Ablation of Atrial Tachycardiaand Atrial Flutter in HeartFailure

Ayotunde Bamimore, MB, ChB,Paul Mounsey, BSc, BM BCh, PhD, MRCP*

KEYWORDS

� Tachyarrhythmia � Heart failure � Atrial flutter � Atrial tachycardia � Ablation

KEY POINTS

� Atrial tachycardia (AT) and atrial flutter (AFL) are common tachyarrhythmias in the heart failurepopulation.

� They commonly lead to, exacerbate, and increase the morbidity and mortality associated with heartfailure and, thereby, warrant urgent and early definitive therapy in the form of catheter ablation.

� Catheter ablation requires careful patient stabilization and extensive preprocedural planning,particularly with regards to anesthesia, strategy, catheter choice, mapping system, and fluidbalance, to increase efficacy and limit adverse effects.

� Heart failure may limit the success of catheter ablation with higher reported recurrence rates and, inselected patients, a hybrid epicardial-endocardial ablation can be considered.

Atrial tachyarrhythmias are common in patientswithheart failure and vice versa.1 Several publicationshighlight the development of heart failure in patientswith poorly controlled atrial tachyarrhythmias aswell as the development of atrial arrhythmias inheart failure patients previously known tobe in sinusrhythm. The structural, electrophysiologic, andneuroendocrine changes that occur in one facilitatethe development of the other, thereby setting up avicious cycle, such that atrial tachyarrhythmiasbeget heart failure and heart failure begets atrialtachyarrhythmias. This statement, however true, isan oversimplification of a complex relationship.

Atrial tachyarrhythmias are those tachycardiasthat are initiated or sustained by the atria and donot require the atrioventricular (AV) node or ven-tricles for perpetuation. They may be regular orirregular. The irregular atrial arrhythmias are atrialfibrillation (AF) and multifocal AT whereas regular

Disclosures: The authors have nothing to disclose.Division of Cardiology, University of North Carolina, ChaCB #7075, Chapel Hill, NC 27599, USA* Corresponding author.E-mail address: Paul_mounsey@med.unc.edu

Heart Failure Clin 9 (2013) 501–514http://dx.doi.org/10.1016/j.hfc.2013.07.0021551-7136/13/$ – see front matter � 2013 Elsevier Inc. All

atrial tachyarrhythmias were previously classifiedas AT and AFL. This outdated classification of reg-ular atrial tachyarrhythmias was based on heartrate and ECG morphology, such that tachycardiaswith atrial rates equal to or greater than 240 beatsper minute (bpm), with an undulating baselinelacking an isoelectric baseline in at least one lead(saw tooth), were classified as AFL and the otherslacking these 2 characteristics as AT. Contem-porary electrophysiology studies (EPSs) andimprovement in mapping techniques have led toa more precise classification based on pathophys-iologic mechanisms.2

Regular atrial arrhythmias are now classified as

1. Focal ATs (formerly ATs), which have thefollowing characteristics� Origin outside the sinus node and from adiscrete portion of the atrium (<2 cm2)

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� Centrifugal spread of activation from thediscrete portion

� Mechanism automatic, triggered activity, ormicroreentry

� Propagation occurring over a short durationof the cycle length (Fig. 1)

� Rate above 100 bpm but less than 240 bpm� Warming up and cooling down properties

2. Macroreentrant AT (formerly AFL), with thefollowing characteristics� Mechanism is macroreentry involving a largeportion of the atrium

� Propagation occurring around an area offixed or functional barrier

� Propagation occurring over most of the dura-tion of the cycle length (Fig. 2)

For the remainder of this review, AT refers tofocal AT and AFL refers to macroreentrant AT,based on the newer classification. This distinctionis not often made in publications. Sometimesthe new classifications are implied and knowl-edge of this by readers is assumed, whereas inother instances, writers use the old classification.Some studies group AT and AFL together as ATs,

Fig. 1. Surface and intracardiac electrograms at 200 mm/s447 ms (153 1 294), which is 134 bpm. Surface leads I, VI,and Halo catheter leads spanning the crista terminalis in thacross large regions of the right atrium (Halo electrodes) aonly 34% of the entire tachycardia cycle length and is de

distinguishing them from AF. Further complicatingthe scenario is that a patient may exhibit each ofthese various tachyarrhythmias at different times.This confusion in terminologies makes the exactprevalence of AT and AFL in the general popula-tion, let alone in heart failure patients, uncertain.Although there is a robust amount of literatureon AF (often including AFL) in the general popula-tion and in heart failure patients, studies on ATand AFL are sparse. Few studies have madeefforts to separate these various atrial arrhythmiasand, from this limited information, the following isknown. The prevalence of AT has been reportedto be 0.34% in an asymptomatic population, ris-ing to 0.46% in a population with symptoms,3

whereas the prevalence of AFL is largely specula-tive. The incidence of AFL is, however, reportedto be approximately 0.07% in the United States,amounting to 200,000 new cases per year, amongwhich 80,000 patients are diagnosed with AFLonly (without AF).4 These numbers are overshad-owed by those of AF, which has a prevalence of2.2 million in the United States (0.7%–1% of thepopulation) and an incidence that stands at0.1%.5 Generally, in cardiac disease states, the

paper speed, showing a focal ATwith a cycle length ofand aVF are shown as well as coronary sinus (CS) leadse right atrium. The duration of endocardial activationnd representing the left atrium (CS) is 153 ms, which ispicted by the first caliper.

