Ablation of Focal Atrial Tachycardias




Abstract


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. Focal AT may result in the initiation of other atrial arrhythmias such as atrial macroreentry or atrial fibrillation 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.




Keywords

3-dimensional mapping, anatomy ablation, atrial tachycardia, crista terminalis, pulmonary veins

 




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.


Multiple Focal Atrial Tachycardia


This term must first be differentiated from the term multifocal AT, which refers to a continuously changing site of focal triggering most commonly observed in patients with advanced lung disease. Multiple focal ATs refer to the situation of having more than one sustained focal tachycardia. The second may be observed after ablation of the first, or rarely there may be competition between the two foci, with one triggering the other and vice versa. Hillock et al. described 10 patients in a series of 258 patients with AT who had more than one focus identified (4%). The mean age of these patients was 54 years, and all were women. There were seven patients with two ATs each and three patients with three ATs each. The locations of AT were the CT, CS ostium, TA, MA, and PV ostium. Successful ablation was performed for 22/23 (96%) tachycardias, and there were no recurrences of AT in those patients with successful ablation during 2 years of follow-up.


Tachycardia-Mediated Cardiomyopathy and Focal Atrial Tachycardia


In a recent series of patients with focal AT, incessant AT occurred in 25% of patients and TCM was present in 10%. TCM occurred in 37% of patients with incessant tachycardia. A comparison of the characteristics of patients with incessant AT who had TCM with those of patients who also had incessant AT but did not have TCM revealed no clear causative clinical differences, and it had been suggested that there may be an underlying genetic predisposition. Origin from atrial appendage sites was associated with a high incidence of incessant tachycardia (84%) and left ventricular (LV) dysfunction (42%). Origin from PV sites also carried a higher likelihood that the tachycardia would be incessant (59%). After successful ablation, LV function was restored in 97% of patients at a mean duration of 3 months. In long-term follow-up, LV function remained normal, but magnetic resonance imaging (MRI) revealed subtle abnormalities including minor LV dilatation, lower ejection fraction than the control group (while nevertheless in the normal range), and possible diffuse mild fibrosis on T 1 mapping. There were no definite regions of delayed enhancement. The clinical relevance of these late findings remains unknown.




Arrhythmia Diagnosis and Differential Diagnosis


Patients with focal AT may present with recurrent nonsustained bursts of narrow complex tachycardia or with sustained tachycardia, which at times can be difficult to differentiate from other SVT mechanisms or from atrial macroreentry.


Inappropriate Sinus Tachycardia Versus Focal Atrial Tachycardia


Differentiating AT from sinus tachycardia on the 12-lead electrocardiogram (ECG) can be difficult, particularly for tachycardias originating at the superior CT. Although the P wave in AT usually has a different morphology to the sinus P wave, in AT from the superior CT, the P wave may be clinically indistinguishable. An abrupt onset and termination of the tachycardia, or warm up and cool down over three to four beats favors AT, whereas sinus tachycardia gradually increases and decreases in rate over approximately 30 seconds to several minutes. Inappropriate sinus tachycardia (IAST) invariably presents as a long RP tachycardia (RP > PR), whereas focal AT may be either long or short RP depending on the AT rate and AV nodal conduction properties.


Patients with IAST have an abnormally fast resting heart rate with acceleration beyond that expected with minimal exercise. In one definition, the resting daytime heart rate exceeds 100 beats per minute and the average heart rate on 24-hour Holter monitor exceeds 90 beats per minute. It is important to exclude secondary causes of sinus tachycardia before making this diagnosis. In general, EP testing is not indicated in these patients unless a focal AT is being considered. Some incessant ATs can have a persistently elevated 24-hour rate with blunted variability. In these cases, the P wave is often abnormal in morphology and the nocturnal rate remains elevated. However, even here there can be considerable variability. IAST should be distinguished from postural orthostatic tachycardia (POT) syndrome, which is characterized by a marked increase in rate (generally >30 beats per minute) during adoption of upright posture. This may represent an overlap syndrome.


In the EP laboratory, the hallmark of AT is that it should be inducible with programmed stimulation. In the presence of isoproterenol, a focal tachycardia will show sudden onset often with the initiating tachycardia P wave located within the preceding T wave, and there is usually a sudden shift in the site of focal activation. In the case of IAST, there is a gradual increase in sinus rate with earliest activation at the superior CT.


To summarize, in comparison with IAST, focal AT (1) has sudden onset and termination; (2) frequently demonstrates tightly coupled activity with the P wave in the T wave at the time of onset (by contrast, IAST has gradual increase in rate); (3) has a fixed site of origin. Acceleration may occur in response to isoproterenol, but the site of origin does not change (by contrast, in IAST, the site of activation shifts superiorly along the CT with isoproterenol); (4) demonstrates normal heart rate in between paroxysms of AT; and (5) frequently demonstrates a nonsinus PWM.


