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1 Original Article Radiofrequency Ablation for Atrial Tachycardia and Atrial Flutter Tomos E. Walters, MBBS c, Peter M. Kistler, PhD b and Jonathan M. Kalman, PhD a, a The Department of Cardiology, Royal Melbourne Hospital and the Department of Medicine, University of Melbourne, Melbourne, Australia b The Department of Cardiology, Alfred Hospital and the Baker IDI, Melbourne, Australia c The Department of Cardiology, Princess Alexandra Hospital, Brisbane, Australia Atrial tachycardia is a generic term for a range of tachyarrhythmias with their origin in the atria. These can be broadly divided by mechanism into macro-reentrant, focal and small circuit re-entry. Atrial flutter is a term which, today, should be restricted to those classical circuits around the tricuspid annulus dependent on the cavo-tricuspid isthmus. The advent of sophisticated mapping solutions has rendered the vast majority of these atrial circuits curable with catheter ablation, with high success rates and very low incidence of complications. (Heart, Lung and Circulation 2012;21: ) 2012 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier Inc. All rights reserved. Keywords. Atrial tachycardia; Cavo-tricuspid isthmus; Atrial flutter; Catheter ablation Classification C onsensus groups from the European Society of Cardiology and the North American Society of Pacing and Electrophysiology have defined regular atrial tachycardia (AT) as either focal or macro-reentrant, classified according to electrophysiological mechanisms and anatomical structures [1]. Focal ATs are characterised by a focal origin with subsequent centrifugal spread, with a mechanism based in abnormal automaticity, triggered activity or micro re-entry [2]. Macro-reentrant ATs, by contrast, involve a larger re-entry circuit, conventionally defined by a diameter in excess of 2 cm. The most common form of macro-reentrant AT involves the cavo-tricuspid isthmus (CTI) as a critical region and has traditionally been referred to as typical atrial flutter. Since this classification, a third category of atrial tachycardia has been defined. This is termed small circuit re-entry and is somewhere between micro and macro. These circuits most commonly occur after atrial fibrillation (AF) ablation procedures involving extensive left atrial ablation. CTI-Dependent Macro-reentrant AT Anatomy/Mapping So-called typical atrial flutter accounts for 90% of macroreentrant ATs and the re-entry circuit has been well defined. The tricuspid valve annulus stands as a fixed Available online 29 March 2012 Corresponding author at: Department of Cardiology, Royal Melbourne Hospital, Melbourne 3050, Australia. Tel.: ; fax: addresses: tomoswalters@me.com (T.E. Walters), jon.kalman@mh.org.au (J.M. Kalman) Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier Inc. All rights reserved. anatomic barrier to electrical conduction anterior to the circuit whilst the posterior barrier is formed by the crista terminalis and the Eustachian ridge [3 5]. No anatomic barrier has been identified between the termination of the Eustachian ridge at the ostium of the coronary sinus and the superomedial aspect of the crista terminalis anterior to the superior vena cava, but only the portion of the atrial septum immediately adjacent to the tricuspid annulus was shown in early studies to be part of the re-entry circuit. It has, therefore, been thought likely that this part of the posterior barrier is functional, with alternative pathways having a longer propagation time [5]. Activation of the atrial septum typically proceeds in an inferior to superior direction and that of the lateral right atrial wall in a superior to inferior direction, with activation around the tricuspid annulus proceeding counter-clockwise [4,5]. In only 10% of macro-reentrant ATs using this circuit does activation proceed clockwise [6]. The CTI in this circuit has been demonstrated to be critical to maintenance of the tachycardia and thus these tachycardias are referred to as CTI-dependent. Subsequent to its initial description, further studies using three-dimensional electroanatomic mapping have confirmed the presence of a re-entry circuit around the tricuspid annulus. Activation through the CTI is a constant, but a degree of heterogeneity has been demonstrated in other parts of the circuit. Chen et al. [7] observed that the crista terminalis can be the sole posterior barrier to transverse conduction but a second line of block can at times be seen along the sinus venosus. Shah et al. [8] found that the pathway of ascending septal activation from the ostium of the coronary sinus is heterogeneous, with activation proceeding either anterior to the superior vena cava or fusing around it. Santucci et al. [9] also reported /04/$36.00 doi: /j.hlc

