How to Use Electroanatomic Mapping to Rapidly Diagnose and Treat Post–AF Ablation Atrial Tachycardia and Flutter
Aman Chugh, MD
Patients who undergo catheter ablation of AF may develop AT during follow-up, which may require a repeat ablation procedure. These tachycardias may arise from the LA, RA, and also the CS. Unlike CTI-dependent AFL, which can be readily recognized based on its stereotypical ECG features and can be eliminated in virtually every patient without significant difficulty, mapping and ablation of postablation AT remains challenging. The reasons for this include lack of specific ECG clues, the diversity of mechanisms, multiplicity of tachycardias in the individual patient, and sites of origin. Nonetheless, these tachycardias can be eliminated in the vast majority of patients. This chapter will offer a practical approach to mapping these tachycardias using electroanatomic mapping.
The planning phase in some ways has its beginnings at the initial consultation for consideration of AF ablation. We discuss with patients, particularly those with persistent AF, that they may require a repeat ablation procedure for AT and AFL. The referring physicians are also included in this discussion, since they are part of the team that will be managing the patients even after the procedure. Approximately 50% of patients will require a repeat procedure after an ablation procedure for persistent AF. Not uncommonly, patients may develop AT shortly after LA ablation for persistent AF. However, these patients should not necessarily be committed to a repeat procedure since in some patients, the AT may be a transient finding. In our practice, all patients with a recurrence within the first few months after an ablation procedure undergo transthoracic cardioversion or are treated medically in case of paroxysmal AT. If the arrhythmia then recurs, we consider a catheter ablation procedure. Most patients elect to undergo a repeat ablation procedure as opposed to taking antiarrhythmic therapy because many patients have either failed medical therapy for AF and/or wish to be arrhythmia-free without the need for long-term rhythm-controlling medications and anticoagulation.
If patients were taking antiarrhythmic medications to suppress the arrhythmia while waiting for the procedure, these medications should be discontinued at least 5 half-lives before the procedure. Amiodarone should be discontinued at least 2 months before the procedure. In patients with paroxysmal AT, we typically discontinue the rhythm-controlling medications, except for amiodarone, about 4 to 6 weeks prior the procedure to increase the chance of arrhythmia recurrence. Ideally, the ablation procedure for AT should be performed during the arrhythmia. In some patients, AT may not be inducible in the EP laboratory despite isoproterenol infusion and an aggressive induction protocol. An empiric ablation strategy in such an instance may not eliminate the culprit arrhythmia, leading to recurrence.
Rate-controlling medications are usually discontinued a few days prior to the procedure. For patients with persistent AT, this may be associated with improvement in AV nodal conduction. In most patients, transient tachycardia is reasonably well tolerated. However, in others, abrupt discontinuation of rate-controlling medications may be associated with 1:1 AV nodal conduction during AT, leading to hemodynamic compromise. These patients may require urgent cardioversion, which of course helps alleviate the acute symptoms but also results in interruption of the clinical tachycardia. To guard against this possibility, patients who are known to have very facile AV nodal conduction are admitted to the hospital on the day prior to the procedure for washout of cardiac medications. If they develop tachycardia, then intravenous rate-controlling medications can be used in a monitored setting. These medications can then be discontinued a few hours before the procedure.
Our preference is to perform LA ablation procedures on therapeutic oral anticoagulation with warfarin. This has been shown to be safe and is probably associated with not only a lower risk of thromboembolic complications but also decreased prevalence of access-site complications. The decision to perform TEE to rule out thrombus is individualized. In patients with therapeutic international normalized ratio, who lack significant structural heart disease and present in sinus rhythm, TEE may be deferred. Patients presenting in AT routinely undergo TEE prior to the procedure. Patients with significant structural heart disease (e.g., severe left ventricular dysfunction or severe LA enlargement (> 5.5 cm) or atrial myopathy or delayed activation of the LAA noted during a prior procedure) should probably undergo TEE irrespective of their presenting rhythm or anticoagulation status.