Atrial Tachycardia Versus Atrioventricular Nodal Reentrant Tachycardia/Atrioventricular Reentrant Tachycardia


Differentiation of AT from atrioventricular nodal reentrant tachycardia (AVNRT) or atrioventricular reentrant tachycardia (AVRT) on the 12-lead ECG can be difficult. Although most commonly associated with a long RP interval, AT can occur with either a short RP interval or a long RP interval depending on the tachycardia rate and the AV conduction interval at a given rate. It can therefore mimic either typical or atypical AVNRT and AVRT. If the ECG trace shows persistent tachycardia with AV block or inconsistency (unhooking) of the ventriculoatrial (VA) relationship during ongoing tachycardia, then this suggests an AT. The observation of termination in which the last event is a nonpremature P wave generally excludes AT. Another clue to the diagnosis is the presence of an inferior P wave axis. With some rare exceptions, this excludes AVRT or AVNRT as it suggests an origin high in the atrium. A superiorly directed P wave vector may indicate AVRT or AVNRT or an AT focus originating from the CS ostium or annular structures. Automatic AT may also manifest with recurrent self-limiting bursts of tachycardia that can exhibit warm up and cool down phases, and this appearance is almost diagnostic of focal AT.


Several classical studies have proposed a variety of tachycardia features and pacing maneuvers to differentiate AT from AVNRT and AVRT in the EP laboratory. Knight et al. investigated the diagnostic value of these features and pacing maneuvers in 196 patients with SVT, of whom 25 had AT. Multiple baseline observations and tachycardia features were evaluated. Pacing maneuvers assessed were atrial pacing during SVT just below the tachycardia cycle length (TCL); atrial pacing during SVT at the longest cycle length that resulted in AV block; ventricular pacing during SVT just below the TCL; burst ventricular pacing for three to six beats at a cycle length of 200 to 250 ms; and scanning diastole with a premature ventricular extrastimulus. AT could not be consistently identified by any single feature or maneuver; however, certain features were useful: AT required isoproterenol for induction more often than AVNRT or AVRT, although the predictive value was poor. Surprisingly, the presence of AV block with persistent tachycardia did not discriminate between AVNRT and AT. However, spontaneous termination of tachycardia with AV block excluded AT. This was seen in 28% of patients. Following ventricular pacing with atrial entrainment and an atrial activation sequence different from tachycardia, the presence of a V-A-A-V response was diagnostic of AT ( Fig. 10.2 ). Inability to entrain the atrium during ongoing tachycardia caused by VA block had an 80% positive predictive value (PPV) for AT. Conversely, tachycardia termination during burst ventricular pacing that did not depolarize the atrium excluded the diagnosis of AT. AT was also excluded when a premature ventricular beat was introduced during the refractory period of the His bundle, and there was either advancement of atrial activation or tachycardia termination without atrial depolarization. The presence of a fixed VA interval on the first beat after atrial pacing (within 10 ms of the VA interval during tachycardia) had a high negative predictive value (NPV) for AT. However, this observation did not completely exclude AT, as apparent VA linking may occur because of coincidental events. Conversely, if the VA interval could be unhooked after the cessation of pacing, then AT is likely to be present. However, variable VA conduction can occur after pacing in AVNRT, and therefore this observation is not specific for AT.




Fig. 10.2


Surface electrocardiography and intracardiac recordings at the initiation of an atrial tachycardia. Last two beats of a ventricular drive train followed by a ventricular extrastimulus (left) . The atrial activation follows the ventricular pacing. There is initiation of tachycardia with a V-A-A-V response indicating an atrial tachycardia. Note that this response applies equally on initiation as during entrainment. CS , Coronary sinus; d , distal; HBE , His bundle electrogram; p , proximal.


Focal Atrial Tachycardia Versus Macroreentrant Atrial Tachycardia


In most cases of focal AT, it is possible to observe a discrete P wave with an intervening isoelectric interval ( Table 10.1 ). However, when the atrial rate is very rapid and if atrial conduction slowing is present, there may be no isoelectric baseline and the appearance may mimic that of macroreentrant AT. Conversely, whereas macroreentrant AT frequently demonstrates a continuous undulation without an isoelectric period on the 12-lead ECG, patterns resembling focal AT (with an isoelectric period) have also been described particularly in the context of extensive atrial scarring and LA foci. LA macroreentry in such patients can classically exhibit low-amplitude P waves and long isoelectric intervals. Ultimately, an EP study is required for a definitive diagnosis of focal AT.



