Abstracts
Cavotricuspid isthmus (CTI)-dependent atrial flutter (AFL) is a common atrial arrhythmia, often occurring in association with atrial fibrillation, that may cause significant symptoms because of a rapid ventricular response, and it may cause embolic stroke, and rarely a tachycardia-induced cardiomyopathy. CTI-dependent AFL has been shown to be caused by macroreentry around the tricuspid valve annulus (TVA), with an area of concealed conduction in the CTI, anatomically bounded by the TVA anteriorly and the inferior vena cava (IVC) and Eustachian ridge posteriorly, with a line of conduction block along the crista terminalis. This electrophysiologic milieu produces a long enough reentrant path length, relative to the average tissue wavelength around the TVA annulus, to allow for sustained reentry. The triggers of AFL, commonly premature atrial contractions or nonsustained atrial fibrillation originating from the left atrium and pulmonary veins, most likely account for the fact that counterclockwise AFL (typical AFL) occurs most frequently clinically. AFL is also relatively resistant to pharmacologic suppression. Because of its well-defined anatomic substrate and frequent pharmacologic resistance, radiofrequency (RF) catheter ablation has been established as a safe and effective first-line treatment for CTI-dependent AFL. Although several approaches have been described for ablating CTI-dependent AFL, the most widely accepted technique is an anatomically-guided approach targeting the entire CTI, resulting in a high efficacy rate for cure of AFL, with minimal risk. This chapter reviews the electrophysiology of CTI-dependent AFL and the techniques currently used for its diagnosis, mapping, and ablation.
Keywords
atrial flutter entrainment ablation, atrial flutter intra-isthmus, atrial flutter lower loop, partial-isthmus reentrant, reverse typical atrial flutter, typical atrial flutter
Key Points
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The mechanism of most cavotricuspid isthmus (CTI)-dependent atrial flutter (AFL) is macroreentry around the tricuspid valve annulus (TVA).
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The diagnosis of CTI-dependent atrial flutter is made by demonstration of macroreentry around the TVA during entrainment at two or more sites around the tricuspid valve, and demonstration of concealed entrainment from the CTI during AFL.
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The target for ablation of CTI-dependent AFL is the CTI, between the TVA and the inferior vena cava (IVC).
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Special equipment that may improve outcome or may be required to ablate the CTI includes a large-tip catheter (8- or 10-mm ablation electrode) with a high-power radiofrequency generator (up to 100 watts) or an externally irrigated ablation catheter, a large-curve catheter, and a preformed or steerable sheath. An intracardiac echocardiographic (ICE) catheter, electroanatomic or noncontact 3-dimensional mapping systems, or a multielectrode Halo catheter may be useful but are not required.
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Sources of difficulty in assuring successful long-term success may include complex anatomy (e.g., pouches, prominent Eustachian ridge) of the CTI, leading to failure to achieve bidirectional isthmus conduction block.
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Long-term success rates range from 90% to 95%, after achieving acute bidirectional CTI conduction block.
Cavotricuspid isthmus (CTI)-dependent atrial flutter (AFL) is a common atrial arrhythmia, often occurring in association with atrial fibrillation. It can cause significant symptoms because of a typically rapid ventricular rate, and may cause embolic stroke, and rarely a tachycardia-induced cardiomyopathy. The electrophysiologic substrate underlying CTI-dependent AFL has been shown to be macroreentry around the tricuspid valve annulus (TVA), with an area of concealed conduction in the CTI, anatomically bounded by the TVA anteriorly and the inferior vena cava (IVC) and Eustachian ridge posteriorly, with a line of conduction block along the crista terminalis. This electrophysiologic milieu produces a long enough reentrant path length, relative to the average tissue wavelength around the TVA, to allow for sustained reentry. The triggers of AFL, commonly premature atrial contractions or nonsustained atrial fibrillation originating from the left atrium and pulmonary veins, most likely account for the fact that counterclockwise AFL (typical AFL) occurs most frequently clinically. AFL is also relatively resistant to pharmacologic suppression.