CT or MRI may have a role in the management of a patient presenting for an AT procedure. In most instances, preprocedure imaging is obtained to evaluate for variant PV anatomy. However, this information is unlikely to alter the approach to the patient with AT. The course of the circumflex or the sinus nodal artery may influence the operator’s decision to perform prophylactic linear ablation at the mitral isthmus and the LA roof, respectively. The anatomy of the coronary branches may be difficult to interpret on imaging studies for most electrophysiologists and consultation with a cardiothoracic radiologist may be needed.
Mapping and Ablation of Postablation AT
Venous and LA Access
A minimum of two catheters is required for a repeat procedure for postablation ATs. Occasionally, patients presenting for a repeat procedure may have significant soft tissue resistance or scarring over the femoral vessels, making it challenging to utilize 3 sheaths within an ipsilateral femoral vein. In this circumstance, the operator has the option to simply use 2 sheaths or obtain venous access on the contralateral side. Our practice is to use 2 sheaths, especially in female patients or those with small stature, to minimize the risk of vascular complications. LA access may also be challenging owing to a thickened interatrial septum secondary to repeat transseptal punctures. In such an instance, the transseptal puncture may be performed using RF energy applied at the tip of the needle.
The ECG can be helpful in not only delineating the mechanism of the arrhythmia but may also guide mapping and ablation. Lack of a significant isoelectric interval between successive p-waves favors macro-reentry as a mechanism. Although the majority of postablation ATs arise from the LA, AFL from the CTI is frequently encountered. A transition from positive to negative flutter waves in the precordial leads, point to right atrial source (Figure 27.1).1 Negative flutter waves in the inferior leads are also suggestive but less specific for a RA origin. The flutter waves may not be readily apparent during 2:1 AV nodal conduction. Adenosine can also help visualize atrial activity but the fact it may result in AF or alter the tachycardia makes it less attractive. Identifying a RA origin should not preempt transseptal catheterization since documenting PV isolation after elimination of the tachycardia is critical in preventing recurrence. The ECG is also helpful in ruling out organized AF. During AT, the P-wave morphology should be consistent, owing to consistent atrial activation. During organized AF, the P-wave morphology should vary, even subtly, which should prompt mapping of AF most often by targeting complex EGMs or rapid activity.
Defining the Reference for Electroanatomic Mapping
A stable reference is required for both activation and entrainment mapping. Typically, a decapolar catheter is inserted into the CS for this purpose. During activation mapping, it is preferable to use the CS bipole with the largest atrial and smallest ventricular EGM. Rarely, the EGM amplitude of the CS EGM is extremely small or the catheter may not be stable within the CS. In this instance, the reference catheter can be placed in the RAA.
Unless the P-wave morphology is suggestive of an RA origin, we typically obtain LA access prior to RA mapping, since about 80% tachycardias are successfully ablated from the LA. Activation mapping is more efficiently performed using a multipolar catheter, either a circular mapping catheter (Lasso, Biosense Webster, Diamond Bar, CA) or the “flower” catheter (PENTARAY, Biosense Webster). The latter is preferred based on a greater number of electrodes and closer electrode spacing. These features facilitate the creation of a high-density map, which can be constructed within 10–15 minutes and also decrease the probability of inclusion of far-field activity. It should be noted that these catheters may become entrapped in mitral valve prosthesis, and the flower catheter is specifically contraindicated in such a setting. There are other mapping systems available, such as the NavX (St. Jude Medical, St. Paul, MN) and the Rhythmia (Boston Scientific).2 We utilize all 3 mapping systems in our practice, but our experience with CARTO (Biosense Webster) is greater compared with the others. A noninvasive mapping system (utilizing unipolar EGMs extracted from the body surface) has also been used in patients with post AF atrial tachycardias but is not yet widely available.3
It is important to document CL stability prior to constructing an activation map. Variability of more than 10% may be associated with a nonsensical activation pattern. The mechanism of these tachycardias is probably best explored by mapping the diastolic interval.