2 Heart, Lung and Circulation Walters et al ;21: Atrial Tachycardia and Atrial Flutter marked variability in the upper part of the circuit, which was seen to pass anterior to the right atrial appendage close to the tricuspid annulus, posterior to the appendage or even posterior to the superior vena cava across the crista terminalis. Circuits which cross the crista terminalis have been termed lower loop or upper loop reentry [10,11]. Catheter Ablation Catheter ablation of CTI-dependent macro-reentrant AT targets the critical isthmus between the tricuspid valve annulus and the inferior vena cava. Creation of a complete line of conduction block between these structures was shown to terminate and prevent re-induction of the arrhythmia almost 20 years ago [12,13]. It has become the first line approach to the treatment of symptomatic CTI-dependent macro-reentry AT since Natale et al. [14] performed a randomised comparison of pharmacotherapy with linear ablation of the CTI and observed catheter ablation to initially be successful in all patients. At a mean follow-up period of 22 months 80% of patients who underwent catheter ablation were maintained in sinus rhythm without use of anti-arrhythmic drugs. By contrast in the group initially treated with anti-arrhythmic medication only 36% were maintained in sinus rhythm, and this group was significantly more likely to require hospitalisation for recurrence of severely symptomatic arrhythmia. Catheter ablation of CTI-dependent macro-reentrant AT may be performed during tachycardia or during sinus rhythm, usually with pacing from the proximal coronary sinus to facilitate identification of conduction block across the CTI. Early studies of linear ablation across the CTI were usually performed with a 4 mm tip ablation catheter but a higher rate of procedural success has been demonstrated with use of either an 8 mm tip ablation catheter or an externally irrigated ablation catheter, both capable of generating a larger ablation lesion. Early studies of catheter ablation of CTI-dependent macro-reentry AT used tachycardia termination and an inability to re-induce tachycardia as the procedural endpoint. Whilst these studies reported a high rate of acute procedural success, long-term recurrence rates were as high as 40% [12,13]. The accepted procedural endpoint has since become bidirectional conduction block across the CTI, which is associated with a long-term recurrence rate of less than 5% [15]. A change in the activation pattern of the low lateral right atrium during coronary sinus pacing is a readily appreciated marker of isthmus block, but does not preclude the presence of ongoing slow conduction across an incomplete ablation line. Pacing should be performed from both sides of the ablation line, from the proximal coronary sinus and from the low lateral right atrium, to confirm bi-directionality of conduction block [16]. If suspicion of incomplete block persists then the ablation line itself should be mapped for the continuous presence of widely spaced (> ms) double potentials [17], with convergence of double potentials indicating a functional gap in the ablation line. The use of three-dimensional electroanatomic mapping systems can shorten ablation and fluoroscopy times [18,19]. Remote magnetic navigation systems, in which alterations in a magnetic field across the patient are used to deflect the tip of catheters to a desired location, have also been used for catheter ablation of typical atrial flutter with early success in small series [20,21]. A measure of the effectiveness of catheter ablation of CTI-dependent macro-reentry AT, using a variety of the approaches discussed above, is the pooled data from a number of electrophysiology laboratories surveyed for a review published by Morady [15]. In a total of 7071 patients undergoing catheter ablation of CTI-dependent macro-reentry AT, the long-term success rate for prevention of recurrent atrial flutter was 97%, with 4% of patients requiring a repeat procedure. The reported rate of serious complications was 0.4%, with the most common being high-grade atrioventricular block. More recently Spector et al. [22] performed a systematic review of all published reports of the efficacy and safety of radiofrequency catheter ablation of CTI-dependent macro-reentry AT in adults between 1990 and They