Because of the consistent and well-defined anatomic substrate and the typical pharmacologic resistance of CTI-dependent AFL, radiofrequency (RF) catheter ablation is established as a safe and effective first-line treatment. Although several approaches have been described for ablating CTI dependent AFL, the most widely accepted technique is an anatomically-guided approach targeting the entire CTI, resulting in a high efficacy rate for cure of AFL, with minimal risk. This chapter reviews the electrophysiology of human CTI-dependent AFL and techniques currently used for its diagnosis, mapping, and ablation.
Atrial Flutter Terminology
Because of the variety of terms used to describe AFL in humans in the past, including type 1 and type 2 AFL, typical and atypical AFL, counterclockwise (CCW) and clockwise (CW) AFL, and isthmus-dependent and non–isthmus-dependent AFL, the Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology published a consensus document in 2001 in an attempt to develop a generally accepted standardized terminology for AFL. The consensus was that the terminology “typical” and “type 1” AFL were most commonly used to describe CTI-dependent, defined as a macroreentrant right atrial tachycardia, and included both the CCW and CW variants rotating around the TVA. Therefore the working group determined that CTI-dependent, right atrial macroreentrant tachycardia, rotating in the CCW direction around the TVA (when viewed from the right ventricle) would be termed typical AFL, and the similar tachycardia rotating in the CW direction around the TVA would be termed reverse typical AFL. For the purposes of this book, we will use the terms typical and reverse typical AFL, or CTI-dependent AFL when being referred to jointly. Other rare isthmus-dependent AFL variants, including lower loop reentry and partial isthmus-dependent AFL, are also discussed in this chapter.
Anatomy and Pathophysiology
The development of successful RF catheter ablation (RFCA) techniques for CTI-dependent AFL depended in part on the delineation of its electrophysiologic mechanism. Using advanced electrophysiologic techniques, including intraoperative and trans catheter activation mapping, CTI-dependent AFL was shown to be caused by a macroreentrant circuit rotating in either a CCW (typical) or a CW (reverse typical) direction in the right atrium around the TVA, with an area of relatively slow conduction velocity in the low posterior right atrium ( Figs. 11.1 and 11.2 ). The predominant area of slow conduction in the AFL reentry circuit has been shown to be in the CTI, through which conduction times may reach 80 to 100 ms, accounting for one-third to one-half of the AFL cycle length.
The CTI is the target for ablation and warrants special attention. The CTI refers to right atrial myocardium between the TVA and IVC, which courses from the inferolateral to the posteromedial low right atrium and is anatomically bounded by the IVC and Eustachian ridge posteriorly and by the TVA anteriorly (see Figs. 11.1 and 11.2 ). These boundaries form lines of conduction block delineating a protected zone in the reentry circuit. The presence of conduction block along the Eustachian ridge has been confirmed by the demonstration of double potentials along its length during AFL ( Fig. 11.3 ). The superomedial boundary of the CTI is the line between the septal insertion of the Eustachian ridge and the most inferior para-septal insertion of the tricuspid valve (TV) (i.e., the base of the triangle of Koch). The inferolateral border of the CTI comprises the final ramifications of the pectinate muscles of the crista terminalis, but a precise lateral boundary is not well defined. In attitudinal orientation, the portion of the CTI adjacent to the tricuspid annulus is anterior and sometimes referred to as the vestibular portion of the CTI. The portion of the CTI that is adjacent to the IVC is attitudinally posterior and referred to as the membranous CTI. The middle portion of the CTI is referred to as the trabeculated CTI.
