Color Atlas and Synopsis of Electrophysiology, 1st Ed.

44. INCISIONAL ATRIAL FLUTTER: INSIGHTS ON HOW TO MAP AND ABLATE NON–ISTHMUS-DEPENDENT ATRIAL FLUTTERS

Emile G. Daoud, MD, FACC, FHRS

CASE PRESENTATION

The patient is a 64-year-old man who underwent mitral valve repair 12 years earlier. He presents with fatigue and palpitations and is found to be in atrial flutter (AFlr). After a transesophageal echocardiogram excludes left atrial clot, he is referred to the electrophysiology laboratory for catheter ablation.

A 20-pole catheter is positioned in the right atrium (Figure 44-1). The flutter wave morphology suggests a non–isthmus-dependent, incisional AFlr. To confirm this diagnosis and to map and ablate the tachycardia, the strategy is to utilize the response to pacing to assess the postpacing interval, assess for concealed entrainment of the tachycardia, and identify low-amplitude/fractionated atrial electrograms and activation and voltage map information from the electroanatomic map.

Images

FIGURE 44-1. This is an LAO fluoroscopic image of a 20-pole catheter in the right atrium. Poles 1 and 2 (distal) are located in the proximal coronary sinus and poles 19 and 20 are in the high right atrium. The catheter lies across the cavotricuspid isthmus (poles 1-10) and then along the right atrial free wall (poles 11-20). The diagram in the lower right corner depicts a right atrial free wall atriotomy with a macroreentrant circuit rotating around the scar/incision (yellow arrows).

MAPPING OF INCISIONAL, PATCH, AND SCAR- RELATED MACROREENTRANT ATRIAL FLUTTER

This case is an example of atrial reentry around an area of scar/incision, termed “incisional flutter.” As is common with these tachycardias, the patient has undergone an atriotomy several years prior to onset of the tachycardia as part of valve surgery.1 Incisional AFlr usually does not respond to antiarrhythmic medication and typically requires ablation.

In addition to understanding the anatomy based on prior operative procedure notes, there are four features that aid in mapping AFlr due to incision-related scar. These features are also equally applicable to mapping and ablating any form of macroreentrant AFlr (inclusive of isthmus-dependent AFlr, AFlr/atrial tachycardias following congenital heart surgery, and postatrial fibrillation ablation AFlr):

1. Postpacing intervals.2 The differential diagnosis of the tachycardia mechanism for this case is clockwise rotation of an isthmus-dependent flutter or an incisional flutter. To diagnose the mechanism, the response to pacing is helpful. When the tachycardia is entrained by atrial pacing, the tip of the pacing catheter is in or near the reentrant circuit if the first return beat of the tachycardia recorded from the pacing catheter, after pacing is stopped, is within 30 ms of the tachycardia cycle length: post-pacing interval (PPI) measured from the pacing catheter minus the tachycardia cycle length (TCL) ≤ 30 ms.

2. Atrial concealed entrainment.3,4 When an atrial tachycardia is entrained, there is often fusion between the wave of depolarization generated from the pacing catheter colliding with the wave of depolarization of the tachycardia. The resultant P wave is a fusion beat: a P-wave morphology that is “fused” between the two sources. Progressive fusion, meaning that the P-wave morphology is changing during the first several beats of pacing, confirms that the pacing catheter is not in the reentrant circuit. However, when pacing from within the circuit, there is no fusion, and the P-wave morphology generated from the pacing catheter is identical to the P wave generated by the tachycardia. This is called “concealed entrainment” and implies that the pacing catheter is within the circuit. Although this technique is effective for mapping reentrant ventricular arrhythmias since changes in QRS morphology are obvious, change in the P-wave morphology using surface ECG analysis is subtle. Concealed entrainment, for any mechanism of macroreentrant AFlr, is therefore determined by the absence of change in the atrial activation sequence, amplitude, and morphology of intracardiac atrial recordings when pacing from within the reentrant circuit.

3. Low amplitude/fractionated electrograms.4 An essential feature of ablating non–isthmus-dependent AFlr is to identify the zone of slow conduction that is critical to the reentrant arrhythmia. This slow zone of conduction is characterized by anisotropic conduction. Anisotropic conduction is slow conduction related to local disorganized atrial architecture, often at sites of atrial myocardium intertwined with atrial scar/fibrosis. Atrial electrograms at these sites have low amplitude and are highly fractionated. Identification of these electrograms coupled with response to pacing and atrial entrainment (listed previously), help to identify the zone of slow conduction and sites to target for ablation.

These three features of assessing a macroreentrant arrhythmia (postpacing intervals, atrial concealed entrainment, and low amplitude/fractionated electrograms) are demonstrated in Figures 44-2 to 44-6 for this case of incisional AFlr (see figure legend for further explanation).

