Ablation of Nonisthmus-Dependent Flutters and Atrial Macroreentry

Key Points

Atypical or nonisthmus-dependent atrial flutter and atrial macroreentry requires fixed or functional barriers and regions of slow conduction.
Atypical flutters are often recognized after catheter ablation or surgical treatment of atrial fibrillation (AF) or after surgery that involves right or left atriotomies.
Activation mapping is used to demonstrate reentrant circuits, middiastolic potentials, fractionated potentials, and double potentials.
A multipolar electrode catheter is useful to map atypical flutter in either atrium.
An electroanatomic mapping system is useful in most cases.
An irrigated-tip or large-tip (8 mm) ablation catheter is usually employed.
Sources of difficulty include defining complex reentrant circuits, particularly those with irregular oscillations in atrial cycle length; achieving durable lines of conduction block; and spontaneous conversion of atypical flutter to atrial fibrillation or other arrhythmias.

Introduction

Atypical atrial flutters refer to a spectrum of arrhythmias that vary in location and circuit dimensions. In many cases these arrhythmias may also coexist with atrial fibrillation (AF) or play transitional roles in the initiation or termination of AF, or in the transformation to typical atrial flutter. Atypical flutters are increasingly recognized after catheter ablation or surgical treatment of AF or after surgery that involves right or left atriotomies.

Historically there has been confusion over the use of the terms atrial flutter and atrial tachycardia (AT). It has been proposed that these terms be applied based on rate or the presence of isoelectric intervals on the electrocardiogram. The term atrial flutter is often used to refer to regular tachycardias with rates of 240 beats per minute or higher and lacking an isoelectric interval between deflections, whereas atrial tachycardia refers to arrhythmias with isoelectric intervals between P waves and/or slower cycle lengths. However, these characteristics are not specific for the mechanism of tachycardia. In this chapter, the term atypical atrial flutter will be used preferentially to refer to reentrant circuits that are not dependent on the cavotricuspid isthmus (CTI). Atypical flutters may be classified based on their chamber of origin, site within a given atrium, and size of the reentrant circuit ( Table 12.1 ).

TABLE 12.1

Types of Nonisthmus-Dependent Atrial Flutters

Right Atrium
Circuit	Boundaries	Clinical Scenarios
Upper-loop reentry	SVC and crista terminalis	De novo or with CTI-dependent flutter
Right atrial free-wall reentry	Right atrial scar, lateral tricuspid annulus	Prior right atriotomy, atrial myopathy
Dual-loop reentry (combined lower loop, upper loop, free wall, and/or tricuspid valve)	Combinations of right atrial scar, SVC, tricuspid annulus, with or without CTI	De novo or with CTI-dependent flutter, prior right atriotomy, atrial myopathy
Left Atrium
Circuit	Boundaries	Clinical Scenarios
Perimitral annular reentry	Mitral annulus, left atrial isthmus	Following left atrial ablation for AF, after maze surgery, de novo
Roof-dependent reentry	Linear ablation lines around left and/or right pulmonary veins, possibly electrically active pulmonary vein tissue	Following left atrial ablation for atrial fibrillation with encircling lesions, after maze surgery, de novo
Periseptal tachycardia	Right pulmonary veins and mitral annulus or fossa ovalis with right pulmonary veins or mitral annulus	Following atriotomy, left atrial ablation for atrial fibrillation, de novo
Miscellaneous
Circuit	Boundaries	Clinical Scenarios
Lesional tachycardias	Surgical scars	Following left atriotomy, post maze surgery
Microreentry or localized reentry	Variable	Following left atrial ablation for AF, after maze surgery, atrial myopathy
Coronary sinus mediated reentry	Coronary sinus with left or right atrial myocardium	De novo

AF, Atrial fibrillation; CTI, cavotricuspid isthmus; SVC , superior vena cava.

Anatomy

The specific configuration of a reentrant circuit is dependent on the local or global anatomy of the atrium, as well as conduction and refractory properties of the atrial myocardium. As a general rule, reentry requires the presence of two limbs, which are anatomically and/or functionally contiguous but dissociated. These limbs are dependent on the presence of an inexcitable central barrier (i.e., atrioventricular annulus, venous ostium, or scar) or a functional line of block. In the right atrium (RA), natural barriers to conduction are the tricuspid annulus, inferior vena cava (IVC), superior vena cava (SVC), crista terminalis, Eustachian ridge, and fossa ovalis. In the left atrium (LA), the mitral annulus and pulmonary venous ostia serve as critical conduction barriers, along with electrically silent areas that may be found in myopathic atria or result from prior ablation or surgery.

