Macroreentrant Atrial Tachycardia (“Atypical Atrial Flutter”)

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Chapter 13 Macroreentrant Atrial Tachycardia (“Atypical Atrial Flutter”)

Pathophysiology

The term typical atrial flutter (AFL) is reserved for an atrial macroreentrant arrhythmia rotating clockwise or counterclockwise around the tricuspid annulus and using the cavotricuspid isthmus (CTI) as an essential part of the reentrant circuit. Atypical AFL is a term commonly used to describe all other macroreentrant atrial tachycardias (MRATs), regardless of the atrial cycle length (CL), but the former term introduces unnecessary confusion, and a mechanistic description of the tachycardia circuit is preferred.

The mechanism of MRAT is reentrant activation around a large central obstacle, generally several centimeters in diameter, at least in one of its dimensions. The central obstacle can consist of normal or abnormal structures. Additionally, the obstacle can be fixed, functional, or a combination of both. There is no single point of origin of activation, and atrial tissues outside the circuit are activated from various parts of the circuit.

A description of MRAT mechanisms must be made in relation to atrial anatomy, including a detailed description of the obstacles or boundaries of the circuit and the critical isthmuses that may be targets for therapeutic action. Typically, chronic or long-lasting atrial tachycardias (ATs) are macroreentrant. Focal ATs are more frequently responsible for irregular ATs with frequent spontaneous interruption and reinitiation than are ATs observed with macroreentry. Microreentrant ATs, by definition, use a smaller circuit and in many regards behave more like other forms of focal ATs.

Atypical Isthmus-Dependent Right Atrial Macroreentry

Lower loop reentry and intraisthmus reentry are macroreentrant circuits that are confined to the right atrium (RA) and incorporate the CTI as a critical part of the circuit. However, in contrast to typical AFL, the circuit is not peritricuspid (Fig. 13-1). Nevertheless, because the CTI is still a necessary part of the circuit, these arrhythmias are amenable to CTI ablation, as is true for patients with typical AFL.1

Lower Loop Reentry

Lower loop reentry is a form of CTI-dependent AFL with a reentrant circuit around the inferior vena cava (IVC); therefore, it is confined to the lower part of the RA (see Fig. 13-1). It often coexists with counterclockwise or clockwise typical AFL and involves posterior breakthrough across the crista terminalis. Lower loop reentry can rotate around the IVC in a counterclockwise (i.e., the impulse within the CTI travels from the septum to the lateral wall) or clockwise fashion. A breakdown in the inferoposterior boundaries of the CTI produced by the eustachian ridge and lower crista terminalis causes the circuit to revolve around the IVC (instead of around the tricuspid annulus), across the eustachian ridge, and through the crista terminalis, with slow conduction because of transverse activation through that structure. Alternatively, the circuit can exit at the apex of Koch triangle and come behind the eustachian ridge to break through across the crista terminalis behind the IVC and then return to the CTI. This arrhythmia is usually transient and terminates by itself or converts spontaneously into AFL or atrial fibrillation (AF).1

Intraisthmus Reentry

Intraisthmus reentry is a reentrant circuit usually occurring within the region bounded by the medial CTI and coronary sinus ostium (CS os; see Fig. 13-1). Circuits in the lateral portion of the CTI can also occur but are less common. This arrhythmia can be sustained and usually occurs in patients who have undergone prior, and often extensive, ablation at the CTI. Intracardiac recordings usually resemble typical AFL. However, in this form of CTI-dependent AFL, entrainment pacing from the lateral CTI demonstrates a post-pacing interval (PPI) longer than the tachycardia CL, a finding indicating that the lateral CTI is not part of the reentrant circuit. On the other hand, pacing from the region of medial CTI or CS os demonstrates concealed entrainment with PPI equal to the tachycardia CL. Fractionated or double potentials usually can be recorded in this area and can be entrained. Although the anatomical basis of this arrhythmia remains unknown, a linear lesion across the medial CTI, usually at the site of a very prolonged electrogram, can cure the tachycardia.

