Ablation of Cavotricuspid Isthmus–Dependent Atrial Flutters


Key Points

  • The mechanism of most cavotricuspid isthmus (CTI)-dependent atrial flutter (AFL) is macroreentry around the tricuspid valve annulus (TVA).

  • 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.

  • The target for ablation of CTI-dependent AFL is the CTI, between the TVA and the inferior vena cava (IVC).

  • 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.

  • 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.

  • 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.

Fig. 11.1, A and B, Schematic diagrams showing the activation patterns of CTI-dependent AFL, as viewed from below the tricuspid valve (TV) annulus, looking up into the right atrium. In typical AFL (A), the reentrant wave front rotates counterclockwise in the right atrium (RA), but in reverse typical AFL (B), reentry is clockwise. Note that the Eustachian ridge (ER) and crista terminalis (CT) form lines of block and that an area of slow conduction (wavy line) is present in the CTI (between the ER and TV annulus). CS , Coronary sinus ostium; His , His bundle; SVC , superior vena cava. C–E, Anatomy of the CTI. The schematic diagram of the right atrium (C) shows the CTI (expanded insert), which is posterior and inferior to the triangle of Koch. D, Pathologic specimen showing the heart in right anterior oblique (RAO) view. The hinge of the TV is shown by the dotted line. Note the complex anatomy along the inferior isthmus line, with a fenestrated Thebesian valve present. SI , Septal isthmus; II , inferior isthmus; EV , Eustachian valve; OF , foramen ovale; N , AV nodal area; SVC , superior vena cava. E, RAO angiogram of the CTI. A pouch-like sub-Eustachian sinus (SE) is seen adjacent to the vestibule region of the isthmus (V). H , His catheter.

Fig. 11.2, A, The endocardial surface of the right atrial cavotricuspid isthmus (CTI) is displayed to show the three levels. Note the pouch at the central isthmus and the distal ramifications of the terminal (Term.) crest that feed into the inferolateral CTI. B and C, The CTI viewed in profile. The histologic section shows myocardium in red and fibrous tissue in blue . The anterior sector corresponds to the vestibule leading to the tricuspid valve (TV) and is related to the right coronary artery (RCA). The posterior sector is closest to the orifice of the inferior caval vein and contains the Eustachian valve or ridge (ER) (Masson trichrome stain).

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.

Fig. 11.3, A, Surface electrocardiographic leads I, aVF, and V 1 and endocardial electrograms (EGMs) in a patient with typical atrial flutter (AFL) demonstrating double potentials (x,y) recorded along the Eustachian ridge (ER) by the ablation catheter (RFd and RFp). Note that the x and y potentials straddle the onset of the initial downstroke of the F wave in lead aVF (vertical line), indicating that the x potential is recorded immediately after the activation wave front exits the sub-Eustachian isthmus and circulates around the coronary sinus above the ER. The y potential is recorded after the activation wave front has rotated entirely around the atrium and is proceeding through the sub-Eustachian isthmus below the ER. Double potentials may similarly be recorded along the crista terminalis (CT). B, A schematic diagram of the right atrium indicates where double potentials (x,y) may be recorded along the ER and CT during typical AFL. CSp, CSm, and CSd are electrograms recorded, respectively, from the proximal, middle, and distal electrode pairs on a quadripolar catheter in the coronary sinus (CS) with the proximal pair at the ostium. His , Electrogram from the His bundle catheter; IVC , inferior vena cava; RFp and RFd, electrograms from the proximal and distal electrode pairs of the mapping and ablation catheter with the distal pair positioned on the ER; RV , right ventricle electrogram; SVC , superior vena cava; TV , tricuspid valve.

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.

Fig. 11.4, Electrograms and schematic representation of atrial activation in lower-loop reentry and partial isthmus-dependent flutter. A, During lower-loop reentry, the posterior right atrium is part of the reentry circuit around the inferior vena cava, and wave fronts collide in the lateral right atrium. The electrograms show multiple collisions at recording sites on the lateral right atrial wall TA1 and TA8 ( stars ). B, During partial isthmus-dependent flutter, the wave front bypasses the anterior CTI near the TVA by passing through the Eustachian ridge posterior to the coronary sinus ostium (CS os ). The coronary sinus ostium is activated prematurely, and the tachycardia is not entrained from the medial CTI itself. IVC , Inferior vena cava; SVC , superior vena cava; TA10 , proximal recording electrodes on halo catheter near upper septum; TA1 , distal recording electrodes on Halo catheter near lateral aspect of the CTI.

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.

Fig. 11.5, A, A CARTO map in a patient with typical atrial flutter (AFL) with a counterclockwise activation sequence around the tricuspid valve annulus (TVA). In the left anterior oblique (LAO) view, the earliest activation was at the septal cavotricuspid isthmus (CTI) and latest activation at the lateral CTI, resulting in an “early meets late” activation pattern at the CTI. The mapped cycle length spanned 99% of the tachycardia cycle length (TCL). However, the postpacing interval (PPI)-TCL interval, measured at different sites around the TVA, showed that only the septal CTI was in the circuit. B, Simultaneous surface electrocardiogram recordings (leads I, II, and V1), a His bundle (HBE), coronary sinus (CS), and duo-decapolar catheter positioned around the TVA, with its distal electrode (TA1) across the CTI at CS ostium and proximal electrode (TA10) close to the high lateral TVA in a patient with typical AFL (cycle length 250 ms). The electrodes TA1–3 were located within the septal CTI (from the CS ostium to 6:00 o’clock on the TVA). Note the low amplitude fractionated potentials (FPs) with a duration of 159 ms, recorded at TA2, which spanned 64% of the TCL, and the double potentials (DPs) with E1 to E2 interval of 127 ms recorded at TA3. A combination of the recordings from TA1 to TA3 (i.e., both FPs and DPs) spanned more than 2/3 of the TCL. In this patient, entrainment pacing from the septal CTI during the tachycardia showed a PPI–TCL ≤ 25 ms, whereas pacing from the lateral CTI showed a PPI–TCL greater than 25 ms. Radiofrequency catheter ablation at the septal CTI, where the FPs were recorded, terminated the AFL, and it was no longer inducible after ablation. The schematic diagram to the right of the figure shows the proposed reentrant circuit.

Diagnosis

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