Impact of Mapping Technologies

Extensive activation sequence mapping is typically used in the electrophysiology laboratory to define the presumptive mechanism of AT and plan an ablation strategy. Technologies for mapping arrhythmias include basket mapping, electroanatomic mapping, and noncontact mapping systems. The mapping technologies have definite advantages over point-by-point catheter mapping, including the ability to map unstable, poorly reproducible, and nonsustained arrhythmias. With these technologies, short episodes of arrhythmias can be mapped with one or several beats, or the arrhythmia substrate can be mapped for areas of low voltage or double potentials. Many series describing the use of each of these new technologies to map and ablate ATs have been reported.17,18 These technologies typically are accompanied by decreased fluoroscopic exposure for the operator, more precise localization of tachycardia, and a better appreciation of atrial anatomy.

These advanced mapping systems have been found to facilitate identification and ablation of ATs arising from the atrial chamber, the atrial septum, pulmonary veins, superior vena cava (SVC), or coronary sinus. Color-coded display of activation timing is highly useful in demonstrating the site of origin of focal ATs. The color-coded display of chamber geometry within three-dimensional space provided by these mapping systems helps to visualize the complex anatomy and relationships between cardiac structures that cannot be fully appreciated with the use of fluoroscopic imaging. The three-dimensional anatomic display is useful in defining the left atrial anatomy along with the locations of pulmonary veins. The variable projections of the electroanatomic system allow individually optimized views of the target area, display of the tip and distal shaft of the ablation catheter, and the potential for precise navigation to predetermined sites. Furthermore, newer mapping technologies can overcome some of the difficulties of traditional point-to-point catheter mapping of activation sequence, which is burdensome and compounded by the lack of accurate reproducibility of catheter location based on fluoroscopic projection alone. The ability to collect a large number of points with high spatial resolution (1 to 2 mm) enables the construction of a detailed activation map that is combined with the three-dimensional anatomy of the relevant chamber. This information provides valuable insight into the mechanism of tachycardia, the anatomic origin, and the relationship to other cardiac and extracardiac structures that are useful to guide ablation. Color-coded maps of myocardial voltage at each point also can provide a map of the cardiac chamber voltage, which is helpful for identifying areas of scar and substrate abnormalities and could provide insight into the underlying disease process or pathophysiology. The ability to navigate the catheter in three-dimensional space without exposure to ionizing radiation is a valuable benefit for both patient and operator. Furthermore, use of these systems can reduce procedural time and promote success and safety during ablation of complex arrhythmias. Finally, the ability to register the precise location of individual ablative lesions within the heart offers a significant advantage over fluoroscopy alone.

A limitation of these systems that must be recognized and is important in studying focal ATs is that the earliest activation within a given chamber will be recorded as the site of origin (i.e., earliest activation within that chamber), even if the arrhythmia arises from another chamber. This is especially important to recognize in performing electroanatomic mapping of the right atrium when the tachycardia originates from the left atrium (LA) or pulmonary veins. Failure to appreciate this issue fully can result in unsuccessful prolonged attempts being made to ablate focal tachycardias from the right atrium before the need to perform detailed left-sided mapping is recognized and successful ablation is ultimately enabled.

In one study, electroanatomic mapping (CARTO; Biosense, Webster, California) of the right atrium was performed during 13 tachycardia episodes in 10 patients who had previous cardiac surgery.¹⁹ Focal ATs were defined in three patients, and macroreentrant circuits were found in seven patients. The mapping system allowed rapid distinction between a focal AT and a macroreentrant mechanism. In the patients with focal mechanisms, a radial spread of activation was noted from the site of earliest activation in all directions on an isochronal map (Figure 73-1). The right atrial activation time was markedly shorter than the tachycardia cycle length, accounting for, an average of 14% of the tachycardia cycle length. In patients with a macroreentrant mechanism, isochronal maps showed a continuous progression of activation around the right or left atrium, with close proximity of earliest and latest local activation (Figure 73-2). The right atrial activation time was in a range similar to that of tachycardia cycle length, occupying 70% or more of the tachycardia cycle length.

Sanders et al.²⁰ reported on the use of high-density mapping of focal AT. They used a high-density mapping catheter (PentaRay; Biosense) to characterize a group of patients in whom prior attempts at atria tachycardia ablation or atrial fibrillation ablation were unsuccessful.²⁰ They noted that a localized focus was found in 70%, whereas 30% had evidence of localized reentry characterized by the ability to record electrograms during 95% of the tachycardia cycle length. They demonstrated that with high-density mapping, it was possible to define regions of preferential conduction and intraatrial conduction delay. Higa et al.²¹ associates made similar observations using the technique of noncontact mapping. These investigators demonstrated that focal AT originates from a small area of tissue but spreads through the atrium by way of regions of preferential (rather than centrifugal) conduction. These investigators made several other notable observations: most ATs originate near a border of a low-voltage zone or an area of anisotropic conduction, and the site of successful ablation is near the site of tachycardia origin or the proximal portion of the preferential conduction pathway, rather than at the “breakout” point.

Atrial Tachycardia Arising from the Crista Terminalis

Atrial tachycardias can be located all along the CT, which has been described as a “ring of fire” because it is a common location for ATs in patients without structural heart disease, accounting for two thirds of right ATs in one study (Figures 73-5, 73-6). One physiological factor contributing to the clustering of ATs in this area is that the CT demonstrates marked anisotropy because of poor transverse cell-to-cell coupling, which could contribute to slow conduction and microreentry. Another contributing factor is that the CT contains clusters of cells with automaticity. The ECG characteristics of these tachycardias were described earlier and depend on site of origin from the CT (e.g., superior versus inferior). Intracardiac echocardiography can be useful to demonstrate the close anatomic proximity of the tachycardia focus to the crista during mapping. Ablation of tachycardias arising from the superior CT carries a small risk of damage to the phrenic nerve resulting in diaphragmatic paralysis.

