), the majority of foci originate from the pulmonary vein (PV) ostia followed by the mitral annulus (MA), left septum, LA appendage (LAA), and musculature within the CS body. It is important to be aware that despite this characteristic anatomic distribution, tachycardia foci may occur from unusual or previously undescribed sites.

Fig. 10.1, A, Schematic showing anatomic distribution of focal atrial tachycardias. B, Distribution of tachycardia originating from the annular region and aortic cusp. AT , Atrial tachycardia; AV , atrioventricular; CS , coronary sinus, CT , crista terminalis, HBE , His bundle electrogram; LAA , left atrial appendage; MV , mitral valve; Os , ostium; PN , perinodal; PV , pulmonary vein; RAA , right atrial appendage; RS , right septum; TV , tricuspid valve.

Crista Terminalis

In seminal work by Kalman et al. using intracardiac echocardiography, the CT was noted to be the location of two-thirds of focal AT arising from the RA. The superior CT was the most common site followed by the mid CT. Foci originating from the inferior CT were uncommonly observed. Focal AT from this site is more common in women particularly above the age of 40 years, frequently has features to suggest microreentry (onset and termination with programmed stimulation), and may have multiple foci. Although the reason for this characteristic distribution is unclear, there are certain electrophysiologic (EP) properties of the CT that may be important. The CT is a region of conduction anisotropy with poor transverse and rapid linear conduction, potentially creating a substrate for microreentry in the context of atrial remodeling. Furthermore, the CT is the anatomic site along which the sinus pacemaker complex is distributed, and therefore richly innervated with automatic tissue.

In a discussion of tachycardias arising from the CT, it is worthwhile considering whether sinus node reentry represents a distinct clinical entity. This tachycardia has been defined as an arrhythmia that can be induced and terminated with programmed stimulation with P wave morphology (PWM) identical or similar to that of the sinus P wave. However, it is difficult to apply this definition strictly because of the variability in sinus PWM (e.g., sinus arrhythmia), and it can be argued that this arrhythmia is synonymous with an AT arising from the CT. As such, the use of this term should probably be discontinued.

Tricuspid Annulus

In a series of consecutive patients with focal right atrial AT, 13% were reported to originate from the TA. In this study, foci arose from either the superior TA or the inferoanterior TA with the latter the most common site. An alternative series of patients with focal AT only observed foci arising from the superior TA. Isolated case reports have reported focal AT originating from the inferolateral TA and the anterolateral TA. In two animal studies, McGuire et al. described the presence of cells with atrioventricular (AV) nodal–type characteristics around the entire TA. These cells were histologically similar to the atrial cells but resembled nodal cells in their cellular electrophysiology, response to adenosine, and lack of connexin 43. One may speculate that these cells serve as the substrate for AT originating from around the TA.

Coronary Sinus Ostium

Kistler et al. reported in approximately 7% of patients undergoing radiofrequency ablation (RFA) for focal AT, the AT focus originated from the CS ostium. The CS ostium is characterized by the abrupt change in myocardial fiber orientation in the region of the Thebesian valve. Most focal ATs originating from the CS ostium demonstrate properties suggestive of reentry. It is speculative whether this change in fiber orientation may provide the anisotropic conduction necessary to initiate reentry.

Midline Atrial Structures: Parahissian (Perinodal), Atrial Septal (Left or Right), and Noncoronary Cusp

There is considerable confusion about the origin and nomenclature of focal AT originating from the abovementioned anatomic regions. The terms parahissian and perinodal have been used interchangeably. In addition, tachycardias described as arising from either the left or right side of the septum have also included tachycardias originating in the perinodal region. Furthermore, others have suggested that parahissian tachycardias are a subset of TA tachycardias because of their similar EP properties. In addition, ATs originating from the noncoronary cusp have been viewed either as a distinct entity or, alternately, as an early exit region for a tachycardia that originates from the perinodal region or anterior septum. In the latter of these hypotheses, the noncoronary cusp is thought to simply provide a safe approach to ablation of an AT that actually originates from the perinodal area. It is the authors’ opinion that tachycardias arising from each of the abovementioned regions should be viewed as a distinct clinical entity with careful mapping in each region. Rarely, AT has been described as arising from the left or right coronary cusps.