Pathophysiology

Although atypical atrial flutters can arise in structurally normal hearts, these arrhythmias predominantly occur in patients with organic heart disease, after cardiac surgery, or AF ablation. In patients with organic heart disease, the pathogenesis is thought to involve elevated atrial pressure, which causes interstitial fibrosis resulting in conduction slowing and block. LA reentry that arises de novo in the atria frequently involves regions of patchy scar, which presumably occurs as the result of atrial myopathy. These areas of patchy scar can be identified as electrically silent areas during electroanatomic mapping. Other important determinants are slowing of atrial conduction velocity, heterogeneity of atrial refractoriness, and initiating or triggering foci.

In response to premature stimuli, arcs of functional block develop and—if of sufficient length—initiate and support reentry. Functional lines of block develop in structures such as the crista terminalis and the Eustachian ridge, both of which play a critical role in the formation of CTI-dependent atrial flutter. Gaps in these functional lines of block, as in the crista terminalis, permit formation of atypical circuits. Functional lines of block may develop in many other locations, including variable sites in the LA. A combination of fixed and functional block has been demonstrated in animal models of lesional tachycardia, in which a line of functional block develops as an extension to a fixed anatomic lesion. In this case, the anatomic lesion might not be large enough to support reentry, but the combined fixed and functional barrier provides the critical path length needed to maintain reentry. Formation and breakdown of these arcs of block are responsible for interconversion of flutter circuits with each other and the transition to AF.

With the growth of ablation procedures for AF, atypical flutters have become increasingly frequent after both catheter and surgical ablation. Discontinuities in ablation lines can result in unidirectional rate-dependent block or conduction slowing. Furthermore, areas of excluded myocardium, such as those occurring with wide encircling pulmonary vein isolation, give rise to large central barriers that permit circus movement reentry. Many reentrant ATs are complex circuits that involve dual loops (figure-of-eight reentry) or less commonly triple loops. In multiple loop tachycardias, conduction times are nearly equal around the individual loops, but sometimes a dominant circuit exists as a driver, which entrains other loops.

Small reentrant circuits, known as localized reentry or microreentry , can occur in a variety of clinical circumstances, such as catheter ablation of AF, surgical maze procedures, and surgical repair of congenital heart disease. These small circuits can also occur de novo in diseased atria. A unifying condition in cases of localized reentry is the presence of an atrial scar, and these circuits usually localize near prior ablation lines or surgical incisions. Disruption of the myocardial architecture may give rise to markedly slow conduction, anisotropic differences in conduction velocity, and unidirectional block, which allow small circuits to develop and perpetuate.

Cardiac surgery that involves atrial incisions is an important cause of atypical flutter. The location and extent of an incision, in addition to intrinsic disease of the atria, influence the likelihood of developing atypical flutter. Patients who have right atrial surgery are also at risk of developing atypical flutter involving the surgical scar in the lateral RA, whereas those who have a left atriotomy may develop atypical flutter in the LA. In addition, patients who have right or left atriotomies are also prone to develop CTI-dependent flutter.

Diagnosis

Macroreentrant Versus Focal Atrial Tachycardia

A fundamental consideration in evaluating atypical flutter is to establish if the arrhythmia is macroreentrant or focal in origin ( Box 12.1 ). In general, P wave durations are shorter and surface isoelectric intervals are longer with focal tachycardias than with macroreentry. A study of 75 patients with atypical flutters after AF ablation found that a P wave duration of less than 185 ms had a sensitivity of 85% and specificity of 97% in identifying a small reentrant circuit. However, it is possible for a macroreentrant tachycardia to have an isoelectric interval if part of circuit consists of a slowly conducting isthmus generating little electric force. When the tachycardia cycle length varies by 15% or more, a focal mechanism is suggested, but a regular cycle length can occur with both focal and macroreentrant atrial tachycardias (ATs).