The anatomy of the CTI can be assessed by computed tomography (CT) or magnetic resonance imaging (MRI) before ablation or by angiography, electroanatomic mapping, or echocardiography intraoperatively. The CTI is typically 34 ± 5 mm in length when measured angiographically from the IVC to the TV. The CTI is usually subdivided into three sections: septal isthmus, central isthmus, and lateral isthmus (see Figs. 11.1 and 11.2 ). In the electrophysiology laboratory, the septal isthmus is defined as that portion between 4 and 5 o’clock when visualized in the left anterior oblique (LAO) projection fluoroscopically. The central isthmus is that portion located at 6 o’clock, and the lateral isthmus is that starting at 7 o’clock. The central isthmus (6 o’clock) marks the shortest distance between the IVC and tricuspid annulus (19 ± 4 mm, range 13–26 mm). In addition, the central isthmus is the thinnest portion, ranging from an average of 3.5 mm near the TV to 0.8 mm in the middle portion. The anterior (vestibular) portion of the CTI adjacent to the TV is entirely muscular, whereas the posterior (membranous) portion closest to the IVC is primarily fibro-fatty tissue. The muscle thickness is least in the central isthmus, greatest at the septal isthmus, and intermediate in the lateral isthmus.
The anatomy of the CTI is highly variable but usually classified into three categories. A flat CTI shows 2 mm or less inferior concavity between the IVC and TV and is found in about 28% of patients. A concave CTI with inferior concavity more than 2 mm in depth is found in about 20% of patients. In these, the average depth is 3.7 ± 0.8 mm. In up to 83% of patients, the CTI shows a distinct inferior pouch (sub-Eustachian pouch or sinus of Keith) averaging 6.5 ± 2.2 mm in depth but up to 12.4 mm deep (see Figs. 11.1 and 11.2 ). The pouch is separated from the TV by a smooth vestibular area (see Figs. 11.1 and 11.2 ). The pouch itself may be symmetrical or asymmetrical, with extension toward the atrial septum. In anatomic studies, pouches are confined to the medial or septal CTI but are not seen in the lateral third of the CTI. Other notable anatomic features influencing the success of CTI ablation are the presence of a prominent muscular Eustachian ridge in about 26% of patients, extension of pectinate muscles into the CTI in 70% of patients, and even into the coronary sinus in 7%. The thickness of the pectinate muscles is greatest laterally and diminishes toward the atrial septum. The presence of pectinate muscles in the CTI may be suggested by recording high voltage electrograms (EGMs) from this area. In autopsy specimens, CTI pectinate muscle extensions and CTI pouches tend to occur together.
The crista terminalis forms another important boundary for CTI-dependent AFL. The crista terminalis leaves the superior right atrial septum and courses superiorly and anteriorly to the superior vena cava, and inferiorly along the posterolateral right atrial free wall to the IVC, where it then continues anteriorly and medially to form the Eustachian ridge. Double potentials have also been recorded along the crista terminalis, suggesting that it too forms a line of block during AFL, separating the smooth septal right atrium from the trabeculated right atrial free wall (see Fig. 11.3 ). Such lines of block, which may be either functional or anatomic, are necessary for an adequate path length for reentry to be sustained, to prevent “short-circuiting” of the reentrant wave front. Thus during typical AFL, the activation wave front traverses the CTI and exits medially, ascends the atrial septum, courses over the anterior right atrium, descends the right atrial lateral wall between the crista terminalis posteriorly and the TV anteriorly, and then enters the CTI laterally to complete the circuit.
The medial and lateral CTI, which are contiguous, respectively, with the interatrial septum near the coronary sinus (CS) ostium and with the low lateral right atrium near the IVC (see Figs. 11.1 and 11.2 ), correspond to the exit and entrance to the CTI, depending on whether the direction of reentry is CCW or CW in the right atrium. The presence of slow conduction in the CTI, relative to the interatrial septum and right atrial free wall, may be caused in part by the anisotropic fiber orientation in the CTI. This may also predispose to the development of unidirectional block during rapid atrial pacing, accounting for the observation that typical (CCW) AFL is more likely to be induced when pacing is performed from the CS ostium, and reverse typical (CW) AFL when pacing is from the low lateral right atrium.
Lower-loop reentry is an isthmus-dependent flutter in which the caudal-to-cranial limb of the wave front crosses over gaps in the crista terminalis in the inferior to middle right atrium ( Fig. 11.4 ). The circuit is essentially around the ostium of the IVC in the right atrium. The direction of rotation may be CW or CCW. This variant activation sequence may be sustained, or it may interconvert with other forms of AFL.