reported a single-procedure efficacy rate of 92%, a multi-procedure efficacy rate of 97% and a repeat ablation procedure rate of 8%, with procedural efficacy having steadily increased over time. There were no procedure-related deaths, no vascular access complications, and no reported instances of cardiac tamponade or stroke/tia. The rate of atrioventricular block was 0.4%, of pulmonary embolus was 0.1% and of pericardial effusion was 0.3%. Other Macro-reentrant ATs Macro-reentant ATs in which the circuit does not involve the CTI as a critical isthmus have often been grouped together and referred to as atypical atrial flutter, although a more accurate designation is non-cti dependent flutter. These include re-entry circuits which develop around surgical scars following correction of valvular or congenital disease (lesional AT) [23,24], circuits which develop following surgical or catheter ablation of atrial fibrillation, and circuits around areas of spontaneous scarring in the right and left atria [25,26]. These circuits most often develop in a structurally abnormal heart. They may be complex or multiple, and may change even as mapping and ablation is undertaken. Conventional mapping techniques include activation and entrainment mapping. A macro-reentrant circuit includes large portions of the atria in which continuous activation can be recorded throughout the tachycardia cycle length (Fig. 1), including during apparent isoelectric intervals on the surface ECG. Unlike in focal AT the concept of early activation is inapplicable as, with continuous circus activation, a site with earlier activation time can always be located. Lines of block, which create a substrate suitable for re-entry, are reflected by the recording of double potentials that result from sequential activation on either side of the line. Pacing within a protected isthmus results in concealed entrainment, with no fusion discernable on the surface ECG, no change in local atrial activation, a post-pacing interval within 30 ms ORIGINAL ARTICLE

3 388 Walters et al. Heart, Lung and Circulation Atrial Tachycardia and Atrial Flutter 2012;21: Figure 1. (A) Surface ECG and endocardial recordings from a 20-electrode catheter during clockwise atrial flutter (left) and counterclockwise atrial flutter (right). There is continuous undulation of the baseline in the surface ECG leads consistent with continuous circus activation of atrial myocardium. This is reflected in endocardial activation recorded throughout large portions of the tachycardia cycle. (Reproduced with permission of the Journal of Cardiovascular Electrophysiology). (B) Surface ECG and endocardial recordings from a 20-electrode catheter during focal atrial tachycardia from the high crista terminalis (left) and during sinus rhythm (right). Atrial activation, reflected in the P-wave on the surface ECG and in the endocardial recordings, is confined to a limited portion of the tachycardia cycle. (Reproduced with permission of the Journal of the American College of Cardiology.) of the tachycardia cycle length and a stimulus-to-activation time of <30 ms. An isthmus within the re-entry circuit may also manifest slow conduction with broad, fractionated electrograms. A macro-reentrant circuit is confirmed if such electrophysiologic features can be demonstrated by atrial pacing at multiple sites separated by at least 2 cm. Contemporary practice now involves the additional use of three-dimensional mapping systems. These allow reconstruction of atrial geometry with identification of important anatomic landmarks, on which background electrophysiologic data can be displayed. Voltage mapping and mapping of double potentials allows the atrial substrate to be determined, with areas of scar and lines of conduction block defined. Mapping the timing of atrial activation then facilitates generation of propagation maps of the re-entry circuit. In lesional macro-reentrant AT the central obstacle within the circuit is an atriotomy scar, a septal prosthetic patch, a suture line or a line of fixed block created by radiofrequency ablation. Re-entry circuits around such obstacles may be complex or multiple, with entrainment critical to confirming the participation of particular areas of the atria in the circuit and thence identification of a suitable target for ablation. Macro-reentry around an existing scar often co-exists with CTI-dependent macro-reentrant AT in the form of dual loop or figure of 8 reentry [27]. Ablation of one may unmask the other and ablation of both is necessary for durable elimination of tachycardia.