Prior to collecting activation data, the window of interest is defined on the 3D mapping system. There are a number of methods in defining the window of interest. A practical approach is to aim to cover approximately 90% of the TCL. For example, for an AT with a CL of 230 ms, the window is selected to span 210 ms. This interval is then divided in half, and values of –105 ms and 105 ms (before and after the reference, respectively) are entered to define the window of interest.4 One may also define the window based on the mechanism of the tachycardia, i.e., focal versus macroreentrant. In the case of the former, the window of interest would be set to account for a fraction of the TCL. However, this presupposes the mechanism, which in itself may be problematic.
A point-by-point activation map is then constructed utilizing a multipolar mapping catheter. “Respiratory gating” avoids creation of inaccurate geometry due catheter movement related to respiratory excursion. Within approximately 15 minutes, a high-density map can be created using a few thousand points. Unfortunately, user intervention is still required for accurate annotation of EGMs. For example, automated mapping is not able to consistently exclude ventricular EGMs near the valve plan, leading to erroneous activation patterns. Also, the system often misses low amplitude local EGMs, which may make it more difficult to identify areas of slow conduction. The operator is able to override the system and assign timing to such points but at a cost of prolonging the mapping portion of the procedure. Areas that are not well defined by the multipolar mapping catheter can be further investigated by the ablation catheter.
With low-amplitude signals, it may difficult to identify true local activation. Differentiating far- from near-field signals may also be difficult. Pacing may help discern between near- and far-field potentials; however, it may alter or terminate the tachycardia. Adjudicating local activation timing to fractionated or split EGMs may also be challenging. In this case, it is best to be consistent and revisit these sites after completion of the map to ensure that the EGMs were correctly annotated. If EGMs consistently span beyond the window of interest, it is possible that the window was not defined appropriately or that there is significant CL variation. If a small part of the EGM does span beyond the window, it is reasonable to assign timing to the earliest or the latest portion of the EGM within the window of interest. It is important to be consistent in annotating EGMs; otherwise one will end up with a meaningless map.
While creating an activation map, it is helpful to accurately define anatomic obstacles, which will serve as anchors to linear lesions. Areas without appreciable electrical activity should be tagged as “scar.” Sites of conduction block, defined as widely split potentials that are separated by an isoelectric interval, should be tagged as “double potentials.” The mitral and tricuspid annuli should be accurately depicted. Not uncommonly, one may encounter fractionated, long-duration EGMs early during the mapping procedure, and it may be tempting to perform entrainment mapping at or even ablate such an “attractive” site. However, it is best to construct the map and understand the mechanism of the tachycardia prior to entrainment mapping and ablation.
Classically, an activation map during macroreentrant tachycardias should reveal an early-meets-late pattern (areas color coded as red (early) and purple (late) adjacent to each other). In addition, mapping should account for nearly the entire CL of the tachycardia. Otherwise one should suspect an origin from the contralateral chamber or the CS. It is important to bear in mind that in a large reentrant circuit, there are no absolute early or late areas, and are only deemed such with respect to an arbitrary reference. To target the “early” area on such a map with RF energy would be the wrong approach. One first confirms the mechanism with entrainment mapping and then identifies anatomical barriers to which the linear lesion is anchored. For focal tachycardias, one should observe a centrifugal activation from the point of origin (red followed by yellow, green, blue, and purple). Despite sampling the entire chamber of origin, only a fraction of the CL may be covered.
Prior to commencing with ablation, it is critical that one understand the mechanism of the tachycardia. It must be borne in mind that patients presenting for AT have previously undergone an extensive ablation procedure for persistent AF, including ablation of PV antra, complex, fractionated EGMs, and lines at the roof and/or mitral isthmus. Thus, one should expect to encounter areas of scar, slow conduction, and conduction block. These findings may obfuscate the activation patterns, leading to nonsensical maps. This is why it is good practice to confirm the findings of activation mapping with (limited)entrainment mapping. Other than macroreentry and focal mechanisms, ATs may also be generated by small areas of reentry. These tachycardias are constrained to one of the walls of the atrium, as opposed to multiple/opposite walls as in macroreentrant ATs (see below).
