Interdependence of Atrial Fibrillation and Atrial Flutter

Animal and human studies of induced and spontaneous AFL have shown that AFL is usually preceded by a transitional period of AF.² It has been suggested that the critical functional line of block between the venae cavae develops during transitional AF, thereby establishing the necessary boundaries for reentry required for AFL maintenance. The absence of the functional line of block results in either in persistence (no conversion to AFL) or termination of AF. Conversely, shortening of the line of block results in conversion of AFL to AF. The coexistence of both arrhythmias is evidenced by the fact that nearly 75% of patients with AFL will have had documented AF at the time of presentation.² Furthermore, the incidence of AF after an AFL ablation is time dependent, with one study finding an 82% incidence of new-onset, drug-refractory AF during a 39-month follow-up.⁴ Indeed, AFL ablation alone does not modify the natural course of arrhythmia progression to AF, and data suggest that a high percentage of patients will ultimately develop AF after ablation of AFL. Furthermore, antiarrhythmic drugs causing atrial conduction slowing (class I_a, class I_c, amiodarone) can convert AF to AFL in part related to the creation of a posterior or intercaval functional line.²

Although AF and AFL frequently coexist, in the clinical presentation one arrhythmia frequently predominates over another. The predominance of AFL presentation over AF in some patients might be explained by more advanced right atrial remodeling with slowed conduction and regional conduction block, particularly occurring in the posterior right atrium (RA). This distribution of remodeling can facilitate the stabilization of AFL and facilitate persistence of this as the dominant clinical arrhythmia.⁵ Furthermore, when studied remote from episodes of arrhythmia, patients with AFL demonstrate significant and diffuse atrial abnormalities characterized by atrial structural changes, conduction abnormalities, and sinus node dysfunction. These changes might explain the predisposition to the development of AFL and the subsequent propensity for AF.⁶

Counterclockwise and Clockwise Atrial Flutter (Typical Flutter)

The circuits of counterclockwise and clockwise atrial flutter can be characterized as right atrial with a broad activation wavefront rotating between the tricuspid annulus (TA) as the anterior barrier and the crista terminalis-eustachian ridge/inferior vena cava (IVC) as the posterior barrier in either a counterclockwise or a clockwise direction. The CTI provides the narrowest segment of the circuit (Figure 74-1, A, B).^9,10 Although these are the critical barriers, significant variations in the leading edge or active region of the reentrant loop have been described. In an entrainment study, Santucci et al.¹¹ demonstrated that only approximately one third of typical AFL cases had an active circuit adjacent to the TA. In others, the circuit took an oblique course between the anterior and posterior barriers, with the upper circuit off the annulus and posterior to the right atrial appendage (RAA) base. Of these, some coursed anterior to the superior vena cava (SVC), others behind the SVC (across the crista terminalis). In others, bifurcation of the upper circuit was seen around the RAA, around the SVC, or around both.¹¹

Counterclockwise typical AFL is the most common form of macroreentrant AFL. The classical inferior lead flutter waves (sawtooth pattern) demonstrate an initial gradual downsloping segment followed by a deeply inverted component with a terminal positive component (of variable amplitude; see Figure 74-1, C). Although the flutter wave typically appears inverted in inferior leads, variations in the amplitude of both the negative and positive components can create atypical patterns. In the precordial leads, V₁ classically demonstrates an initial isoelectric component followed by an upright component. With progression across the precordial leads, the initial component becomes inverted, and second component becomes isoelectric such that V₅ and V₆ demonstrate an inverted flutter wave.¹² Lead I is low amplitude–isoelectric, and aVL is usually upright (see Figure 74-1, C). Unusual flutter wave morphologies can be seen with counterclockwise AFL and a left AFL might mimic the counterclockwise AFL appearance.

Clockwise AFL is seen in approximately 10% of cases, and its boundaries are identical to counterclockwise AFL, but with reverse direction of wavefront rotation. The surface ECG appearance tends to be more variable, but with some characteristic features. Flutter waves in the inferior leads are usually broadly positive, and the upright component is preceded by an inverted component of variable amplitude. There is characteristic notching on the upright component, which has a bifid appearance. V₁ is characterized by a broad, negative, and usually notched deflection with transition to an upright deflection in V₆. Lead I is usually upright and aVL is low amplitude negative, overall giving an appearance that is the reverse of counterclockwise AFL (see Figure 74-1, C).