TABLE 10.1

Focal Atrial Tachycardia Versus Macroreentry or Small Circuit (Microreentry)












































Focal Macroreentry Microreentry
Most common SHD None SHD/CHD/AF RFA AF RFA
ECG isoelectric interval Yes No Yes
Record from >80% of CL No Yes Yes
Entrain with PPI-TCL <20 ms Yes Yes Yes
Entrain PPI-TCL < 20 ms, two sites > 2 cm apart No Yes No
Activation pattern Radial Large loop Radial
Ablation approach Focal Linear or focal Focal

AF, Atrial fibrillation; AT, atrial tachycardia; CHD, coronary heart disease; CL, cycle length; PPI, postpacing interval; RFA, radiofrequency ablation; SHD, structural heart disease; TCL, tachycardia cycle length.


In focal AT, the origin of atrial activation can be localized with endocardial mapping to a small area from which there is radial spread. Occasionally, the presence of anatomic or functional barriers conduction may result in regions of preferential conduction. Nevertheless, in focal AT, intracardiac recordings demonstrate large portions of the cycle length without activity, correlating with the isoelectric interval on the surface 12-lead ECG. Conversely, in macroreentrant AT, it is generally possible to record activity throughout the TCL. Furthermore, whereas focal AT caused by microreentry may be successfully entrained, the ability to entrain an AT with characteristics of being in the circuit (postpacing interval [PPI] minus the TCL of < 20 ms) from two sites greater than 2 cm apart is diagnostic of macroreentry. It will be possible to entrain a reentrant focal AT, but the PPI-TCL will only indicate a site in the circuit in the immediate vicinity of the focus.


The rate of the tachycardia does not help in discriminating between focal and macroreentrant AT, as the rate ranges of both focal AT and macroreentrant AT are too wide to be reliably used for determination of arrhythmia mechanism. The rate range of focal AT is usually between 130 and 250 beats per minute, but may be as low as 100 beats per minute or as high as 300 beats per minute. Similarly, although macroreentrant AT usually has a rate between 240 and 310 beats per minute, conduction delays within the circuit either caused by atrial pathology or use of conduction slowing antiarrhythmic medications may slow the rate to less than 150 beats per minute.


With the advent of 3-dimensional mapping systems, small circuits with properties between those of microreentry and macroreentry have been described. , These reentrant circuits occur in a localized region with a diameter of 1 to 2 cm and have been described around a PV, in the anterior LA and in the septum. Evidence of markedly slowed conduction is usually present, and many of these patients have had prior ablation procedures. These tachycardias often have a PMW consistent with a focal AT , ( Box 10.1 ).



BOX 10.1


Focal AT may be a long or short RP tachycardia. No single diagnostic maneuver for focal AT. Therefore multiple approaches are used.




  • Focal AT suggested in the following cases:




    • Inferior P wave axis.



    • Multiple spontaneous bursts of tachycardia with warm up and cool down.



    • V-A-A-V response to ventricular overdrive pacing.



    • Unhooking of the VA relationship (can occur in AVNRT).




  • AT ruled out in the following cases:




    • V-A-V response to ventricular overdrive pacing.



    • Spontaneous termination with a nonpremature A as the last event.



    • Advancement/delay or termination of the tachycardia with a ventricular extrastimulus when His bundle is refractory.



    • Tachycardia termination with burst ventricular pacing that does not depolarize the atrium.



    • Inability to entrain the atrium during ongoing tachycardia caused by VA block (can occur in AVNRT).



    • VA interval hooked on first return beat after atrial pacing (rarely can occur fortuitously).




  • In comparison with IAST, focal AT




    • Has sudden onset and termination or warms up and cools down within several beats.



    • Frequently demonstrates tightly coupled activity with the P wave in the T wave at the time of onset. By contrast, IAST has gradual increase in rate.



    • Has a fixed site of origin. Acceleration may occur in response to isoproterenol administration, but site of origin does not change. By contrast, in IAST the sites of activation shift superiorly along the crista with isoproterenol.



    • Demonstrates normal heart rate in between paroxysms of atrial tachycardia.



    • Frequently has a nonsinus P wave morphology.




AT, Atrial tachycardia; AVNRT, atrioventricular nodal reentrant tachycardia; IAST, inappropriate sinus tachycardia; VA, ventriculoatrial.

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Feb 21, 2019 | Posted by in CARDIOLOGY | Comments Off on Ablation of Focal Atrial Tachycardias

Full access? Get Clinical Tree

Get Clinical Tree app for offline access