Non–Isthmus-Dependent Right Atrial Macroreentry

Lesional Right Atrial Macroreentrant Tachycardia

Atrial macroreentry in the right free wall is the most common form of non–CTI-dependent RA MRAT. These circuits can propagate around a central obstacle of a low-voltage area or scar in the lateral or posterolateral RA wall, arising spontaneously or as a consequence of prior atrial surgery.The central obstacle of the macroreentrant circuit can be an atriotomy scar (in patients who have undergone surgery for congenital or valvular heart disease), a septal prosthetic patch, a suture line, or a line of fixed block secondary to radiofrequency (RF) ablation. Other obstacles can also include anatomical structures located in the vicinity of the scar (superior vena cava [SVC], IVC). Occasionally, these ATs are associated with areas of electrical silence, a finding suggesting atrial scarring in patients who have not undergone prior atrial surgery. These patients have a characteristic posterolateral and lateral distribution of RA scarring and frequently have more than one tachycardia mechanism. Low-voltage electrograms characterizing areas of scar and double potentials characterizing a line of block can be observed during both normal sinus rhythm (NSR) and AT. In one study, electroanatomical mapping revealed that RA electrically silent areas (electrogram amplitude 0.03 mV or lower) were involved in the tachycardia mechanism in two thirds of the patients with non–CTI-dependent RA MRAT.2,3

Patients with congenital heart disease have a high prevalence of AT, particularly after they have undergone reparative or palliative surgical procedures. For MRATs in adults with repaired congenital heart disease, three RA circuits are generally identified: lateral wall circuits with reentry around or related to the lateral atriotomy scar, septal circuits with reentry around an atrial septal patch, and typical AFL circuits using the CTI. These arrhythmias are discussed separately in Chapter 14.1,4

Left Atrial Macroreentry

LA MRATs are less common than typical AFL and are frequently related to or coexist with AF. LA MRAT is a known complication of surgical and catheter-based therapies of AF, and it can occur in up to 50% of patients following extensive catheter ablation strategies (see Chap. 15).8 Additionally, cardiac surgery involving the LA or atrial septum can produce different LA macroreentrant circuits. However, LA circuits also can be found in patients without a history of atriotomy or prior ablation. Electroanatomical maps in the latter group often show low-voltage or areas of scar in the LA, which act as a central obstacle or barrier in the circuit. These areas are typically located at the posterior wall (45%), superior region (roof, 28%), or anteroseptal region (27%) of the LA. The pathogenesis of these areas with no electrical signals is not well established. Potential causes include volume and pressure overload (mitral valve disease, hypertension, heart failure), ischemia (atrial branch occlusion), postinflammation scarring (after myocarditis), atrial amyloidosis, atrial dysplasia, and tachycardia-related structural remodeling. These macroreentrant circuits show considerable anatomical variability and frequently involve multiple simultaneous loops.1,2

Clinical Considerations

Electrocardiographic Features

P wave morphology on the surface ECG is usually of limited value for precise anatomical localization of macroreentrant circuits. Analysis of the P wave can be impeded by partial or complete concealment of the P wave within the QRS complexes or T waves when the AT is associated with 1:1 or 2:1 AV conduction. Additionally, P wave morphology of a spectrum of RA and LA MRATs is highly variable. The presence of complex anatomy secondary to congenital abnormalities, prior atrial surgery, or a large low-voltage zone (secondary to underlying atrial substrate or extensive catheter or surgical atrial ablation) can modify atrial wavefront propagation in a nonuniform manner, resulting in deviated atrial activation vectors or low amplitude P waves. Furthermore, P waves produced by different underlying substrates may appear similar if the direction of activation of the atrial septum and LA is similar. The surface ECG morphology is most characteristic (and hence predictive) for establishing a diagnosis of counterclockwise typical AFL. Nevertheless, atypical ECG patterns have been described for typical AFL after AF ablation. Although clockwise typical AFL also has a characteristic appearance, this is more variable, and it can be mimicked by various other MRATs.5,10 On the other hand, AFL may show distinct isoelectric intervals between P waves, especially in the presence of extensive atrial scarring or a localized macroreentrant circuit, similar to focal AT.