Mapping

Although the ECG appearance of the flutter waves may be highly characteristic, it is always important to confirm the arrhythmia mechanism with activation and entrainment mapping before performing ablation. The RA activation sequence during counterclockwise and clockwise AFL can be delineated with multipolar catheters or the use of high-density three-dimensional (3D) electroanatomic mapping systems. Typically, multipolar catheters are placed in the coronary sinus (CS), around the TA and in the His bundle position (see Figure 74-1, D). In patients with paroxysmal AFL who are in sinus rhythm, rapid atrial pacing can be used to initiate the arrhythmia, although AF might also ensue. Onset is characteristically with unidirectional block within the CTI such that pacing from the CS ostium most usually will induce counterclockwise AFL, whereas low lateral RA pacing will most usually induce clockwise AFL.

Entrainment

Electrophysiological testing of typical AFL is primarily aimed at confirming that the circuit is macroreentrant and that the CTI is integral. A minimum requirement would be to entrain within the CTI to demonstrate that this is within the circuit (postpacing interval [PPI]–tachycardia cycle length [TCL] < 20 ms). We use entrainment pacing with a cycle length 10 to 20 ms less than TCL. It is important to initiate entrainment with synchronization to the entraining electrode in order to avoid initial introduction of a tight-coupled stimulus, which can terminate or change the circuit. If the entraining cycle length is too short, it is possible to introduce decrement into the circuit, which will prolong the PPI and produce an erroneous result. To confirm the arrhythmia mechanism we will also perform entrainment from several sites around the TA, which should be in the circuit, and from the mid and distal CS, which should be out of the circuit in typical flutter. In general terms, the farther away from the circuit that entrainment is performed the longer the PPI. When entrainment is “in” at two sites more than 2 cm apart, the presence of macroreentry is confirmed.

During transient entrainment of a tachycardia with a pacing cycle length 10 to 20 ms shorter than the flutter cycle length, the wavefront from each pacing impulse orthodromic and antidromic fashion.¹³ The antidromic wavefront will collide with the preceding orthodromic wavefront as it exits the critical isthmus. Entrainment will result in acceleration of the atrium to the pacing cycle length, with each antidromic wavefront colliding with the orthodromic wavefront of the preceding pacing stimulus (constant fusion). When pacing stops, the orthodromic wavefront of the last pacing stimulus has a cycle length equal to the cycle length of entrainment, but as it does not encounter a further pacing-induced antidromic wavefront, it is not fused (the last entrained but not fused beat). When pacing rate is further increased, the collision site between orthodromic and antidromic wavefronts is shifted farther from the pacing site so that more of the ECG complex appears paced (progressive ECG fusion) and more electrogram sites are antidromically captured (progressive electrogram fusion). When entrainment is performed in a narrow isthmus, the extent of antidromic capture is limited within the isthmus, and fusion will not be evident on the surface ECG (concealed entrainment; Figure 74-2). When outside a protected isthmus antidromic atrial capture or penetration is more extensive and therefore manifest on the surface ECG (manifest fusion).

However, although the presence of concealed entrainment can be an extremely useful tool for mapping ventricular arrhythmias, in practice it is of limited utility for atrial arrhythmias. The flutter wave morphology is of relatively low amplitude and is frequently obscured by overlap with QRS complexes and T waves, making it difficult or impossible to detect changes in morphology. Furthermore, the distortion of the stimulus artifact can render it difficult to detect subtle degrees of fusion. Thus, although entrainment remains one of the cornerstone tools for evaluation of atrial arrhythmias, the focus is on the PPI-TCL to determine which sites are within the circuit.