Differentiating ATs originating at the superior CT from sinus tachycardia can be difficult at times in diaphragm paralysis. There may be subtle differences in the P wave morphology in AT originating in the superior CT compared with the sinus P wave. Administration of isoproterenol can help to differentiate sinus tachycardia from superior crista, focal AT. The origin of earliest activation in sinus tachycardia will move superiorly up the CT with isoproterenol, whereas in focal AT, isoproterenol will increase the AT rate, but the location of earliest atrial activation will not change substantially.

Atrial Tachycardia Arising from the Tricuspid Atrioventricular Annulus

The tricuspid annulus probably represents the second most common location of right-sided ATs. In several series, tachycardias arising from the tricuspid annulus accounted for 13% to 22% of right ATs.³³ Tricuspid annular AT has negative or notched P waves in V1 and invariably positive P waves in lead aVL. Reports describe foci from around the entire circumference of the tricuspid annulus. Inferior foci tend to have negative P waves in leads II, III, and aVF, whereas superior foci are usually isoelectric or positive in these leads. Foci from the superior tricuspid annulus and the RAA have similarity P wave morphologies, consistent with their close proximity. The presence of myocytes with AV nodal-type electrophysiologic characteristics around the entire tricuspid annulus has been described in animals.³⁴ These cells are histologically similar to the atrial cells but resemble nodal cells in their cellular electrophysiology, response to adenosine, and lack of connexin43. These cells can serve as the substrate for AT originating from around the tricuspid annulus.

Atrial Tachycardia Arising from the Right Atrial Appendage and Superior Vena Cava

The RAA is an uncommon site of origin for AT (<5% of ectopic ATs in several series), although both appendages are a more common site for incessant ATs.35–37 The appendage is composed of ridges formed by pectinate muscles, which arise from the CT. The characteristic electrocardiographic pattern associated with RAA tachycardia shows negative P waves in lead V₁ that become progressively positive across the rest of the precordial leads, along with upright P waves in the inferior leads, positive or isoelectric-positive in lead I, and an inverted P wave in lead aVR. As with other right ATs that arise from the superior crista, RAA can be confused with sinus tachycardia. At least one case series has suggested that RAA tachycardias arise more commonly in younger male patients and can manifest as an incessant tachycardia resulting in left ventricular dysfunction secondary to tachycardia-induced cardiomyopathy.^35,38

Catheter ablation of focal RAA tachycardia is relatively straightforward and has high success rates.35,38 However, there are at least two case reports of RAA tachycardias that were more challenging to eliminate with catheter ablation. One case of RAA tachycardia that which originated in the inferior/lateral aspect of the appendage could not be ablated despite multiple attempts using manual catheter ablation, but it was successfully ablated using magnetic navigation.³⁹ Another case of an AT that originated at the apex of the RAA was resistant to catheter ablation and required surgical right atrial appendectomy to eliminate the tachycardia.⁴⁰

The SVC is an uncommon site of origin for focal ATs (<2%).41,42 Cardiac muscle extends for a distance into the SVC in human hearts, and the electrophysiological characteristics of the SVC and RA muscle are similar. AT originating in the SVC can arise from 1 to 3 cm above the SVC-RA junction and conduct to the right atrium in a 1 : 1 manner or with variable conduction delay or block. AT arising from the area of the SVC demonstrates a P wave morphology that is positive in leads I, II, III, and aVF, isoelectric or negative in lead aVL, biphasic (positive then negative) in lead V₁, and positive or isoelectric in leads V₂ to V₆ (Figures 73-7, 73-8). Radiofrequency (RF) catheter ablation of SVC foci is usually successful in eliminating tachycardia. Rather than directly targeting the AT focus in the SVC, an alternative strategy is electrical disconnection of the SVC muscle sleeve at the SVC-RA junction in a circumferential or segmental fashion or isolation of the arrhythmogenic area from the rest of the SVC. Careful attention should be paid to avoid injury to the phrenic nerve during ablation in this region, and complete SVC isolation is best avoided because of the risk of SVC stenosis.⁴³ The SVC also has been reported as having a role in arrhythmia initiation and maintenance in 5% to 10% of patients with paroxysmal AF.⁴⁴ Fibrillatory conduction from a focus in the SVC with exit block to the right atrium masquerading as a focal right AT also has been reported.⁴⁵

Atrial Tachycardia Arising from the Coronary Sinus

Focal ATs were reported to arise from the coronary sinus area in up to 10% of patients in one study.²⁶ Most patients had tachycardia arising from outside the coronary sinus or just inside the os (Figures 73-9, 73-10).⁴⁶ AT also arose from deep within the coronary sinus, presumably from the coronary sinus musculature, based on the observation that the tachycardia could not be ablated from the left atrial endocardium but could be ablated from within the coronary sinus.⁴⁷ The arrhythmogenic substrate is believed to be the muscular sleeves on the epicardial atrial surface surrounding the coronary sinus and extending from the CS ostium to the lateral aspect of the mitral annulus. In human hearts, the CS musculature provides electrical connections to the LA most prominently at the proximal portion and activation from the RA can conduct to the LA via these electrical connections. A discrete potential is noted after the coronary sinus electrogram in sinus rhythm and preceding the surface P wave by 30 to 50 ms during tachycardia. Successful ablation sites typically have activation at least 20 ms before the onset of the P wave.⁴⁷ Macroreentrant ATs can also involve the coronary sinus and require ablation on the left atrial endocardial surface as well as the coronary sinus.