Perimitral Atrial Macroreentry

Most of these tachycardias show prominent forces in leads V1 and V2, with diminished amplitude in the inferior leads (see Fig. 13-2). It has been suggested that a posterior LA scar allows for domination by anterior LA forces. This constellation of findings may mimic counterclockwise or clockwise CTI-dependent AFL, but the decreased amplitude of frontal plane forces suggests an LA circuit. In patients with prior PV isolation procedures, the surface ECG morphology of counterclockwise perimitral MRAT can be different from that in patients without prior ablation, possibly related to varying degrees of prior LA ablation or scar. In these patients, counterclockwise perimitral MRAT demonstrates positive P waves in the inferior and precordial leads and a significant negative component in leads I and aVL. Furthermore, counterclockwise perimitral MRAT in these patients can have a morphology similar to that of left PV ATs. However, counterclockwise perimitral MRAT is suggested by a more negative component in lead I, an initial negative component in lead V2, and a lack of any isoelectric interval between P waves. Clockwise perimitral MRAT has limb lead morphology that is the converse of that of counterclockwise perimitral MRAT and an initial negative component in the lateral precordial leads. The positive P wave in leads I and aVL differentiates clockwise perimitral MRAT from counterclockwise CTI-dependent AFL and left PV AT.

Electrophysiological Testing

Typically, a decapolar catheter (positioned into the CS with the proximal electrodes bracketing the CS os) and a multipolar (20- or 24-pole) Halo catheter (positioned at the tricuspid annulus) are used to map typical AFL. The distal tip of the Halo catheter is positioned at 6 to 7 o’clock in left anterior oblique (LAO) view, so that the distal electrodes will record the middle and lateral aspects of the CTI, the middle electrodes will record the anterolateral RA, and the proximal electrodes may record the RA septum (depending on the catheter used). Instead of the Halo and CS catheters described, some laboratories use a single duodecapolar catheter around the tricuspid annulus while extending the catheter tip inside the CS. Such a catheter would straddle the CTI and provide recording and pacing from the medial and lateral aspects of the isthmus.

AT = atrial tachycardia; CL = cycle length; LA = left atrium; RA = right atrium.

Tachycardia Features

MRAT is characterized by a constant CL, P wave polarity, morphology, and amplitude of the recorded bipolar electrograms and by the presence of a single constant macroreentrant circuit with a constant atrial activation sequence. The atrial activation sequence and atrial CL depend on the origin and type of the macroreentrant circuit. However, considerable variation in the atrial CL for a single macroreentry circuit is unusual, although it can be observed in the atrium contralateral to atrium of origin of the tachycardia. In contrast, focal ATs classically exhibit alterations in CL with speeding (warm-up) and slowing (cool-down) at the onset and termination of tachycardia. Variation in the AT CL of greater than 15% has been suggested as a reliable marker of a focal AT. However, a regular AT can be either focal or macroreentrant.11 Additionally, focal ATs often manifest as bursts of tachycardia with spontaneous onset and termination, although they can be incessant, and they may accelerate in response to sympathetic stimulus.5 Several criteria can help distinguish focal AT from MRAT (see Table 11-5).