4 Heart, Lung and Circulation Walters et al ;21: Atrial Tachycardia and Atrial Flutter ORIGINAL ARTICLE Figure 2. Macro-reentry atrial tachycardia around regions of spontaneous scar in the right atrial free wall. (A) Electroanatomic voltage maps in 3 different patients demonstrating spontaneous scarring in the right atrial free wall, with the free wall shown en face. Scar is shown in grey and areas of low voltage in red. (B) Activation maps demonstrating tachycardia circuits around regions of scarring, with earliest activation in red and latest in purple. The upper panel demonstrates a clockwise tachycardia circuit around a scarred region, with subsequent successful ablation between the scar and the inferior vena cava. In the lower panel an anticlockwise tachycardia circuit initially passes through a channel between areas of scar and later, after ablation within this channel, passes between the scar and the inferior vena cava. Ablation at this point was successful in terminating the tachycardia. IVC, inferior vena cava; SVC, superior vena cava; TA, tricuspid annulus. Reproduced with permission of Heart Rhythm. ATs, including macro-reentrant forms, have become a relatively common result late after catheter ablation of AF. The rate of development of AT following AF ablation has been reported as high as 50%, and both the incidence and mechanism are dependent on the chosen strategy [28]. The lowest incidence occurs after circumferential pulmonary vein isolation alone. Such ATs are typically focal, due to reconnection of pulmonary veins in >80% of cases [29]. The addition of linear ablation within the left atrium further increases the incidence of AT, with the vast majority due to a macro-reentrant circuit involving a gap in an ablation line. Such circuits are most commonly around the mitral annulus, involving the isthmus between the mitral annulus and the left inferior pulmonary vein, or involve the roof of the left atrium [30,31]. The highest incidence of AT occurs after a strategy involving pulmonary vein isolation, linear ablation and the targeting of complex fractionated electrograms [32]. Multiple reports have demonstrated so-called small circuit re-entry to be a major mechanism of AT following AF ablation with extensive substrate modification [31,33]. Jais et al., for example, reported a cohort of 128 consecutive patients with 246 ATs in the context of prior extensive AF ablation. Forty-six percent were demonstrated to be macro-reentrant ATs whilst 54% were confirmed not to be macro-reentrant. Of these 26% were demonstrated to arise from a discrete point source as a truly focal AT but 74% were found to arise from a small circuit 1 2 cm in diameter, with activation recordable throughout 75% of the tachycardia cycle in this small region and subsequent centrifugal spread to the remainder of the left atrium. Such circuits were preferentially found at the sites of previous ablation, where zones of slow conduction were demonstrable. There remains debate as to whether these circuits represent the underlying primary drivers of AF uncovered by ablation and substrate modification or, more likely, are simply secondary to prior ablation with reentry around scar due to previous ablation lesions. Non CTI-dependent circuits have also been described in patients without prior ablation or surgery. Stevenson et al. [25], for example, described a group of eight patients with macro-reentrant AT related to an area of spontaneous scar in the posterolateral right atrium manifest by electrical silence or low voltage electograms (Fig. 2). These patients had no history of cardiac surgery or congenital cardiac abnormalities, had preserved ventricular systolic function and relatively mild atrial dilatation. The tachycardia circuit was targeted at the isthmus between the region of scarring and the inferior vena cava, superior vena cava or tricuspid annulus, or at a channel within the scar. There was a high rate of success with catheter ablation, with 75% of patients free from tachycardia recurrence at 20 months of follow-up. Jais et al. [26] performed a detailed study of left atrial macro-reentrant ATs. Seventy-seven percent of the study cohort had significant structural heart disease, including significant mitral valve dysfunction, previous mitral valve surgery or left ventricular systolic dysfunction with marked left atrial dilatation. This left atriopathy was frequently associated with an area of scar, reflected by electrical silence, most often in the posterior wall. Most