The electrocardiographic pattern of ATs arising from the CS musculature is somewhat typical, with deeply negative P waves in the inferior leads and positive P waves in aVR. As such, the morphology of the ECG during focal AT arising from CS can be similar to and can be confused with that of typical counterclockwise atrial flutter (AFL), which has an exit site at the CS ostium. Notably, tachycardia foci from the CS ostium have characteristic P wave morphologies in the precordial leads. Lead V₁ is biphasic with an initial component that is either isoelectric or mildly inverted (when timed to onset of the P wave in inferior leads) followed by an upright component. Across the precordial leads, the initial component becomes more negative and the second component becomes isoelectric. Foci located within the body of the CS will have a P wave in V₁ that is upright from the onset, without an isoelectric segment and P waves across the precordial leads that are frequently upright (Figure 73-11).

Atrial Tachycardia Arising from the Atrial Septum and Para-Hisian Regions

Focal ATs originating in the area of the atrial septum in the vicinity of the atrioventricular node include AT arising from the anterior, mid-, and posterior septal regions and from the apex of the triangle of Koch (e.g., the para-Hisian region).48–52 These tachycardias, like ones arising from near the tricuspid and mitral annuli, tend to be more sensitive to lower doses of adenosine than ATs arising from the CT. In addition, in one study, 45% of patients with a septal tachycardia required isoproterenol for tachycardia induction, compared with 32% of patients with AT originating in the right atrial free wall.

Anteroseptal and midseptal right ATs have a biphasic or negative P wave morphology in lead V₁. The combination of a negative or biphasic P wave in V₁ and a positive or biphasic P wave in all inferior leads favors an anteroseptal AT. The presence of a negative or biphasic P wave in V₁ and a negative P wave in at least two of the three inferior leads favors a midseptal AT. The presence of a positive P wave in V₁ and a negative P wave in all three inferior leads favors a posteroseptal AT. The electrophysiology study is critical for differentiating these tachycardias from atypical AV node reentry or a septal accessory pathway. In several series, 27% to 35% of patients had tachycardias originating from this region.

Atrial tachycardias can originate from near the apex of the triangle of Koch (i.e., anteroseptal tricuspid annulus, in close proximity to the His bundle recording) in 10% or more of patients with tachycardias arising from the right atrium. A location is considered para-Hisian when either a His deflection is observed at the site of earliest atrial activation during tachycardia or the successful ablation site along the tricuspid annulus is within 1 cm of a site recording the His bundle potential.⁵²

It has been proposed that para-Hisian ATs have properties consistent with AT arising circumferentially along the tricuspid annulus, and as such should be considered a subset of this broader group of annular ATs.⁵² Atrial tissue surrounding the AV annuli is specialized and distinct from other atrial myocytes. Periannular cells are similar to atrial cells histologically, but can resemble AV nodal transitional cells electrophysiologically. There is controversy in the literature regarding the pharmacologic behavior and mechanism of these para-Hisian ATs. Some reports indicate that these tachycardias are adenosine and verapamil-sensitive, whereas others report that they are adenosine-insensitive.⁵³ Some reports of ATs from the apex of the triangle of Koch suggest reentry as the underlying mechanism, whereas others argue that triggered activity is the most likely potential mechanism.^52,54

ECG findings suggestive of a para-Hisian AT include narrowing of the P wave during AT compared with sinus rhythm, and biphasic P waves in V₁, with the dominant positive or negative component having a polarity opposite to that observed in the inferior leads (Figures 73-12, 73-13). Some but not all reports suggest that a left-sided para-Hisian AT origin is associated with positive P waves in lead V₁.^50,51 The P waves are consistently positive or isoelectric in leads I and aVL. The P wave morphology in the inferior leads may show two distinct patterns: (1) negative or biphasic with terminal negativity or (2) positive or biphasic P waves and terminal positivity. The P wave morphology in the inferior leads during tachycardia is determined largely by the route of left atrial activation: via the posteroinferior input from the coronary sinus versus via the Bachmann bundle.

Catheter ablation of this form of AT originating in the perinodal region is safe and effective. In most patients, these tachycardias can be ablated without damage to AV nodal conduction. In a recent detailed multicenter report of focal ATs arising exclusively from the para-Hisian region in 38 patients, catheter ablation was attempted in 30 patients and was successful in 26 (87%).⁵² Notably catheter ablation was not attempted in eight patients because of patient preference in avoiding the potential risk of complete AV block or left heart catheterization. RF energy was applied in 22 patients, and cryoenergy was applied in eight patients. Two patients had transient 2 : 1 AV block that resolved during the procedure. Two other patients had a prolonged PR interval after ablation.

In cases of para-Hisian AT, it is important to map both the right and left atrial septum (and the noncoronary cusp; Figure 73-14). Atrial activation mapping on the right side alone will not differentiate between a right and left atrial site of tachycardia origin, implying rapid direct transseptal conduction by way of the Bachmann bundle, which results in an early right-sided breakthrough. In one series of 16 patients with the earliest atrial activation in the triangle of Koch, a left atrial focus was found in nearly 40% of patients.

There are a number of reports demonstrating that RF energy applications within the aortic sinuses of Valsalva can eliminate focal ATs originating from near the atrioventricular node or para-Hisian region.55–64 Of note, many of the patients in these reports had undergone multiple previous unsuccessful ablation procedures before successful ablation of ATs from the aortic sinuses. When earliest activation is recorded in the proximal electrode of the His-bundle catheter, but ablation in this region cannot eliminate tachycardia, then consideration should be given to attempting ablation from within the aortic sinus of Valsalva.

