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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.
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.
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.
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