BOX 12.1

Diagnostic Criteria

Macroreentrant Tachycardias

Entrainment with fusion (with last beat entrained but not fused)
Electroanatomic mapping of >90% of tachycardia cycle length with adjacent early and late areas of activation
Insensitivity to adenosine (in dose sufficient to cause AV block)

Microreentrant Tachycardias or Localized Reentry

Fragmented electrograms that encompass a large proportion of the tachycardia cycle length on single electrode or multiple closely spaced electrodes
Entrainment with progressively longer postpacing intervals at increasing distances from the apparent source
Insensitivity to adenosine (in dose sufficient to cause AV block)

Left Atrial Tachycardias

Passive conduction in the right atrium, with early septal activation and fusion of wave fronts in the RA lateral wall
Absence of RA activation during long segments of the cycle length (mapping <50% of tachycardia cycle length)
Large variations in the RA cycle length with a relatively fixed cycle length in the LA
Entrainment pacing at multiple sites in the RA yielding postpacing intervals >30 ms

AV, Atrioventricular; LA, left atrium; RA, right atrium.

The electrocardiographic (ECG) morphology of atypical flutters is highly variable, and substantial overlaps exists between flutter morphologies arising from different anatomic circuits, so that localization of atrial flutters from the surface ECG has limited utility. However, some broad generalizations can be made that distinguish CTI-dependent from non-CTI-dependent flutters, as well as right from left atrial tachycardias. CTI-dependent flutters often show characteristic morphologies, and recognizing deviation from these patterns allows one to conclude that a tachycardia might be atypical flutter. Typical counterclockwise CTI-dependent flutter often has a superiorly directed flutter wave axis with a small terminal positive deflection in the inferior leads (so called sawtooth pattern). Lead V ₁ has an overall positive deflection with an initial isoelectric or inverted component, and the flutter wave transitions from positive to negative across the precordium. Clockwise CTI-dependent flutter is more variable, but it characteristically shows positive, notched flutter waves in the inferior leads, and lead V ₁ usually shows negative flutter waves. It should be emphasized that even CTI-dependent flutters can show variability in ECG morphology, and the typical patterns described above might also arise from non-CTI-dependent mechanisms. Typical CTI-dependent flutter that occurs after ablation for AF may also present with atypical ECG morphologies.

Generally flutters that are predominately negative in V ₁ arise from the RA, whereas those that show broad positive waves in V ₁ (without isoelectric or negative initial components) usually arise from the LA ( Fig. 12.1 ). Left atrial flutters usually demonstrate either positive flutter waves in the inferior leads or low-amplitude/isoelectric signals in the limb and other precordial leads. Intermediate patterns that do not fit these various descriptions are common and can be difficult to localize. Regardless of the morphology, confirmation of the tachycardia origin with endocardial mapping is required.

Fig. 12.1, Representative examples of atypical flutters. A, Lateral right atrial (RA) reentry in a patient with prior mitral valve repair with a right atriotomy. In this case, flutter waves are negative in V 1 with an inferior axis. B, Localized reentry from the anterior wall of the left atrium (LA) shows positive flutter waves in V 1 with low-amplitude signals in the limb and lateral precordial leads. C and D, Two examples of perimitral annular reentry in a patient with prior mitral valve repair and a patient with ischemic cardiomyopathy. These show positive flutter waves in V 1 with different axes in the inferior leads. Note the isoelectric interval, illustrating that isoelectric intervals are not specific for focal tachycardia.

Evidence for a macroreentrant mechanism can be obtained through manifest entrainment, entrainment with concealed fusion (concealed entrainment), or electroanatomic mapping (see Mapping section). Manifest entrainment is recognized as fixed fusion at any given paced cycle length and by progressive fusion with progressively rapid overdrive pacing. Because the surface flutter wave may not be visible or may be obscured by ventricular depolarization or repolarization, intracardiac electrograms provide a surrogate marker for orthodromic and antidromic capture and the degree of fusion. Manifest entrainment with progressive fusion implies a dimensionality to the tachycardia circuit that includes a separate entrance and exit site, a condition that does not exist for focal tachycardia and is unlikely to be demonstrated for microreentry. The pacing site is considered to be within the tachycardia circuit when the postpacing interval after entrainment is 30 ms (or less) greater than the tachycardia cycle length ( Fig. 12.2 ). Entrainment from two opposite quadrants (such as septal and lateral LA, or anterior and posterior LA), each with return cycle lengths within 30 ms of the tachycardia cycle length, indicates the presence of a macroreentrant circuit. Thus in-circuit entrainment from the septal and lateral LA often indicates perimitral reentry; in-circuit entrainment from the anterior and posterior LA is consistent with a roof-dependent LA flutter. Entrainment may also give indirect information about the distance of a pacing site from the reentrant circuit, with shorter postpacing intervals indicating closer proximity to the circuit.