Each of the aortic sinuses of Valsalva, is in contact with the atrial myocardium, which enables mapping and ablation of some ATs from the aortic sinuses of Valsalva. In a recent series, among 113 patients with AT, 13 patients had midseptal to anteroseptal AT and 12 patients (9%) underwent successful ablation from the noncoronary cusp (n = 10), right coronary cusp (n = 1) or left coronary cusp (n = 1) without complication.⁶⁴ During long-term follow up, AT recurred in only one patient.

The majority of these ATs are successfully ablated within the noncoronary sinus of Valsalva (NSV). ATs successfully ablated from the NSV typically have a negative/positive P wave in lead V₁, isoelectric P in lead I, and upright or biphasic (with terminal positivity) P wave morphology in the inferior leads. The NSV is adjacent to the epicardial aspect of the atrial myocardium located between the right and left atria, immediately anterior to the interatrial septum. The fast pathway input to the AV node is located in close proximity to the anterior portion of the NSV. RF applications at the NSV result in left atrial lesions located between the floor of the fossa ovalis and the mitral annulus. This area can be difficult to position an ablation catheter with sufficient stability and adequate tissue contact using either a retrograde or transseptal approach. Catheter stability within the NSV allows for the creation of lesions in the deeper tissues that are otherwise not accessible.

A few ATs have been reported to have been successfully ablated within the right or left sinus of Valsalva.61–63 In one study, a negative/positive or isoelectric P wave in leads I and aVL was supportive of a left sinus of Valsalva AT versus an NSV AT in which positive P waves in leads I and aVL were observed.

Analysis of electrograms can be helpful for identifying the correct positioning of the mapping and ablation catheter at the aortic sinuses of Valsalva during the ablation procedure. NSV electrograms during sinus rhythm have a larger atrial amplitude than ventricular amplitude, which differs from left and right sinus of Valsalva electrograms.⁶³

Most reported cases of catheter ablation of NSV tachycardias originating from near the AV node or His bundle region have not resulted in impairment of AV conduction. Whether or not a His-bundle potential can be recorded at the NSV should be assessed before the RF energy application to avoid this particular complication.

In addition, before performing catheter ablation within the aortic sinuses of Valsalva, coronary angiography or selective angiography of the aortic sinuses should be performed to ensure that the distance between the ablation catheter and coronary ostium is more than 10 mm. Coronary angiography should be performed again after the ablation procedure to rule out any coronary spasms, stenoses, or occlusions. An alternative approach to coronary angiography uses intracardiac echocardiography to localize the catheter within the NSV.

In summary, tachycardias located in atrial septal region require careful mapping of both sides of the septum and, in some cases, mapping and ablation in the aortic sinuses of Valsalva. The aortic root occupies a central location between the tricuspid and mitral annulus and in close vicinity to the His bundle. Because of the close proximity of these ATs to the AV node, care needs to be taken to avoid AV block during ablation. However, successful radiofrequency ablation is achievable in the majority of cases without complication.

Left Atrial and Pulmonary Vein Tachycardias

Focal tachycardias originating in the LA and pulmonary veins not associated with prior catheter ablation for AF form an important subset of all ATs, reportedly constituting 10% to 40% of all focal ATs.26,65 These tachycardias can occur in a wide spectrum of clinical settings ranging from structurally normal hearts to advanced cardiac disease and in patients who have undergone a cardiac or lung transplant.^32,65,66 Catheter ablation is a generally successful treatment for these focal ATs, including those refractory to pharmacologic therapy. Left atrial and pulmonary vein tachycardias occur commonly in patients following ablation for AF, but will not be discussed here.

The pulmonary veins and mitral valve annulus are the main source of focal left ATs. A majority of pulmonary vein tachycardias originate from the ostium, rather than from deep inside the veins with a strong propensity for the superior veins. In addition, it is rare for ATs to recur from different sites in the pulmonary veins or for atrial fibrillation to develop after a pulmonary vein focal ablation.67–69 Therefore, unlike patients with PV triggers and atrial fibrillation in which there are usually multiple triggers in multiple veins and the pathophysiology involves a diffuse, chronic process often with extensive atrial remodeling, patients whose sole clinical arrhythmia is AT appear to have an isolated or focal process. As such, patients with focal left-sided AT are curable in the long term with focal ablation.

Superior (Bachmann bundle), inferior (coronary sinus), and septal (fossa ovalis) interatrial electrical connections exist between the right and left atria. Additional posterior electrical connections between the right-sided pulmonary veins and right atrial posterior walls exist in human hearts. This can compound the difficulty differentiating between an AT originating from the pulmonary veins and one arising from the posterior right atrium. Focal AT from the PV usually has a positive P wave across the precordium, from V₁ to V₆. Careful analysis of the P wave configuration in V₁ may be helpful; the posterior right atrial sites have a biphasic P wave in V₁, with a positive-negative configuration, and the right superior pulmonary vein sites have a positive P wave in V₁ (Figure 73-15). A second differentiating feature is that P waves from the right superior pulmonary vein show notching in lead II in 80%, but are smooth in those coming from the region of the SVC.