Atrial activation during MRATs spans the whole tachycardia CL. In contrast, intracardiac mapping in the setting of focal ATs shows significant portions of the tachycardia CL without recorded atrial activity, and atrial activation time is markedly less than the tachycardia CL, even when recording from the entire cardiac chamber of tachycardia origin (see Fig. 11-2). However, in the presence of complex intramyocardial conduction disturbances, activation during focal tachycardias can extend over a large proportion of the tachycardia CL, and conduction spread can follow circular patterns suggestive of macroreentrant activation.5 On the other hand, long isoelectric intervals can occur between P waves during MRATs, especially when mapping is limited to only the atrium contralateral to the origin of the macroreentrant circuit or to only parts of the ipsilateral atrium; a focal activation can be observed, incorrectly suggesting a focal mechanism. This is particularly observed for LA MRATs in the presence of large areas of electrical silence. However, a thorough intracardiac activation mapping reveals atrial activation spanning the tachycardia CL.

Occasionally, P wave morphology on the surface ECG resembles AFL, but intracardiac recordings show that parts of the atria (commonly the LA) have disorganized atrial activity (Fig. 13-4). Such rhythms behave more like AF than AT, but they may be converted to true typical AFL with antiarrhythmic drugs.

MRAT is usually associated with 2:1 AV conduction, although variable AV conduction and larger multiples are not uncommon. Variable AV block is the result of multilevel block; for example, proximal 2:1 AV block and more distal 3:2 Wenckebach block result in 5:2 AV Wenckebach block. Macroreentrant circuits can have long CLs in the presence of extensive atrial disease and antiarrhythmic agents, in which case fast ventricular response and 1:1 AV conduction may occur.

Diagnostic Maneuvers during Tachycardia

Atrial Pacing

Burst pacing from the CS or along the Halo catheter is started at a CL 10 to 20 milliseconds shorter than the atrial CL, and then the pacing CL is progressively shortened by 10 to 20 milliseconds. The capture of atrial stimuli and acceleration of the atrial rate to the paced rate should be verified before analyzing the tachycardia response to overdrive pacing. The response of AT to overdrive pacing is evaluated for entrainment, overdrive suppression, transformation into distinct uniform AT morphologies or AF entrainment, and ability and pattern of termination.

Entrainment

Overdrive atrial pacing at long CLs (i.e., 10 to 30 milliseconds shorter than the tachycardia CL) usually can entrain MRAT. The slower the pacing rate and the farther the pacing site from the reentrant circuit, the longer the pacing drive required to penetrate and entrain the tachycardia. Achievement of entrainment of the AT establishes a reentrant mechanism of the tachycardia and excludes triggered activity and abnormal automaticity as potential mechanisms (Fig. 13-5). Entrainment can also be used to estimate qualitatively how far the reentrant circuit is from the pacing site (see later).

Entrainment with Fusion

During entrainment of MRAT, fusion of the stimulated impulse can be observed on the surface ECG, but it is easier to recognize on intracardiac recordings from the Halo and CS catheters. The stimulated impulse has hybrid morphology between the fully paced atrial impulse and the tachycardia impulse. The ability to demonstrate surface ECG fusion requires a significant mass of atrial myocardium to be depolarized by both the paced stimulus and the tachycardia. The farther the stimulation site from the reentrant circuit, the less likely entrainment will manifest ECG fusion. It is important to understand that overdrive pacing of a tachycardia of any mechanism can result in a certain degree of fusion, especially when the pacing CL is only slightly shorter than the tachycardia CL. Such fusion, however, is unstable during the same pacing drive at the same pacing CL because pacing stimuli fall on a progressively earlier portion of the tachycardia cycle, thus producing progressively less fusion and more fully paced morphology. Such phenomena should be distinguished from entrainment, and sometimes this requires pacing for long intervals to demonstrate variable degrees of fusion. Focal ATs (automatic, triggered activity, or microreentrant) cannot manifest fixed or progressive fusion during overdrive pacing. Moreover, overdrive pacing frequently results in suppression (automatic) or acceleration (triggered activity) of focal ATs, rather than resumption of the original tachycardia with an unchanged tachycardia CL.

Overdrive Suppression

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