Partial isthmus flutter is another variant in which the CCW reentrant wave front “short circuits” through the Eustachian ridge barrier to pass between the IVC and the CS ostium (see Fig. 11.4 ). The wave front then propagates in a CW direction through the medial end of the CTI to collide with the wave front that is also conducting through the isthmus from its lateral aspect.
Intra-isthmus reentry (IIR) is a microreentrant atrial flutter localized within the septal region of the CTI ( Fig. 11.5 ). In a prospective series of patients with IIR reported by the Yang, et al., around half of patients (57%) with intraisthmus had prior CTI ablation. IIR was often diagnosed in patients (21%) with recurrent atrial flutter after previous CTI ablation.
Diagnosis
Surface Electrocardiography
The surface 12-lead electrocardiogram (ECG) is helpful in establishing a diagnosis of CTI-dependent AFL, particularly the typical form ( Table 11.1 ). In typical AFL, an inverted saw tooth F wave pattern is observed in the inferior ECG leads II, III, and aVF, with low-amplitude biphasic F waves in leads I and aVL, an upright F wave in precordial lead V 1 , and an inverted F wave in lead V 6 ( Fig. 11.6 A ). In contrast, in reverse typical AFL, the F wave pattern on the 12-lead ECG is less specific and variable, often with a sine wave pattern in the inferior ECG leads (see Fig. 11.6 B ). The determinants of F-wave pattern on ECG are largely dependent on the activation sequence of the left atrium, resulting from reentry in the right atrium. Inverted F waves are inscribed in the inferior ECG leads in typical AFL, because of activation of the left atrium initially posteriorly near the CS, and upright F waves are inscribed in the inferior ECG leads in reverse typical AFL because of activation of the left atrium initially anteriorly, near Bachmann’s bundle. However, because the typical and reverse typical forms of CTI-dependent AFL use the same reentry circuit, but in opposite directions, their rates are often similar. It has also been shown that the ECG presentation of typical AFL can be dramatically altered by ablation in the left atrium for atrial fibrillation.
| Type of Flutter | Criteria |
|---|---|
| Surface ECG | |
| Typical flutter | Saw tooth upright F wave pattern in the inferior ECG leads and in V1 |
| Reverse typical flutter | Sine wave or upright F wave pattern in the inferior ECG leads |
| Lower loop reentry | Variable; often resembles typical flutter if counterclockwise; clockwise rotation usually yields upright F waves inferiorly and inverted in V1 |
| Partial-isthmus reentry | Poorly described; probably similar to typical flutter |
| Electrophysiologic Testing | |
| Isthmus-dependent flutters | Demonstration of entrainment criteria during pacing from the CTI,Including the following: |
| First postpacing interval <30 ms longer than tachycardia cycle length | |
| Stimulus-to-F-wave interval equal to electrogram-to-F-wave interval on pacing catheter | |
| Identical paced F wave morphology and atrial activation sequence | |
| Macroreentrant RA activation by standard activation or electroanatomic mapping with entire tachycardia cycle length represented in right atrium | |
| Typical flutter | Concealed entrainment from CTI and counterclockwise macroreentrant RA activation |
| Reverse typical flutter | Concealed entrainment from CTI and clockwise macroreentrant RA activation |
| Lower loop reentry | Concealed entrainment from both CTI and low posterior right atrium with clockwise or counterclockwise macroreentrant RA activation |
| Partial isthmus-dependent | Concealed entrainment from lateral but not medial margin of CTI; early coronary sinus ostium activation during flutter; wave front collision in CTI; counterclockwise macroreentrant RA activation |
The ECG presentation of lower-loop reentry is highly variable, depending on the caudal-to-cranial level of wave front breakthrough across the crista terminalis. CCW lower-loop reentry may resemble typical AFL because of similar patterns of activation of the atrial septum and left atrium. A decrease in the late inferior forces may be evident in lower-loop reentry, because of wave front collision in the lateral right atrium. With multiple or variable wave front breaks in the lateral atrium, unusual and changing ECG patterns may be observed. Alternation of P wave polarity from positive to negative in V 1 may occur. CW lower-loop reentry typically demonstrates positive flutter waves in the inferior leads and negative flutter waves in V 1 .