Analysis of electrograms recorded from the posterior right atrium, CS, and His bundle regions during AT often reveals two components consisting of near-field and far-field components, which can assist in determining whether the tachycardia originates in the right or left atria.⁷⁰ In the right atrial electrograms, when the amplitude of the first component (near-field electrogram, a sharper electrogram) is higher than that of the second component, the AT originates in the right atrium. Likewise, analysis of CS electrograms consisting of a near-field component from CS musculature and a far-field component from left atrial myocardium can uncover LA activation preceding right atrial activation. Similarly, near-field and far-field components from RA and LA activation can be identified on the His bundle atrial electrograms.⁷⁰ A near-field electrogram followed by a far-field signal on the His bundle electrogram during AT suggests a probable right atrial focal AT, whereas a far-field followed by a near-field electrogram sequence predicts the need for LA access.

Although the limitations and accuracies of these algorithms have been discussed previously, P wave characteristics can assist in the localization of the focus to a particular PV. P waves from the left-sided PVs are generally broad in V₁ and are notched, particularly in the inferior leads but also in V₁. A positive P wave in lead I suggests a focus in the right-sided PV, and an inverted P wave suggests a left-sided PV. An upright P wave in aVL is consistent with a right-sided PV focus; however, right-sided PV can also have negative P waves in aVL. The inferior leads can be used to differentiate superior from inferior PV sites (tall and upright versus low amplitude or inverted).

Atrial Tachycardia Arising from the Mitral Atrioventricular Annulus

The mitral annulus is the second most common location of focal AT in the LA, after the pulmonary vein region. Interestingly, there appears to be a clustering of these foci around the superior aspect of the mitral annulus in immediate proximity to the region of the left fibrous trigone at the aortic-mitral continuity. A superior mitral annular location (as well as a location along the left side of the atrial septum or at the noncoronary cusp) should be considered for AT when the earliest right atrial activity is recorded in the para-Hisian region (approximately 0 to 20 ms before P wave onset) and the P wave demonstrates a characteristic morphology consisting of a biphasic (negative followed by positive) appearance in the precordial leads and a low amplitude appearance in the limb leads.71,72 Lead aVL is negative or isoelectric, and the inferior leads are positive during ATs arising from the superior mitral annulus. These ECG findings have a sensitivity of 88% and a specificity of 99%. The initial negative component of the P wave in lead V₁ is unusual for left ATs, but it can be explained by the relatively anterior position of the mitral annulus in this region. Focal ablation of these tachycardias usually is successful. It is speculated that remnants of the developing specialized conduction system at the mitral annulus-aorta junction could be the underlying substrate of this arrhythmia.⁷¹ Myocardial cells at the mitral annulus-aorta junction exhibit AV node–like electrophysiologic properties, respond to adenosine, lack connexin, and give rise to catecholamine-induced triggered activity owing to delayed afterdepolarizations.^73,74

Atrial Tachycardia Arising from the Left Atrial Appendage

Atrial tachycardia can arise from the left atrial appendage (~2% of sustained ATs). LAA tachycardias are often incessant and are associated with tachycardia-mediated cardiomyopathy in some cases. The P wave during LAA tachycardias is deeply negative in leads I and aVL, which has a sensitivity of 92% and a positive predictive accuracy of 92% with a specificity of 97%, highly positive in the inferior leads, and broad and positive in lead V₁.75,76 The atrial activation sequence typically shows activation in the distal coronary sinus earlier than the P wave.

A recent report indicated that focal AT originating from the distal portion of the left atrial appendage could be ablated successfully and acutely with RF energy in 13 of 14 patients, with no long-term recurrences in the 13 successful cases.⁷⁷ However, in some reported cases, elimination of AT arising from the body or apex of the LAA is refractory to endocardial catheter ablation.⁷⁸ This result is similar to what was described earlier for tachycardias arising from the RAA and is likely related to the complex, blind cul-de-sac, heavily trabeculated anatomy of the left atrial appendage that makes it difficult to manipulate catheters safely or to apply sufficient contact force at the LAA apex. Rarely, a left atrial appendage tachycardia will need to be ablated epicardially, eliminated via surgical left atrial appendectomy, or abolished via thoracoscopic appendage exclusion.^79–83

Sinus Node Reentrant Tachycardia

Tachycardias arising from this region are presumed to be due to microreentry in tissue near the sinus node or perinodal region (superior CT). The P wave morphology during tachycardia should be identical to that seen during sinus rhythm.

Inappropriate Sinus Tachycardia

The uncommon, poorly characterized entity of inappropriate sinus tachycardia is probably a heterogeneous disorder. The hallmark feature of this syndrome is a consistently elevated resting heart rate (>95 beats/min) and an exaggerated heart rate response to low levels of physical activity. The average sinus rate during 24-hour Holter monitoring usually is greater than 90 beats/min, and a persistent increase of at least 25 beats/min occurs when arising from supine to an upright position, in the absence of orthostatic arterial hypotension. Some affected patients have an elevated intrinsic heart rate, and others have increased responsiveness to infusions of isoproterenol. The ECG characteristics of this tachycardia include an identical P wave configuration in tachycardia and sinus rhythm. It is likely that some patients have primary autonomic abnormalities, including postural orthostatic tachycardia syndrome in some. Some patients may have primary abnormalities of the sinus node. A recent analysis of 18 patients with inappropriate sinus tachycardia receiving intravenous adenosine (0.1 to 0.15 mg/kg) showed that these patients demonstrated a blunted response, with less sinus cycle length prolongation than age-matched control subjects undergoing electrophysiology studies.⁸⁴ The blunted response was also seen after pharmacologic autonomic blockade. These observations suggest that structural abnormalities of the sinus node are responsible for this syndrome. A recent report⁸⁵ suggested that β-adrenergic receptor autoantibodies are involved in the mechanism of inappropriate sinus tachycardia. In the electrophysiology laboratory, a distinction should be made between inappropriate sinus tachycardia and a focal automatic AT with an origin close to the superior CT.⁸⁵