5 390 Walters et al. Heart, Lung and Circulation Atrial Tachycardia and Atrial Flutter 2012;21: patients had single circuits, with a smaller group having multiple or highly complex circuits. Ablation of a critical isthmus of slow conduction resulted in a 91% acute procedural success rate, with sinus rhythm maintained in 73% at 15 months. Catheter ablation of non CTI-dependent AT, requiring an individually tailored approach specific to the underlying substrate, has therefore been shown to be highly effective. Acute procedural success rates in the contemporary era are in excess of 90% [15,26], with recurrence rates varying markedly from 0% to 59% in the context of different underlying arrhythmia substrates. For example in a recent report of catheter ablation of macro-reentrant AT occurring late after surgical repair of an atrial septal defect (ASD) a CTI-dependent tachycardia circuit was seen in all patients and a non CTI-dependent circuit in 70% [34]. Acute procedural success, demonstrated by bi-directional block across the ablation line, was seen in all patients. Twenty-five percent of patients subsequently required a repeat procedure for recurrent macro-reentrant AT and 90% then remained free of AT three years removed from their last procedure. Late AF was, however, documented in 30%. Focal Atrial Tachycardia Anatomy/Mechanisms Focal AT is defined as activation from a discrete focus with subsequent centrifugal spread. Such focal activity may be due to abnormal automaticity, triggered activity or a micro-reentrant circuit. In general, abnormal automaticity is characterised by spontaneous atrial activity that is enhanced by isoprenaline but not induced by programmed extra-stimululi, whereas triggered activity and micro-reentry can both be initiated and terminated by programmed extra-stimuli. There is, however, much overlap and precise delineation of mechanism is beyond the scope of a standard diagnostic electrophysiology study. Furthermore, in an era where focal ATs are mapped and ablated focally, the underlying mechanism is of limited clinical importance. Focal ATs most often arise in the absence of significant structural heart disease and with histologically normal myocardium [35]. In a series of patients with focal AT who underwent surgical therapy, however, some degree of myocardial inflammation, infiltration or fibrosis was seen in almost half of resected specimens [36]. This may be reflected in electroanatomic maps as areas of low voltage and fractionated electrograms representing slow conduction. These regions can act as the substrate for micro-reentrant circuits and have been described as sites of successful ablation in patients with focal AT [37]. Atrial tachycardia foci have a characteristic anatomic distribution. The crista terminalis, representing the embryological junction between the smooth venous and trabeculated muscular portions of the right atrium, is the site of origin for 2/3 of right-sided focal ATs [37]. As an area of marked anisotropic conduction and with nodal properties conferred by the presence of the sinus node extending a variable portion of its longitudinal span, it is predisposed to both micro-reentry and abnormal automaticity. The tricuspid annulus represents the second most common right atrial location [38], which might be explained by the presence of atrial myocytes with nodal-like electrophysiologic properties around the circumference of the annulus [39]. The ostium of the coronary sinus [40], the atrioventricular node and its surrounding zone of transitional cells, the right atrial appendage [41] (Fig. 3) and the superior vena cava [42] are other recognised areas for clustering of focal AT. In the left atrium focal ATs cluster at the ostia of the pulmonary veins, with a propensity for the upper veins [43,44]. These can develop independent of any history of atrial fibrillation, with pulmonary vein activity more focal, more ostial and slower than that seen in AF. The second most common left-sided focus is the superior aspect of the mitral annulus, in close proximity to the left fibrous trigone and aorto-mitral continuity [44,45]. Atrial myocytes with nodal-like properties have been described within these structures [46,47], which provides an explanation for the relatively high frequency of focal AT from the aorto-mitral continuity and anterior leaflet of the mitral valve [48,49] (Fig. 3). The left atrial appendage, the body of the coronary sinus and the left interatrial septum are other described locations for focal AT [44]. Localisation by P-wave Morphology Atrial activation in focal AT is classically described as being represented on a 12-lead ECG as a distinct deflection with an intervening isoelectric interval (Fig. 1). This contrasts with