Images

FIGURE 44-2. This is the initial intracardiac tracing of the tachycardia, cycle length 300 ms. The activation sequence is earliest at poles 17 and 18 and last at poles 1 and 2. The differential diagnosis is clockwise isthmus-dependent AFlr or incisional AFlr. The widely split electrograms on poles 17 and 18 and the late activation of poles 19 and 20 coupled with the history of a prior atriotomy suggest an incisional flutter, but response to pacing is required to confirm a diagnosis (see Figure 44-3). Abbreviations: aVF, V1, surface ECG I; 20-pole recordings labeled as Duo 1-20; RVa, right ventricular apical recording.

Images

FIGURE 44-3 This demonstrates the response to pacing from poles 5 to 6. These poles are located within the cavotricuspid isthmus. If the tachycardia is an isthmus-dependent AFlr, the response to pacing should confirm this mechanism. However, pacing confirms that the mechanism is not isthmus-dependent. When pacing is stopped, the postpacing interval measured at poles 5 and 6 is 40 ms (340 ms − 300 ms = 45 ms), consistent with poles 5 and 6 not located within the AFlr circuit. Also, the atrial activation sequence during atrial pacing from poles 5 and 6 is not consistent with concealed entrainment of the AFlr. The activation sequence during pacing is not identical to the activation sequence during the tachycardia. Note that the electrogram recorded from poles 1 and 2 during pacing is nearly simultaneous with the electrogram on poles 9 and 10 (dashed green line); however, during the tachycardia, poles 1 and 2 are activated well after poles 9 and 10 (dashed blue line). Abbreviations same as Figure 44-2.

Images

FIGURE 44-4. Since the original tracing (Figure 44-2) showed split potentials at poles 17 and 18 and an isthmus-dependent AFlr is excluded (Figure 44-3), response to pacing is then assessed by pacing at poles 15 and 16, presumably near the circuit. The postpacing interval is quite good, 305 ms (a difference of 5 ms), consistent with pacing from near/within the circuit. Furthermore, pacing from poles 15 and 16 results in an atrial activation sequence that is identical to the activation sequence during the tachycardia, but also note that the atrial electrogram features (amplitude and fractionation) are also nearly identical with pacing as compared to during tachycardia. This response to pacing confirms atrial concealed entrainment, another clue that poles 15 and 16 are within the AFlr circuit. Abbreviations same asFigure 44-2.

Images

FIGURE 44-5. With pacing only at two sites, the mechanism and location of the AFlr is confirmed. The ablation catheter is then advanced into the right atrium and is directed to the region near poles 15 and 16. In this figure, note that the electrograms at the ablation catheter (ABL 1, 2) are low amplitude, fractionated, and split (at times into three components). Also, the electrograms recorded from the ABL 1, 2 span the electrograms on the 20-pole catheter (red dashed lines), indicating that ABL 1, 2 is in a region of slow activation and likely a turnaround point of the tachycardia as it rotates around the edge of the atriotomy incision. Abbreviations same as Figure 44-2.

Images

FIGURE 44-6 Response to pacing at ablation catheter (ABL 1, 2) shows excellent postpacing interval (300 ms, a difference of 0 ms) and atrial concealed entrainment (as explained in Figure 44-4). Abbreviations same as Figure 44-2.

The fourth feature that is quite valuable to map incisional AFlr (as well as other non–isthmus-dependent AFlr) is the activation and voltage map that is completed with an electroanatomic map.

4. Activation and voltage map.5,6 An electroanatomic map allows creation of a voltage and an activation sequence map of the atrium during the tachycardia. Scar is identified by low amplitude or absent atrial electrograms, which can be the area for slow conduction/reentry and often the region for the patch/scar/incisional AFlr. Mapping of the endocardial activation sequence during the tachycardia allows creation of the reentrant circuit by identifying the sites of earliest and latest activation. Figures 44-7 and 44-8 demonstrate the activation maps (CARTO system) that were used in this case to identify the reentrant incisional AFlr and to guide the ablation lesion set (see figure legend for further explanation).

Images

FIGURE 44-7. This is an RAO projection of the electroanatomic map of the right atrium during the incisional AFlr. This map was created by annotating electrograms recorded from the ablation catheter relative to a fixed electrode in the heart (in this patient, it was Duo 1, 2). The ablation catheter was moved throughout the atria, and signals that were “early,” relative to the electrogram on Duo 1, 2, were annotated as red, and “late” signals were annotated as dark colors (latest = purple color). Also shown are the 20-pole electrodes, deployed along the cavotricuspid isthmus and the right atrial free wall. Poles 17 and 18 (noted to have a split electrogram on the first recording, see Figure 44-2) are highlighted in white. The electroanatomic map shows a region of “early meets late,” a dark red zone, squeezed between the early red/yellow colored region and the late blue/purple colored region. The “early meets late” region suggests the turnaround point of the tachycardia. The tricuspid valve annulus is noted by light blue colored dots and ring. The single gold-colored dot represents the location of the His bundle. Abbreviations: CS, coronary sinus; IVC, inferior vena cava; SVC, superior vena cava; TV, tricuspid valve.