Classification

Macroreentrant ATs can be divided into those that are isthmus dependent (i.e., dependent on conduction through the tricuspid annulus–inferior vena cava isthmus) or not isthmus dependent.¹ A majority of macroreentrant ATs in the adult population are isthmus dependent. A majority of non–isthmus-dependent macroreentrant ATs are related to an area of scar, often from a previous surgical incision. Some examples of macroreentrant ATs include typical atrial flutter, lower loop reentry, double-wave reentry, macroreentrant AT from the right atrial free wall, and macroreentrant ATs occurring in the right or left atria related to previous surgery, including atriotomy, surgical scarring, and the presence of septal prosthetic patches, suture lines, or other anatomic obstacles. An increasing frequency of macroreentrant left ATs is currently being seen after atrial fibrillation ablation. Some unusual causes of macroreentrant tachycardia include reentry at sites of donor recipient anastomosis from either orthotopic heart transplantation or lung transplantation.⁹¹ Recently there has been increased recognition of macroreentrant ATs arising from scarring in patients who have not undergone previous atrial surgery or catheter ablation. Such spontaneous scarring has been described in the posterior wall of the LA, as well as in the posterolateral and lateral right atrium, and is recognized as part of an atrial cardiomyopathy.^92,93 The successful ablation electrogram in these cases is frequently characterized by a long fractionated signal, middiastolic signal, broad, fragmented signal that encompasses much of the tachycardia cycle length.

Diagnostic Maneuvers

Electrophysiological characterization, mapping, and ablation of macroreentrant AT has been performed using standard electrophysiological techniques to demonstrate entrainment by recording diastolic atrial potentials from an area of slow conduction. They extrapolated data from animal studies showing that anatomic barriers resulting from residual atrial scars provide the substrate for atrial reentry. Multiple endocardial recordings were made to define the protected zone of slow conduction, generally using standard techniques of entrainment. For example, potential target sites for ablation were defined by determining whether pacing from that site was associated with concealed entrainment. Atrial mapping and pacing were performed to look for the first PPI within 10 to 30 ms of the TCL (Figure 73-16). When a postsurgical structural abnormality was present or a natural anatomic barrier (e.g., venous orifice, valve annulus) was nearby, mapping was more detailed in that region. In contrast with focal AT ablation, in which a single site of origin can be ablated to terminate tachycardia, macroreentrant AT usually requires ablation performed over a larger region, often defined by anatomic barriers or by adjacent scars separated by an isthmus of tissue serving as a critical area of slow conduction. Often these sites are characterized by double potentials or areas with low-voltage, long-duration, and more fractionated electrograms. Cycle length variability (greater than 15%) is rarely seen with macroreentrant AT, but it is not uncommon with focal AT. Atrial macroreentrant tachycardias also occur less commonly in patients without previous cardiac surgery, catheter ablation, or obvious structural heart disease. In these patients, electrically silent areas act as barriers for tachycardia. Like focal ATs, macroreentrant ATs generally incorporate several “typical” areas as part of the reentrant circuit. For example, the most common site involved in the right atrium is the isthmus between the tricuspid valve and the inferior vena cava and in the LA the mitral isthmus, roof, or atrial septum.

The advent of computer mapping techniques has allowed a more precise and rapid identification of arrhythmia mechanisms. A second approach to studying the mechanism of macroreentrant ATs has focused on the concept of macroreentry around a scar or previous surgical incision. These new technologies have allowed anatomic reconstruction of the cardiac chambers with recording of local activation times and identification of atrial scar tissue, allowing for the construction of isochronal maps of a substantial portion of or the entirety of the tachycardia circuit in many patients. Nakagawa et al.⁹⁴ made a fundamental contribution in this area with a study of 16 patients who had congenital heart disease surgery and underwent mapping and ablation of right atrial macroreentrant tachycardias. These workers mapped 15 macroreentrant ATs in 13 patients using the CARTO electroanatomic mapping system. First, they noted that all macroreentrant ATs propagated through narrow channels (<2.7 cm) defined by the mapping system as an area of decreased electrogram voltage between two close dense or thin scars. These workers coined the phrase “no channel–no macro-reentry.” Electrogram morphology, electrogram amplitude, and electrogram timing did not differentiate between sites within and those outside a narrow channel. Entrainment mapping failed to differentiate sites within the circuit but outside the channel (“outer loop” sites) from sites within the circuit and within the channel. Entrainment pacing was not done in many of the patients because it often resulted in the induction of a new tachycardia or in the termination of the original tachycardia. Additional limitations to entrainment mapping include difficulty measuring PPIs because of low amplitude or absence of atrial potentials in scarred atria or inability to pace the tissue. To overcome this limitation, measurements of the PPI-TCL can be made based on the N + 1 difference, or from recording sites remote from the pacing electrode.⁹⁵ Entrainment mapping can also induce atrial fibrillation. Finally, the investigators were able to record double potentials during atrial pacing at slow rates, suggesting fixed sites of anatomic block. In general, it appears that the size and location of the scars or associated natural anatomic barriers (e.g., valve annulus, SVC, pulmonary veins, or inferior vena cava) determine the size and properties of the tachycardia circuit.