the rhythmic undulation typical of a macro-reentrant tachycardia. Particularly in the setting of accelerated heart rates or atrial disease, however, this distinction becomes unclear and so it is not possible to definitively establish the presence of a focal versus a macro-reentrant AT from the surface ECG. The morphology of the atrial P-waves can be used to estimate the likely site of tachycardia origin in patients with structurally normal atria. For accurate analysis the P wave must be seen without superimposition of the T wave or preceding QRS complex. The presence of atrial structural abnormalities, for example following catheter ablation of AF, renders P-wave morphology algorithms inaccurate. An early study identified leads V1 and avl as the most helpful in distinguishing right from left atrial foci [50]. The sensitivity and specificity of a positive P-wave in lead V1 in predicting a left atrial focus were 93% and 88% respectively, with a positive predictive accuracy of 87% and a negative predictive accuracy of 94%. A positive or biphasic P-wave in avl was demonstrated to have a sensitivity of 88% and a specificity of 79% for a right atrial focus, with a positive predictive accuracy of 83% and a negative predictive accuracy of 85%. Other groups have observed that focal ATs arising from the crista terminalis frequently have a negative P-wave in avl and that a negative P-wave in lead I is highly specific for a left atrial origin [35]. From the detailed study of 130 ATs in 126 consecutive patients, Kistler et al. [51] have developed an algorithm that can be used to identify the likely site of origin of a focal AT. The algorithm was subsequently

6 Heart, Lung and Circulation Walters et al ;21: Atrial Tachycardia and Atrial Flutter ORIGINAL ARTICLE Figure 3. Focal atrial tachycardias. (A) Electroanatomic activation maps in the left anterior oblique (LAO) and right anterior oblique (RAO) projections demonstrating centrifugal spread of activation from a focus at the base of the right atrial appendage. The red dots mark the site of successful ablation at the site of earliest atrial activation. (B) Focal tachycardia from the aorto-mitral continuity. In the upper panel an activation map in the LAO projection demonstrates centrifugal spread from the focus of origin, with the successful ablation site at the site of earliest atrial activation marked with a red dot. In the lower panel a transoesophageal echocardiogram shows the ablation catheter tip ( ) in contact with the aorto-mitral continuity at the successful ablation site. Ao, aorta; LA, left atrium; LAA, left atrial appendage; LSPV, left superior pulmonary vein; LV, left ventricle; MA, mitral annulus; MV, mitral valve; RSPV, right superior pulmonary vein; RV, right ventricle; TA, tricuspid annulus. Reproduced with permission of the Journal of Cardiovascular Electrophysiology.

7 392 Walters et al. Heart, Lung and Circulation Atrial Tachycardia and Atrial Flutter 2012;21: applied prospectively to a further 30 patients, with the location of the focal AT correctly determined in 93%. Mapping Endocardial activation mapping is the key to localisation of the AT focus at invasive electrophysiology study. Activation mapping includes the use of multipolar catheters in the right atrium to provide a broad activation picture along with sequential point mapping with the ablation catheter to identify the point of earliest atrial activation. If the onset of the P-wave on the surface ECG during tachycardia is obscured by the T-wave then mapping can be performed with reference to a stable fiducial point with a known relationship to the P-wave onset. Such activation mapping requires an adequate burden of tachycardia or ectopy, which can be stimulated by atrial pacing manouvers and intravenous isoprenaline. When the tachycardia is difficult to induce paced activation sequence mapping may be attempted, with atrial pacing through the ablation catheter used to generate an atrial activation sequence and a P-wave morphology which can be compared to those which occur during spontaneous ectopy. In an early series the combination of endocardial activation and paced activation mapping allowed an 80% success rate from catheter ablation of focal AT [52]. Another specific technique that has been used to map the site of a focal AT is atrial overdrive pacing, with comparison of the postpacing interval (PPI) to the tachycardia cycle length (TCL) [53]. The difference between PPI and TCL was found to be proportional to the distance from the tachycardia focus, and a PPI-TCL of <20 ms was found to localise the tachycardia focus to facilitate successful