LA Macroreentrant ATs
Mitral Isthmus–Dependent AFL
The most common macroreentrant AT after extensive ablation of persistent AF is mitral isthmus–dependent AFL.5 The mitral isthmus is defined as the region between the lateral mitral annulus and the left-sided PVs. Perimitral flutter is usually seen after prior linear ablation at the mitral isthmus, but it may also be encountered even without prior ablation in this region. In contradistinction to typical AFL, which is predominantly due to counterclockwise activation (around the tricuspid valve), mitral isthmus–dependent flutter is equally likely to be due to clockwise or counterclockwise activation around the mitral valve. The following criteria are required for the diagnosis of perimitral flutter: activation mapping accounts for entire CL of the tachycardia; the activation map shows an early-meets-late pattern around the mitral valve (Figure 27.2); and entrainment mapping at any point around the valve reveals a postpacing interval (PPI) within 20 to 30 ms of the TCL (Figure 27.3). (Note: If only entrainment mapping is utilized, PPIs within 20 to 30 ms of the TCL, from opposite, e.g., lateral and septal aspects of the mitral annulus, confirm the diagnosis.)
Linear ablation is commenced from the lateral annulus and extended to the anterior aspect of the left-sided PVs. In about 20% of patients, a pouch is present at the lateral mitral isthmus, making it difficult to create a contiguous lesion.6 If the catheter suddenly “skips” during catheter withdrawal from the lateral annulus, a pouch is likely present. The real-time impedance profile during ablation may also suggest the presence of a pouch. In such a case, it is reasonable to extend the line from the posterolateral or even anterolateral annulus. Typically, high power (35 W of irrigated RF energy; THERMOCOOL SMARTTOUCH, Biosense Webster) is required during endocardial ablation of the mitral isthmus.
Frequently, endocardial ablation fails to terminate the tachycardia. Epicardial ablation within the CS is required in about two-thirds of the cases to terminate perimitral flutter and/or achieve bidirectional block at the isthmus (Figure 27.4). The ablation catheter is advanced into the distal CS to the level of the endocardial line. Prior to commencing with RF energy, the catheter is torqued toward the atrial side to avoid power delivery within a ventricular branch. If a large ventricular EGM is present on the distal bipole of the ablation catheter, it is useful to perform high-out pacing to rule out ventricular capture.
During RF energy delivery within the CS, the power is reduced to 20 W, and the catheter is withdrawn slowly to the mid CS. If the tachycardia does not terminate, the process is repeated until the local atrial EGM is abolished. While ablating in the CS, it is critical to follow the impedance/temperature curves to monitor for overheating or catheter dislodgement into a ventricular branch. The latter will be associated with a sudden impedance rise. If after several attempts there is no slowing of the tachycardia or change in the activation sequence/P-wave morphology with ablation, it is useful to perform entrainment mapping to make sure one is still dealing with the same tachycardia (see “Multi-Loop ATs”).
After tachycardia termination, the next step is to demonstrate linear block at the mitral isthmus. This may be accomplished either during pacing from the proximal CS or the LAA (Figure 27.5). We typically place the ring catheter at the base of the LAA and observe for an abrupt change in activation during RF energy delivery. In the absence of conduction block, pacing from the LAA results in distal-to-proximal activation of the CS. When conduction block is achieved, there is a sudden change in the activation sequence to proximal-to-distal. Pacing from multiple bipoles of the CS catheter is helpful in ruling out slow conduction and confirming bidirectional block. Bidirectional block across the mitral isthmus can be achieved in up to 90% of patients, but it may be quite challenging in some. The most likely reason for the inability to create complete mitral isthmus block is the presence of the circumflex artery, interposed between the CS and the epicardial isthmus.6 The artery likely acts as a heat sink, preventing adequate heating of the mitral isthmus. Herein lies the possibility of injury to the circumflex artery. If block cannot be achieved, the next step might be to attempt ablation using higher power. Since the interposition of the circumflex is the likely reason for lack of success, additional attempts, especially if using higher power, may not only fail to yield block but may also increase the risk of arterial injury.