Right Atrial Appendage

The hallmark of these uncommon tachycardias is that they are frequently incessant and therefore may be associated with TMC. In a series of patients with RAA focal AT, Roberts-Thompson et al. observed that these arrhythmias either arose from the inferolateral base or the tip of the RAA. The inferolateral base of the RAA was the most common location in this study. On the other hand, in a series by Freixa et al., the tip of the RAA was the most common site with 60% of foci arising from this location. Both these studies noted that this tachycardia was more common in men.

Pulmonary Veins

The role of PV foci in the initiation of paroxysmal AF has been extensively documented. These patients frequently demonstrate a spectrum of arrhythmias ranging from focal atrial ectopy and nonsustained AT to paroxysms of atrial macroreentry or AF. In this patient population, there are multiple PV foci within each PV and from multiple PVs. As such, focal ablation is universally unsuccessful, and an approach that encompasses isolation is required. However, there is a group of patients with PV foci who demonstrate only focal AT as the clinical arrhythmia and in these patients the fundamental mechanism appears to be truly focal in the majority. Foci responsible for isolated AT tend to have longer cycle lengths and be ostially located rather than deep within the PV compared with foci associated with AF initiation. In addition, the foci arise more commonly from the superior PVs than the inferior PVs. AT originating from the PVs are virtually always spontaneous and rarely inducible with programmed stimulation, suggesting abnormal automaticity or triggered activity. In rare cases, PV AT has been induced by speech and deglutition. In some patients with PV AT, the arrhythmia may be incessant and result in TMC. Although this appears to be fully reversible following catheter ablation, recent studies have suggested that subtle ventricular abnormalities may persist. Given the focal nature of PV AT, these arrhythmias are curable in the long term with focal ablation. In a study by Teh et al. evaluating the long-term outcomes of patients with PV AT following catheter ablation, 96% were free from recurrence of AT off antiarrhythmic drugs at a mean follow-up 7.2 ± 2.1 years. None of the patients developed AF. In those patients with recurrences, in almost all instances this was from the original focus.

Mitral Annulus

The MA is the second most common location of LA focal AT. In a series of patients with LA focal AT by Hachiya et al., approximately one-third of foci originated from the MA. The superior region of the MA in close proximity to the aorto-mitral continuity (AMC) and the left fibrous trigone has been reported as the most common site of mitral annular focal AT. Gonzalez et al. hypothesized using a murine model that embryologic remnants of specialized conducting tissue located in this region may provide the substrate for focal AT. Furthermore, Wit et al. observed that muscle fibers of the anterior mitral valve leaflet were continuous with the LA myocardium. These fibers exhibited AV nodal–type characteristics with both spontaneous automaticity and anisotropic conduction properties potentially providing the substrate for abnormal automaticity or microreentry.

Left Atrial Appendage

LAA focal AT has been reported to most commonly arise from the base of the LAA. In a series by Yamada et al., all LAA foci arose from the base of the LAA, most commonly the medial side. Rarely, LAA focal AT has been described as originating from the tip of the LAA or the epicardium.

Coronary Sinus Musculature

Badhwar et al. described an uncommon type of focal AT originating from within the CS musculature in approximately 3% of patients undergoing catheter ablation. The mean distance from the CS ostium to the site of earliest endocardial activation recorded within the CS was 3.6 ± 0.5 cm. This site always preceded the earliest LA endocardial site during tachycardia. All patients were noted to have a sharp potential in the CS that preceded the CS atrial signal during tachycardia. In all patients, the tachycardia was successfully ablated within the CS.