Fig. 12.2, Entrainment from multipolar catheters localizes a left atrial tachycardia. Activation of the coronary sinus (CS) is proximal to distal. Entrainment from the proximal and distal poles of the CS catheter (A and B) results in postpacing intervals nearly identical to the tachycardia cycle length. Panel B shows the phenomenon of downstream overdrive pacing. 83 Entrainment from the distal electrode of the CS catheters (downstream from the proximal electrodes) results in orthodromic capture of the proximal poles after conduction delay. Panels C and D show entrainment from the high and low right atrium (RA), respectively, both of which show long postpacing intervals (as well as fusion of intracardiac electrograms during pacing), indicating that they remote from the tachycardia circuit. These responses are consistent with a left atrial tachycardia, which was perimitral reentry.

The response to adenosine is useful in distinguishing reentrant from focal ATs, in that it exerts mechanistic-specific effects on atrial arrhythmias. With rare exceptions, adenosine does not terminate the vast majority of reentrant atrial arrhythmias, whereas it either terminates focal ATs attributed to triggered activity or transiently suppresses focal AT as a result of enhanced automaticity ( Fig. 12.3 ). Adenosine-insensitive ATs with apparently focal activation patterns show characteristics of localized reentrant circuits, including low-amplitude, long-duration fractionated electrograms, and can be entrained. This simple tool provides a reliable means for establishing a tachycardia mechanism before mapping ( Fig. 12.4 ).

Fig. 12.3, Reentrant atrial tachycardia in a patient with a prior lateral right atriotomy. A, The tachycardia is insensitive to adenosine, which is consistent with a reentrant mechanism. B, A duo-decapolar catheter in the lateral right atrium (RA) demonstrates fusion of wave fronts in the lateral wall, in this case consistent with lower-loop reentry, with a circuit around the inferior vena cava (IVC). During ablation in the cavotricuspid isthmus, the tachycardia cycle length prolongs and activation in the lateral right atrium changes (arrow), which is explained by interruption of lower-loop reentry and the existence of a second circuit involving the lateral right atriotomy. C, The change in the tachycardia circuit is illustrated graphically. CS, Coronary sinus; CTI, cavotricuspid isthmus; RF, radiofrequency; SVC, superior vena cava; TA, tricuspid annulus.

Fig. 12.4, Differentiating mechanisms of atrial tachycardia using adenosine and electrophysiological characteristics. Adenosine-sensitive atrial tachycardia is typically focal in origin caused by triggered activity or, far less commonly, automaticity. Adenosine-insensitive atrial tachycardia is either macroreentrant or microreentrant, depending on circuit size and the resolution of the mapping system. Entrainment with the postpacing interval nearly equal to the atrial tachycardia cycle length is typical for macroreentrant or microreentrant tachycardias. Prolonged electrogram durations may be recorded at early sites in microreentrant tachycardias but are not typical at the origin of triggered and automatic rhythms. Electrogram durations at sites around a macroreentrant circuit might vary depending on local conduction characteristics. PES, Programmed electrical stimulation.

Localization of Reentry to the Right Atrium or Left Atrium

The activation pattern of the coronary sinus (CS) is useful in localizing ATs. RA tachycardias typically exhibit proximal-to-distal activation in the CS, unless activation proceeds predominantly over Bachmann bundle (or the catheter is positioned very distally in the CS), in which case the distal CS may be activated earlier. LA tachycardias show a variety of activation patterns depending on the particular reentrant circuit ( Fig. 12.5 ). Some LA tachycardias, such as clockwise perimitral annular reentry and tachycardias originating near the lateral LA (by the left pulmonary veins or appendage), exhibit distal-to-proximal CS activation. However, a proximal-to-distal sequence does not necessarily localize the arrhythmia to the RA and may be seen with counterclockwise perimitral reentry or tachycardias involving the septum or right pulmonary veins. Chevron and reverse chevron activation patterns occur with roof-dependent LA macroreentry. The chevron pattern occurs when a wave front descends the posterior wall and activates the midposterior mitral annulus, and then propagates in both septal and lateral directions along the inferior LA. The reverse chevron pattern occurs when a wave front descends the anterior LA wall and then fuses in the posterior mitral annulus. Focal arrhythmias in the posterior or anterior LA may also produce chevron or reverse chevron patterns. It should be recognized that activation of the CS may be dissociated from the LA endocardium because of a muscular sleeve, which envelops the CS and is attached to the LA through discrete connections. Electrograms recorded in the CS may show disparate activation patterns, and careful analysis may show that the endocardial LA is activated in a pattern different from the CS. Macroreentry involving the CS musculature or the ligament of Marshall as a critical part of the circuit has also been described.