The sensitivity and specificity of classical criteria for concealed entrainment for identification of a critical isthmus are based on studies performed during ventricular tachycardia. The sensitivity and specificity of these criteria for defining entrainment in the atrium were examined by Morton et al.⁹⁶ They used the model of typical atrial flutter and performed entrainment mapping from seven sites at four different cycle lengths. Concealed entrainment identified any isthmus site with 100% sensitivity with the flutter cycle length minus 10 ms but with a specificity of only 54%. Specificity increased to 98% with pacing at flutter cycle length minus 40 ms, but the sensitivity was decreased to 65%. At the flutter cycle length minus 30 ms, sensitivity was 85% and specificity was 90%. Concealed entrainment was seen from a nonisthmus site in 5 of 10 patients. Another caveat is that pacing at cycle lengths more than 10 to 20 ms faster than the tachycardia could results in PPIs that are higher than expected because of local pacing latency.⁹⁷ These findings highlight the observation by Nakagawa et al.⁹⁴ that targeting sites for ablation based solely on entrainment will result in a less than ideal success rate. Nevertheless, the techniques used by Nakagawa et al.⁹⁴ have limitations as well, including the need for meticulous attention to labeling of points acquired by the electroanatomic mapping system, differentiation of electrograms with low voltage from poor contact, selection of the fiducial point on the electrogram for timing, and sensitivity of the map to incorrect labeling of electrograms. These findings underscore the difficulties of relying on any one criterion for defining sites of ablation of these complex macroreentrant tachycardias. In general, current approaches that combine the definition of anatomy with electrophysiologic mapping data are warranted for attempted ablation of these complex arrhythmias.

Right Atrial Macroreentrant Flutters

Right atrial macroreentrant circuits include typical atrial flutter (counterclockwise or clockwise, cavotricuspid, isthmus dependent) and atypical flutters. Atypical flutters include right atrial free wall reentry, upper loop reentry, and lower loop reentry. In addition, during some atypical AFLs, the location of the circuit is variable and may involve dual-loop reentry (figure-eight) or complex reentrant mechanisms. Atypical reentrant circuits usually are related to surgical scars or electrically silent areas and anatomic obstacles (in the RA: SVC, inferior vena cava, CT, tricuspid annulus). As a general rule, the more complex the surgery, the more arrhythmogenic channels between scars exist, which produces a larger number of tachycardias. Single- and multiple-conduction isthmuses bordered by fixed and or functional low-voltage zones are critical for these reentrant circuits.

Right atrial free wall reentry probably is the most common form of right atrial atypical flutter. During right atrial free wall atypical atrial flutter, the activation wavefront circulates around a low-voltage or electrically silent zone in the lateral, posterolateral, or anterior free wall. This low-voltage region could be due to spontaneous scar formation or a prior cardiac surgical procedure. Radiofrequency ablation of the channel between the inferior vena cava or tricuspid annulus and the central obstacle can eliminate this form of macroreentry.

The CT is not always a fixed line of conduction block. Conduction gaps in the CT may provide the substrate for upper loop reentry as well as other double-loop atypical flutters. Upper loop reentry involves the upper portion of the right atrium with a reentrant circuit that rotates around the SVC and a lower turnaround point located at a conduction gap in the CT. Radiofrequency linear ablation of the conduction gap in the CT eliminates reentry. An incomplete line of block in the CT during typical AFL can result in double-loop reentry during typical AFL, one circulating around the tricuspid annulus and the other rotating around a part of the CT through the conduction gap. Radiofrequency ablation of the cavotricuspid isthmus and the gap in the CT eliminates both reentrant loops.

Lower loop reentry (counterclockwise) involves only the lower portion of the right atrium and depends on conduction through the cavotricuspid isthmus. The wavefront rotates around the inferior vena cava and tricuspid annulus with a breakthrough site at the low lateral tricuspid annulus. This arrhythmia will be ablated successfully in the cavotricuspid isthmus.

Left Atrial Macroreentrant Flutters

A number of laboratories have characterized left atrial macroreentrant circuits, or “left atrial flutters.” In two early studies, macroreentrant left atrial flutters were mapped with the CARTO electroanatomic mapping system and were ablated successfully in more than 70% of patients.103,104 Most patients had structural heart disease, and 14% to 32% had mitral valve disease. Multiple left atrial scars and channels are typical. The most frequent locations are between an atriotomy scar and the mitral annulus. The investigators described macroreentrant ATs as having a continuous sequence of atrial activation, with adjacent earliest and latest activation and the range of activation times occupying 90% or more of the tachycardia cycle length. Entrainment mapping was done in some patients to locate a critical isthmus of slow conduction. A right atrial macroreentrant circuit was excluded by showing that the PPI in the right atrium was longer than the tachycardia cycle length by 40 ms or longer from three or more sites in the right atrium, including the cavotricuspid isthmus and right atrial free wall. Spontaneous variation of greater than 100 ms was seen in the right atrium, with concomitant variations in the LA of less than 20 ms, and right atrial activation accounted for less than 50% of the arrhythmia cycle length from more than eight points during sequential catheter mapping. The left atrial flutters typically were characterized by large reentrant circuits that rotated around the mitral annulus, electrically silent areas, and lines of double potentials near acquired or natural anatomic barriers, such as the pulmonary veins (Figure 73-17). Electrically silent areas were defined as those with no recordable electrogram or an electrogram amplitude of less than 0.05 mV. A dual-loop reentrant circuit was defined for 74% of tachycardias, and a single-loop circuit was defined in the remaining 26% of tachycardias in one series of patients. In some studies, the mapping can be highly complex and involve up to four loops rotating simultaneously. The isthmuses described for left ATs may be wider and have greater voltages indicating thicker myocardium.