The ECG description of partial isthmus-dependent flutter is incomplete, but it may be expected to resemble typical AFL, given their similar patterns of atrial activation.
The surface ECG pattern of IIR is variable, with 86% of cases resembling typical CCW AFL and 21% of cases exhibiting atypical AFL (positive F waves in inferior leads and V1). In the majority of patients with IIR (79%), a distinct isoelectric period was observed between surface F waves, which were often low amplitude or flat.
Electrophysiologic Diagnosis
Despite the utility of the 12-lead ECG in making a presumptive diagnosis of typical AFL, an electrophysiologic study with mapping and entrainment should be performed to confirm the underlying mechanism if RFCA is to be successfully performed (see Table 11.1 ). This is particularly true in the cases of reverse typical AFL or CTI-dependent flutter following left atrial ablation, which are much more difficult to diagnose on 12-lead ECG.
For the electrophysiologic study of AFL, activation mapping may be performed using multielectrode catheters or 3-dimensional electroanatomic computerized activation mapping systems. For standard multielectrode catheter mapping, catheters are positioned in the right atrium, His bundle region, and CS. To most precisely elucidate the endocardial activation sequence, a duo-decapolar catheter (e.g., Halo 20-electrode mapping catheter) may be positioned in the right atrium around the TVA ( Fig. 11.7 ). These catheters may extend to the lateral CTI or cross the entire CTI into the CS, depending on design. The latter obviates the need for a separate CS catheter. Recordings obtained during AFL from all electrodes are then analyzed to determine the right atrial activation sequence.
For patients who present to the laboratory in sinus rhythm, it is necessary to induce AFL to confirm its mechanism. Induction of AFL is accomplished by atrial programmed stimulation or burst pacing, usually from the CS ostium or low lateral right atrium. The direction of AFL induced (e.g., CCW vs. CW) may depend in part on the pacing site. For burst pacing, cycle lengths between 180 and 240 ms are typically effective in producing unidirectional CTI block and inducing AFL. Induction of AFL typically occurs immediately after the onset of unidirectional CTI isthmus block, or after a brief period of rapid atrial tachycardia or atrial fibrillation. During electrophysiologic study, a diagnosis of either typical or reverse typical AFL is suggested by observing a CCW or CW activation pattern in the right atrium around the TVA, respectively. For example, as seen in Fig. 11.8 , A in a patient with typical AFL, the initial atrial activation is recorded at the CS ostium (i.e., CS os EGM), which is timed with the initial down stroke of the F wave in the inferior surface ECG leads, followed by caudal-to-cranial activation in the interatrial septum (i.e., His bundle atrial EGM), then cranial-to-caudal activation in the right atrial free wall (i.e., proximal to distal EGMs on the duo-decapolar catheter), and finally to the CTI (i.e., ablation catheter atrial EGM), demonstrating that the underlying mechanism is a CCW macroreentry circuit around the TVA encompassing the entire tachycardia cycle length. In a patient with reverse typical AFL, the mirror image of this activation pattern is seen (see Fig. 11.8 B ).
In addition, confirmation that the AFL reentry circuit uses the CTI, requires demonstration of classical criteria for entrainment, including concealed entrainment, during pacing from the CTI, and constant fusion from a site or sites outside the CTI (often the lateral right atrium). Criteria for demonstrating concealed entrainment of AFL include acceleration of the tachycardia to the pacing cycle length without a change in the F wave pattern on surface ECG or endocardial atrial activation pattern and EGM morphology, as well as immediate resumption of the tachycardia at the original cycle length on termination of pacing, including the first postpacing interval (i.e., the postpacing interval minus tachycardia cycle length, or PPI-TCL, should be less than 30 ms, Fig. 11.9 ). Concealed entrainment is further confirmed, during pacing from the CTI, if the stimulus-to–F-wave or stimulus-to-reference EGM interval during pacing, and the pacing electrode EGM-to–F-wave or pacing EGM-to-reference EGM interval during AFL are the same (see Fig. 11.9 ). Furthermore, during typical AFL, the stimulus-to–F-wave or stimulus-to-proximal CS EGM is shorter when the pacing site is medial, near the exit from the CTI (e.g., 30 to 50 ms), and longer when the pacing site is lateral, near the entrance to the CTI (e.g., 80–100 ms). The converse is true during reverse typical AFL. In contrast, pacing at sites outside the CTI results in manifest entrainment of AFL, with progressive fusion of the F postpacing interval wave pattern and endocardial atrial EGMs at progressively shorter cycle lengths faster than the AFL cycle length.