Fig. 12.5, Activation sequences of the coronary sinus (CS) in various forms of left atrial tachycardia. A, Counterclockwise perimitral reentry gives rise to proximal-to-distal CS activation. B, Clockwise perimitral reentry produces distal-to-proximal CS activation. C, Roof-dependent atrial tachycardia with a descending wave front in the posterior wall causes early activation in the mid CS, after which the impulse propagates both proximally and distally along the mitral annulus (chevron pattern). D, Roof-dependent atrial tachycardia with a descending wave front in the anterior wall causes fusion of wave fronts in the posterior mitral annulus (by the coronary sinus) because the impulse first activates the anterior mitral annulus and then bifurcates to activate the lateral and septal walls before fusing in the posterior annulus (reverse chevron pattern).

It is possible to establish a diagnosis of LA tachycardia during mapping in the RA and thus identify the need for transseptal catheterization and LA mapping. Criteria for identifying an LA origin through intracardiac mapping include the following:

1.
Passive conduction into the RA, which may be demonstrated as fused wave fronts in the lateral wall of the RA.
2.
Earliest RA activation in the septum, typically in the region of Bachmann bundle or the CS ostium, especially if areas of early activation encompass a large area.
3.
Large variations in the RA cycle length with a relatively fixed cycle length in the LA, implying LA/RA dissociation or conduction block.
4.
Entrainment pacing at multiple sites in the RA (including the CTI and the RA free wall) yielding postpacing intervals greater than 30 ms.

Although fusion of wave fronts in the lateral wall of the RA is common during LA tachycardias, it is possible to record a single wave front mimicking counterclockwise or clockwise atrial flutter. This situation depends on (1) the location of the multipolar catheter in the lateral wall, (2) the location of conduction breakthrough from the LA (i.e., preferential conduction over Bachmann bundle or the CS), and (3) the presence of conduction block in the CTI. Typically, activation time in the RA is substantially less than the tachycardia cycle length. Exceptions occur when the tachycardia cycle length is short or if conduction is substantially slowed in the RA, incorrectly implying the presence of a RA tachycardia.

Mapping

Activation Mapping

Conventional activation mapping with multielectrode catheters is usually employed to define the mechanisms of atypical flutters. In the RA, a multielectrode catheter positioned around the tricuspid annulus can provide information suggestive about the tachycardia mechanism. For example, counterclockwise lower-loop reentry reveals lateral-to-septal activation in the CTI and areas of breakthrough in the lateral RA, which can cause fusion of wave fronts or an ascending wave front in the lateral wall (see Fig. 12.3 ).

Double potentials, which usually signify lines of block, may be identified through conventional activation mapping. If reentry proceeds around a line of block, double potentials are widely split in the middle of the line, and they progressively narrow toward the end of the line where the wave front pivots. An example of this may be found in RA free-wall macroreentry ( Fig. 12.6 ). Middiastolic and fragmented potentials can be recorded within critical zones of slow conduction, but verification of participation in the tachycardia circuit is desirable through other means, such as entrainment maneuvers.

Fig. 12.6, Right atrial (RA) free-wall reentry. Double potentials in the lateral wall reflect descending and ascending wave fronts, with narrowing of the intervals between double potentials down the lateral wall and a fragmented electrogram reflecting a pivot point in pole RA-6 (RA-1, low lateral RA; RA-10, high lateral RA). CS, Coronary sinus.

Activation mapping in the LA relative to a fixed reference can identify or exclude mitral reentry or roof-dependent flutter. Opposite activation sequences in the superior and inferior mitral annulus (e.g., lateral-to-septal activation along the superior annulus, and septal-to-lateral activation along the inferior annulus) identify perimitral reentry. By contrast, similar directions of activation (e.g., lateral-to-septal) in both the superior and inferior annulus exclude perimitral reentry. Opposite activation along the anterior and posterior walls is seen with roof-dependent reentry.

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