catheter ablation in all patients. As with macro-reentrant ATs, the mapping of focal ATs has been facilitated by the development of three-dimensional electroanatomic technologies that allow detailed reconstruction of atrial geometry and determination of activation sequence. Higa et al. [54] have used non-contact mapping to perform a detailed analysis of the origin of focal AT and the subsequent atrial activation pattern. They observed the origin to be a single point of activation corresponding to a unipolar QS electrogram. The majority of focal ATs were shown to have their origins in a low voltage zone or at the border of such a zone, suggesting arrhythmia origin in diseased myocardium. Rather than simple centrifugal spread to activate atrial myocardium from this point, a pathway of preferential conduction away from the origin was initially seen, perhaps due to non-uniform anisotropy in diseased myocardium or conduction through islands of scar. Centrifugal atrial activation was then seen from a breakout point at the termination of the preferential pathway, usually outside the low voltage zone or border area. Catheter ablation of the origin or the proximal portion of the preferential pathway rather than at the breakout point was demonstrated to have high acute procedural success and a low rate of arrhythmia recurrence. A similar schema of tachycardia origin, preferential conduction and breakout to atrial myocardium, with successful ablation at the origin or proximally on the preferential pathway, has been confirmed in subsequent reports [55]. Catheter Ablation The first report of catheter ablation of a focal atrial tachycardia involved delivery of a direct current shock at the site of earliest atrial activation in a 10 year-old patient with an incessant focal AT that had lead to development of a dilated cardiomyopathy [56]. Medi et al. [57] have subsequently described tachycardia mediated cardiomyopathy in up to 10% of patients undergoing catheter ablation for focal AT, with the LV function normalising in the majority following successful ablation. Delivery of radiofrequency energy has subsequently become the mainstay of catheter ablation of focal AT. Various series have reported success rates between 69% and 100% [58] with most reporting success rates between 85% and 95%. The major complication rate has been very low. The various methods by which catheter ablation can be directed to the tachycardia focus have been described above. In addition, the electrogram signal characteristics recorded through the ablation catheter can aid in accurately identifying the AT focus. Fractionated electrograms, potentially reflecting abnormal atrial myocardium with abnormal atrial conduction, have been described at the successful ablation site in multiple, but not all, studies [37,59,60]. The unipolar electrogram recorded with contact mapping can also identify a potentially successful site for ablation of focal AT [61]. A QS unipolar electrogram, a pure negative deflection with an initial steep slope, has been reported at all successful ablation sites, with an RS pattern at unsuccessful sites. Using such electrograms as a guide, a success rate of 86% for catheter ablation of focal AT has been reported [62]. Reported rates of recurrence are low, ranging from 0% to 33% [58]. Chen et al. [63] have analysed clinical and electrophysiologic characteristics that predicted success from catheter ablation of focal AT in reports published between 1969 and They reported an overall recurrence rate of 7% after successful catheter ablation, with a right-sided focus being the only independent predictor of successful long-term arrhythmia elimination. Older age, background structural heart disease and multiple foci of AT were risk factors for arrhythmia recurrence. Conclusions Atrial tachycardia is a generic term for a range of differing circuits. These can be broadly divided by mechanism into macro-reentrant, focal and small circuit re-entry. Atrial flutter is a term which is today largely restricted to those classical circuits around the tricuspid annulus involving the cavo-tricuspid isthmus. The advent of sophisticated mapping solutions has rendered the vast majority of these atrial circuits curable with catheter ablation, with high success rates and very low incidence of complications. References [1] Saoudi N, Cosío F, Waldo A, Chen SA, Iesaka Y, Lesh M, et al. A classification of atrial flutter and regular atrial tachycardia according to electrophysiological mechanisms and anatomical bases; a statement from a Joint Expert Group from The

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