The diagnosis of lower loop reentrant AFL is confirmed by demonstration of concealed entrainment of the tachycardia from not only the CTI but also the inferior-posterior right atrium. Partial isthmus-dependent flutter is confirmed by the demonstration of concealed entrainment from the lateral margin of the CTI but not from the medial portion near the TVA. In addition, there is early activation of the CS ostium and evidence of wave front collision within the medial CTI. Concealed entrainment should be demonstrable from the area of short circuit between the Eustachian ridge and CS ostium.
The diagnosis of IIR is confirmed by demonstration of concealed entrainment only within the septal CTI near the CS ostium, while all other areas of the right atrium, left atrium, and CS are out of the circuit (PPI-TCL >25) 27,28 . In addition, fractionated potentials and double potentials are often observed within the septal area of the CTI. In rare instances, concealed entrainment and fractionated potentials have also been observed at the mid or antero-inferior CTI, indicating extension of the circuit more laterally. Electroanatomic mapping may not have adequate resolution to identify this microreentrant circuit. It may demonstrate either a focal pattern with total mapped cycle length less than 60% of the tachycardia cycle length with earliest activation arising from the septal CTI near the CS ostium, or it may demonstrate a CCW reentrant pattern around the TVA, with the total mapped cycle length greater than 90% of the TCL, deceptively suggesting the presence of typical CTI-dependent AFL.
The differential diagnosis of AFL from other supraventricular arrhythmias is usually apparent given typical ECG manifestations and variable ventriculoatrial relationships. The most important distinction to be made is the exclusion of a focal atrial tachycardia. Rarely, focal atrial tachycardia in the low posteroseptal right atrium may be confused with AFL if unidirectional CTI conduction block (i.e., medial to lateral block) is present. Otherwise, the atrial tachycardia can be recognized by failure to entrain it from the CTI and by a radial activation pattern.
Ablation
For ablation of CTI-dependent AFL, the most common approach is to create a line of bidirectional conduction block across the CTI, from the TVA to the IVC. For this purpose, a variety of mapping and ablation catheters, with different shapes and curve lengths, as well as RF generators, are available from several commercial manufacturers. We prefer to use a standard-curve ablation catheter (Blazer™ 8-mm tip, mid-distal standard curve, Boston Scientific, Inc., Natick, MA, USA) or an externally irrigated ablation catheter (Thermocool ST™, Biosense Webster, Diamond Bar, CA, USA; Tacticath, Abbott Laboratories, Chicago, IL, USA) because it has been shown that the use of large-tip (8–10 mm) ablation catheters or irrigated ablation catheters reduces procedure durations and improves success rates compared with standard 4-mm RF electrodes. The smaller electrode (3.5 mm) on irrigated catheter designs may provide better near-field EGM resolution than large-tip electrodes as well. Long, fixed-curve guide sheaths (e.g., SR0 or SL1, St. Jude, Inc., St. Paul, MN, USA) or steerable deflectable sheaths (e.g., Agilis, St. Jude, Inc., St. Paul, MN, USA) are also useful to improve catheter reach, stability, and tissue contact. There is also published evidence that large-tip ablation catheters are most useful for flat CTI anatomy, whereas irrigated designs may be more advantageous in the presence of CTI pouches. When using fixed curve or steerable sheaths, it is important that the curvatures of the sheath and catheter remain coaxial. Paradoxically, rotating the sheath to point into the septum may limit the septal motion of the catheter.