Left AFL includes mitral annular AFL, pulmonary vein-related AFL, and left septal AFL. In some patients, the LA circuits are complex, with two or three loops rotating concomitantly. Electrically silent areas (“scars”) and anatomic obstacles (e.g., pulmonary veins, fossa ovalis, mitral annulus) have a critical role in the pathophysiology of these circuits. The mitral annular AFL macroreentrant circuit rotates around the mitral annulus, either counterclockwise or clockwise.¹⁰⁵ The boundaries of the critical isthmus include the mitral annulus anteriorly and low-voltage zone or scars in the posterior or anterior LA walls. Radiofrequency ablation connecting the mitral annulus to an electrically silent area or an anatomic obstacle can cure this arrhythmia. The usual area of an ablation line at the isthmus between the left inferior pulmonary vein and the mitral annulus can eliminate this AFL. An alternative ablation line connecting the anterior–anterolateral mitral annulus with the left superior pulmonary vein for ablation of perimitral flutter has been suggested.¹⁰⁶ Pulmonary vein–related AFL macroreentrant circuits can rotate around one or more pulmonary veins and a scar in the posterior wall or roof of the LA.¹⁰⁷ Pulmonary vein reentrant circuits can be cured with ablation by creating a lesion from a pulmonary vein to the mitral annulus or to another pulmonary vein. The left septal AFL macroreentrant circuit rotates around the left septum primum, either counterclockwise or clockwise.¹⁰⁸ The electrocardiographic characteristics are dominant positive P (“F”) waves in lead V₁ and low-amplitude waves in the other leads. The critical isthmus is located between the septum primum and the pulmonary veins (posterior isthmus) or between the septum primum and the mitral annulus ring (anterior isthmus). Radiofrequency ablation of either the posterior or anterior isthmus can eliminate this left septal AFL. However, targeting the anterior isthmus might be more effective because the posterior isthmus may be thicker or more difficult to reach with a catheter.

Macroreentrant Atrial Tachycardia Following Cardiac Surgery

The presence of surgical atrial scars (lesion or incisional) provides a substrate for macroreentry, including conduction slowing and block. These surgeries can include correction of congenital heart disease (e.g., atrial septal defect, Fontan, tetralogy of Fallot) or for acquired lesions (mitral valve surgery, occasionally with coronary surgery depending on the location of cardiopulmonary bypass return). Following surgery, the reentrant circuit can use the right atriotomy scar as a central obstacle, rotate around an atrial patch used for ASD closure, or be dependent on the cavotricuspid isthmus. Some circuits may be highly very complex, using channels between multiple dense scars and lines of fixed conduction block within large areas of low voltage.

Markowitz et al.¹⁰⁹ described a series of 10 patients with macroreentrant tachycardias after mitral valve surgery. Six tachycardias originated from the right atrium, four were from the LA, and one was biatrial. In 80% of patients, tachycardia circuits were defined by surgical atrial lesions or cannulation sites. Three macroreentrant tachycardias involved the left atrial septum and right pulmonary veins, with the tachycardia making a single reentrant loop in two patients and a figure-eight reentry in one patient involving a clockwise loop around an area of low voltage in the posterior wall and a counterclockwise loop around the mitral annulus with a central isthmus between two areas of low voltage. Of interest, the tachycardia had a focal origin in three patients.

Macroreentrant Atrial Tachycardia after Previous Atrial Fibrillation Ablation Procedures (Surgical or Catheter)

Atrial macroreentrant tachycardias after atrial fibrillation (catheter or surgical) ablation can be complex and is discussed in more detail in Chapters 78 and 123. These tachycardias typically are microreentrant or macroreentrant. The type of tachycardia observed after atrial fibrillation ablation depends significantly on the previous atrial fibrillation ablation strategy.^110–112 Recurrent organized left ATs may be seen in 5% to 50% of patients and are more likely to be focal in patients with pulmonary vein isolation procedures and more likely to be macroreentrant in patients with linear lesions. Most patients with a focal origin for their tachycardia will have a site mapped to or near a reconnected pulmonary vein, whereas others have small-loop microreentry because of a focally ablatable small isthmus near a pulmonary vein. Typically, these patients will have fragmented, long-duration, and low-voltage electrograms, presumably owing to incomplete ablation of atrial tissue (e.g., gap-related) in their previous procedure (Figure 73-18). Others have been noted to have a macroreentrant tachycardia, which most commonly involves conduction across the mitral isthmus, the posterior wall, or gaps from previous ablation. The explanation for this abnormal atrial electrogram is believed to be altered intraatrial conduction and decreased left atrial voltage.¹¹³ Unusual forms of atrial macroreentry can occur after atrial fibrillation ablation, including circuits that incorporate the coronary sinus and its musculature, necessitating ablation inside the coronary sinus.¹¹⁴

Macroreentrant Atrial Tachycardia without Structural Heart Disease or Previous Surgical or Catheter Intervention

In a recent study, electroanatomic mapping revealed that right-sided, electrically silent areas (electrogram amplitude < 0.03 mV) were involved in the tachycardia mechanisms in two thirds of patients with non–isthmus-dependent right AFL.¹¹⁵ In half of the cases, a single-loop reentry circuit rotated around the areas of electrical silence, which constituted a central obstacle. In the remaining half, a dual-loop reentry with a narrow isthmus within electrically silent areas was observed. The pathogenesis of these electrically silent scars is not known, but it could be related to volume and pressure overload, impaired vascular compliance and diastolic dysfunction, atrial ischemia, postinflammatory scarring, or atrial amyloidosis. Understanding of the anatomic basis of these circuits has been greatly aided by three-dimensional mapping systems. Searching for low voltage areas, double potentials, complex fractionated electrograms, and conventional entrainment could help to determine circuit boundaries and critical isthmuses.

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