Pathophysiology

The pathophysiology leading to the development of focal AT remains unknown. When histologic examination has been possible in cases of focal AT, both normal and abnormal myocardium at the focal origin have been reported. McGuire et al. reported four patients with abnormalities, two with extensive myocardial fibrosis and two with myocyte hypertrophy and endocardial fibrosis. All had structural heart disease. Other reports have found mononuclear cell infiltration, mesenchymal cell proliferation, islets of fatty tissue, thinning, and blebs. These may produce the substrate required for microreentry or abnormal automaticity.

Higa et al. demonstrated the existence of low-voltage zones suggesting the existence of localized atrial pathology in patients with focal AT. The majority of focal ATs in this series originated within or on the border of a low-voltage zone. Many of these arose from the CT, which showed conduction anisotropy with rapid linear conduction and slowed transverse conduction. It is possible that localized atrial myocardial abnormalities represent the substrate for focal AT. Consistent with these observations, several studies have found low-amplitude, fractionated electrograms at the site of successful ablation in patients with focal AT, representing slowed conduction and possibly atrial pathology. Nevertheless, this has not been a universal finding and may be dependent on anatomic location such as the CT.

Whereas local structural abnormalities appear to most likely create the substrate for focal discharge or microreentry, focal AT may also exhibit EP characteristics suggestive of abnormal automaticity or triggered activity. Chen et al. performed a comprehensive evaluation of the mechanisms of AT in 36 patients using both pacing and pharmacologic maneuvers. Automatic ATs were identified in seven patients by the following characteristics: (1) AT could be initiated only with isoproterenol; (2) programmed stimulation could not initiate or terminate AT; (3) AT could be transiently suppressed with overdrive pacing; (4) propranolol terminated all of the AT; (5) adenosine, dipyridamole, verapamil, Valsalva maneuver, carotid sinus massage, and edrophonium could not terminate the AT; and (6) monophasic action potential recordings did not find afterdepolarizations. AT related to triggered activity occurred in nine patients with the following features: (1) the initiation of AT was reproducible with atrial pacing and was dependent on achieving a critical range of atrial pacing cycle lengths; (2) just before the onset of AT, delayed afterdepolarizations were observed in the monophasic action potential recordings; (3) termination of AT was reproducible with programmed stimulation; (4) entrainment was not found, but overdrive suppression could be demonstrated; (5) adenosine, dipyridamole, propranolol, verapamil, Valsalva maneuvers, carotid sinus massage, and edrophonium terminated the AT. AT arising from microreentry was identified in 20 patients. Their characteristics included the following: (1) AT could be reproducibly initiated and terminated with programmed stimulation; (2) fulfillment of the criteria for manifestation and concealed entrainment; (3) the interval between the initiating premature beat and the first beat of AT was inversely related to the premature coupling interval of atrial extrastimuli; (4) adenosine, dipyridamole, and verapamil terminated the AT in most cases.

The limiting factor in the analysis of mechanisms is the significant overlap in EP characteristics. For example, programmed stimulation may initiate and terminate both triggered activity and microreentry. However, although triggered activity may be dependent on cycle length, abbreviation of pacing cycle lengths may also predispose to reentry.

The use of adenosine to differentiate between AT mechanisms has provided inconsistent results, which may in part reflect different definitions used in a range of studies. However, more recent studies using a strict differentiation between focal and macroreentrant AT have reported more consistent results. Markowitz et al. observed that focal automatic ATs could be transiently suppressed but not terminated with adenosine, and ATs with characteristics consistent with microreentry or triggered activity terminated with adenosine use. By contrast, macroreentrant ATs were insensitive to adenosine. Iwai et al. observed similar responses to adenosine and used 3-dimensional electroanatomic mapping to delineate the tachycardia circuit, ensuring a clear distinction between focal and macroreentry.

In the era of catheter ablation, the relevance of tachycardia mechanism has been questioned. Chen et al. performed a literature search to determine whether mechanistic information altered ablation outcomes in patients with AT. The ATs were categorized as either automatic or nonautomatic. This study found that the mechanism of AT did not predict successful ablation or recurrence of AT after the initial success.

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here