Images

FIGURE 44-8 With the tachycardia mechanism confirmed and mapping completed, a line of ablation (red dots) is completed between the superior vena cava and the tricuspid valve annulus, resulting in termination of the tachycardia. During this line of ablation, careful attention was made not to ablate at sites near the phrenic nerve, identified by activation of the diaphragm with high-output pacing from the ablation catheter. Abbreviations same as Figure 44-7.

For incisional AFlr, successful ablation sites often have all four of these features, yet ablation is unlikely to be successful with a single application of radiofrequency energy. The zone of slow conduction is often broad and, similar to ablation of isthmus-dependent AFlr, a permanent elimination of a patch/scar/incision-related AFlr requires a line of ablation to another electrical inert region of the heart. In the current case example, a line of ablation was completed between the superior vena cava and the tricuspid valve annulus, thus transecting the critical zone of slow conduction.

The key to long-term freedom from AFlr is confirmation of bidirectional conduction block, not merely termination of the tachycardia.7 The mechanism to confirm bidirectional conduction block in this case is the same technique to confirm bidirectional block across any linear ablation lesion (eg, a cavotricuspid isthmus line for isthmus-dependent AFlr, or a roof line or mitral valve line created as part of ablation for atrial fibrillation). The concept is that two catheters are positioned on either side of the line of ablation. When pacing from one catheter, the time to the atrial signal recorded on the second catheter will be longer as the recording catheter is moved toward the line of block, compared to when the catheter is further from the line of ablation (but closer to the pacing source). In other words, if the line of ablation is complete, and there are no gaps, the wave of depolarization from the pacing catheter must travel in only one direction and hence activate the other side of the ablation line last (Figure 44-9).

Images

FIGURE 44-9 Confirmation of bidirectional conduction block. Figure 44-9 is an electroanatomic map (abbreviations same as Figure 44-7) after completion of the line of ablation and termination of the AFlr. The goal is to confirm bidirectional conduction block. Pacing will be completed from the tip of the catheter highlighted by the * and labeled as HRAd on the intracardiac tracings. HRA catheter is visualized on the electroanatomic map and is positioned just lateral to the line of ablation. The ablation catheter (ABL 1, 2) is located at the white dot, which is anatomically further away from the pacing tip compared to the pink dot. However, if there is complete block along the ablation line, then the pacing impulse must first travel past the white dot before reaching the area near the ablation line, noted by the pink dot.

Shown is the response to pacing from the HRAd catheter and the time to the local atrial signal recorded when the ablation catheter is first at the white dot and then located at the pink dot. With the ablation catheter located at the white dot, the time from the pacing stimulus from HRAd to the atrial electrogram on the ablation catheter (ABL 1, 2) is 120 ms (upper electrogram tracing). When the ablation catheter is then moved to the pink dot, even though it is anatomically closer to the pacing catheter (*, HRA), because there is complete conduction block across the ablation line (ie, no gaps), the time from the HRAd to the ABL 1, 2 at the pink dot is longer (240 ms; lower electrogram tracing) compared to the time recorded at the white dot (120 ms). Bidirectional block is confirmed when the same maneuver is performed with pacing from the ablation catheter and recording from the HRA catheter (not shown).

REFERENCES

  1. Pap R, Kohári M, Makai A, et al. Surgical technique and the mechanism of atrial tachycardia late after open heart surgery. J Interv Card Electrophysiol. 2012;35:127-135.

  2. Santucci PA, Varma N, Cytron J, et al. Electroanatomic mapping of postpacing intervals clarifies the complete active circuit and variants in atrial flutter. Heart Rhythm. 2009;6:1586-1595.

  3. Coffey JO, d’Avila A, Dukkipati S, et al. Catheter ablation of scar-related atypical atrial flutter. Europace. 2013;15:414-419.

  4. Wu RC, Berger R, Calkins H. Catheter ablation of atrial flutter and macroreentrant atrial tachycardia. Curr Opin Cardiol. 2002;17:58-64.

  5. Peichl P, Kautzner J, Cihák R, Vancura V, Bytesník J. Clinical application of electroanatomical mapping in the characterization of “incisional” atrial tachycardias. Pacing Clin Electrophysiol. 2003;26:420-425.

  6. Reithmann C, Hoffmann E, Dorwarth U, Remp T, Steinbeck G. Electroanatomical mapping for visualization of atrial activation in patients with incisional atrial tachycardias. Eur Heart J. 2001;22:237-246.

  7. Snowdon RL, Balasubramaniam R, Teh AW, et al. Linear ablation of right atrial free wall flutter: demonstration of bidirectional conduction block as an endpoint associated with long-term success. J Cardiovasc Electrophysiol. 2010;21:526-531.