Electroanatomic Mapping

High-density, 3D electroanatomic mapping (contact or noncontact mapping) is able to delineate the right atrial circuit during typical AFL with the use of activation maps represented as a continuous progression of colors (see Figure 74-1, B). A key point with activation mapping using electroanatomic mapping systems in macroreentrant circuits is that early activation is not applicable to any specific point in the circuit, because activation is continuous and the origin of activation is always arbitrary with respect to the particular reference chosen for illustration. Therefore, color coding will be represented in red or white at the site with earliest activation with respect to the arbitrarily defined zero point and will progress through a spectrum of colors to purple representing latest activation, again with respect to the arbitrarily chosen point. Activation timing should span the entire cycle length of a macroreentrant circuit. Where earliest meets latest activation in a continuous circuit is the point where “head meets tail,” which is again an arbitrary anatomic point determined by choice of the zero point.

Using 3D mapping, the activation wavefront in counterclockwise AFL will most typically appear as a broad wavefront that exits the medial CTI, ascends the septum, passes anterior to the SVC, and descends the anterolateral RA to enter the CTI laterally (see Figure 74-1, B). Passive wavefronts will activate the left atrium and the posterior RA, where conduction delay or block at the crista terminalis will prevent a short-circuiting of the TA (see Figure 74-1).^9,10 As described earlier, entrainment mapping and noncontact mapping have both been used to define the many variants on the location of the active circuit of typical AFL. 3D mapping can also characterize tissue voltage of the CTI, which could be useful in planning the path of the ablation line because lower voltage can predict an easier ablation path.¹⁴

Treatment

Pharmacologic

Principles of pharmacologic treatment are to control the ventricular rate during AFL with the use of atrioventricular (AV) node blocking agents (β-blockers, cardiac-selective calcium channel blockers) or maintenance of sinus rhythm with class I or III antiarrhythmic drugs. Class 1c agents can stabilize the flutter by slowing rate, increasing excitable gap, and can result in 1 : 1 AV conduction. Because of the presence of postreversion atrial stunning, whether pharmacologic or electrical, it is mandatory to follow anticoagulation guidelines as for reversion of AF. Because of the high late incidence of AF after successful flutter ablation coupled with the documented late risk of stroke,¹⁸ it is common to make decisions regarding ongoing anticoagulation (with coumadin or an equivalent) based on the CHADS₂ score. In the absence of supporting data, an alternate approach is to continue to monitor closely for development of late AF particularly in those patients with stroke risk factors.

Catheter ablation

Pharmacologic treatment results in long-term maintenance of sinus rhythm in 36% to 73% of patients with AFL; moreover, complete arrhythmia suppression can be difficult.¹⁹ Evidence from randomized studies has demonstrated the superiority of catheter ablation over antiarrhythmic drugs in the treatment of AFL, with higher rates of maintenance of sinus rhythm, improvement in quality of life, and reduction in the recurrence of future AF.^20,21 Thus, catheter ablation is a class I recommendation for AFL if it is recurrent, is poorly tolerated, or reemerges after using a class I antiarrhythmic or amiodarone.¹⁹

Catheter ablation can be performed in either the septal or mid aspects of the CTI and will be determined by stability of catheter access and anatomic variation (see Figure 74-1, D). It is important to be aware that inadvertent AV block has rarely been reported during ablation at the septal aspect of the CTI because of the proximity to posterior extensions of the AV node. The lateral isthmus is generally longer and is not usually the primary ablation target. Ablation can be performed during AFL or proximal CS pacing (in sinus rhythm). The latter allows identification of a change in activation sequence on the tricuspid annular catheter, signifying slowing of CTI conduction or block (Figure 74-3, A).

Figure 74-3 Methods of assessing block across the cavotricuspid isthmus (CTI). A, Coronary sinus (CS) pacing (representing pacing septal to the CTI) is depicted before CTI block (first three panels). A clockwise wavefront traveling across the CTI from the distal to proximal tricuspid annulus (TA) collides with the counterclockwise wavefront ascending up the interatrial septum and down from the proximal to the distal TA. During ablation, there is a progressive increase in transisthmus conduction (first three panels) until CTI block is achieved (last panel). Note that in the last panel there is a change in activation sequence on the TA catheter where the distal TA located lateral to the CTI is activated last and there is reversal of electrogram polarity. B, Inset

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