The target for CTI-dependent AFL ablation is the CTI ( Table 11.2 ), which when standard multipolar electrode catheters are used for mapping and ablation, is localized with a combined fluoroscopically and electrophysiologically guided approach. The usual target for the ablation line is the central isthmus because the CTI is narrowest at this point (i.e., distance from TVA to IVC) and has the thinnest musculature. This site is located at 6 o’clock in the LAO view (see Fig. 11.7 ). One drawback to ablation of the central isthmus is the frequent occurrence of pouches in this region. Pouches may be avoided by ablating the lateral isthmus (7 o’clock in LAO projection). However, there are thicker right atrial musculature and terminal pectinate muscles found here. The medial isthmus is devoid of pectinate musculature but contains the thickest atrial muscular layer and is nearest to the right coronary artery and AV nodal extensions. Typically, the ablation catheter is positioned using fluoroscopic guidance (see Fig. 11.7 ) or electroanatomic mapping, in the central CTI, with the distal ablation electrode on or near the TVA in the right anterior oblique (RAO) view, and midway between the septum and low right atrial free wall (6- or-7 o’clock position) in the LAO view. The distal ablation electrode position is then adjusted toward or away from the TVA, based on the ratio of atrial and ventricular EGM amplitudes (A/V ratio) recorded by the bipolar ablation electrode. An optimal ratio is 1:2 or 1:4 at the TVA, as seen in Fig. 11.8 , A on the ablation electrode. After the ablation catheter is positioned on or near the TVA, it is very slowly withdrawn during ablation toward the IVC while RF energy is applied continuously.
| Type of Flutter | Targets |
|---|---|
| CTI-dependent | CTI from TVA to IVC |
| TVA to Eustachian ridge isthmus | |
| TVA to CS ostium to Eustachian ridge isthmus | |
| Maximal electrogram voltage recorded on-line | |
| Partial isthmus-dependent | CS ostium to IVC |
Alternatively, the ablation catheter can be withdrawn in a stepwise manner, a few millimeters at a time (usually less than or equal to the length of the distal ablation electrode), with 30- to 60-second pauses at each location, during a continuous or interrupted energy application. For irrigated electrodes, a maximal power of 35 to 50 W and a temperature of 40°C to 45°C should be used. In contrast, the large-tip (i.e., 8–10 mm) ablation catheters require a higher power, up to 100 W, to achieve target temperatures of 50°C to 60°C, because of the greater energy-dispersive effects of the larger ablation electrode. Use of large-tip ablation catheters also requires the use of two grounding pads applied to the patient’s skin to avoid skin burns. Excessive impedance drops (i.e., >10–20 Ω from baseline) should be avoided, to prevent tissue overheating and steam pops. CTI ablation can be performed with standard 4-mm-tipped RF catheters (50 W, 50–65°C); however, use of these catheters is associated with longer procedure and ablation times, lower acute success rates, and much higher recurrence rates. EGM recordings may be used in addition to fluoroscopy to ensure that the ablation electrode is in contact with viable tissue in the CTI throughout each energy application. However, recent studies have suggested that real-time contact force measuring catheters may help reduce total ablation time required to produce acute CTI conduction block, and that standard surrogates of tissue contact (e.g., impedance, EGM amplitude) may not ensure adequate tissue contact during ablation as measured by contact force sensing catheters.
Ablation across the entire CTI ( Fig. 11.10 ) may require several sequential 30- to 60-second energy applications during a stepwise catheter pullback, or a prolonged energy application of up to 120 seconds or longer during a continuous catheter pullback. The catheter should be gradually withdrawn until the distal ablation electrode no longer records an atrial EGM, indicating that it has reached the IVC, or until the ablation electrode is noted to abruptly slip off the Eustachian ridge. RF energy application should be immediately interrupted when the catheter has reached the IVC, because ablation in extracardiac venous structures is known to cause significant pain. Computerized 3-dimensional mapping systems are useful to document the anatomic placement of ablation lesions and decrease fluoroscopy use. As the ablation catheter approaches the IVC, it is often useful to release the catheter curve slightly and withdraw the sheath and catheter as a unit to allow greater contact between the electrode and the CTI, before the catheter is withdrawn into the IVC.