Fig. 2. Surface and intracardiac electrograms at 200 mm/s paper speed, showing macroreentry in the right atrium(typical AFL), with a cycle length of 240 ms (first set of calipers), which is 250 bpmwith a 3:1 AV block. Intracardiacleads consist of a 20-pole catheter that has its proximal 10 electrodes (RA 1–2 to RA 9–10) along the right atriumlateral wall and the distal 10 (CS 1–2 to 9–10) in the coronary sinus. Endocardial activation spans a large portion ofthe entire tachycardia cycle, and its duration depicted by the second caliper is 204 ms, which is 85% of the entiretachycardia cycle length.

Ablation of Atrial Tachycardia 503

prevalence of these arrhythmias increases ascorroborated by a study of 917 patients post–acute myocardial infarction, of whom 7% hadAF, 3% had AFL, and 3.6% had AT.6 In heartfailure, which may represent a final commonpathway for many cardiac conditions, the preva-lence of AF is reported to be between 20% and50% (depending on New York Heart Associationclass)7,8 and, although the exact prevalence ofAFL and AT are not as well known, their numbersmost likely increase as the prevalence of AFincreases.

WHY ARE AT AND AFL MORE PREVALENT INHEART FAILURE PATIENTS?

First, the risk factors for atrial arrhythmias are thesame as those for heart failure, so these condi-tions afflict the same patients. These risk factorsinclude advanced age, hypertension, diabetes,obesity, and cigarette smoking.4,8,9 In addition,some of the structural changes in the atria of

heart failure patients are shared by those withatrial arrhythmias. Wyndham and colleagues10

excised tissue samples from the culprit AT focusin a patient, and histology revealed markedlyincreased levels of mononuclear infiltrates andconnective tissue. Josephson and colleagues11

also demonstrated an increase in wall thickness,endocardial thickness, and inflammatory cells aswell as increased mesenchymal cells. In addition,they noted multicomponent atrial electrogramsaround the foci of atrial tachyarrhythmias depict-ing slow and asynchronous conduction similarto that seen in diseased ventricles in ventriculartachycardia studies. Similar findings are seen inthe atria of patients with heart failure and areattributable to myocardial stretch from pressureand volume changes. In essence, the structuraland neuroendocrine alterations in heart failureprobably facilitate the development of atrialtachyarrhythmias by complex and interrelatedmechanisms (discussed in articles elsewhere inthis issue).

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WHAT ARE THE EFFECTS OF AT AND AFL ONHEART FAILURE?

Tachyarrhythmias with uncontrolled ventricularresponse can be the sole cause of heart failure inpatients with no other risk factors. The first re-ported case of suspected tachycardia-mediatedcardiomyopathy (TCM) was by Gossage and Hicksin 191312 and, since then, animal models ofchronic atrial pacing mimicking AT have confirmedthe predictable development of reversible heartfailure.13

Given the aforementioned observations, AT andAFL may, therefore, be either the cause or conse-quence of heart failure, thereby evoking uncer-tainty and confusion in the management of newpatients with both disorders. This scenario mayrequire aggressive treatment of the arrhythmiaand subsequent observation for a few monthsbefore it can be determined whether a patienthas TCM or heart failure due to another causewith concurrent tachyarrhythmia. Sometimes theleft ventricle end diastolic dimension may helpdistinguish between the two, with left ventriculardimension less than or equal to 6.1 cm being100% sensitive for TCM and 71.4% specific in apatient presenting with heart failure and an appar-ently new tachyarrhythmia.14

Uncertainty and confusion may also be found inscenarios in which heart failure coexists with AToriginating from sites close to the sinoatrial nodehaving a positive P-wave axis on ECG leads II, III,and aVF, giving the initial impression of sinustachycardia secondary to heart failure.15 It maytake several days to weeks of Holter monitoringof the pattern of tachycardia to make the distinc-tion. Patterns of sudden dips in the heart rate to anew lower baseline alternating with sudden jumpsto the higher baseline heart rate may be the firstclue that the diagnosis is AT rather than sinustachycardia, which shows more gradual diurnalfluctuations. EPS may be required in difficultcases.AT and AFL are common causes of heart failure

exacerbation and hospitalization. In patients withpreexisting heart failure, they may result in furtherdeterioration in ejection fraction, pushing patientswith mild systolic dysfunction to severe dysfunc-tion. This worsening in ejection fraction affectsthe prognosis and could, for example, be of impor-tance in determining whether a patient requiresprophylactic implantable cardioverter defibrillator(ICD) therapy.8

Uncontrolled ventricular rates in patients withatrial tachyarrhythmias may increase the likelihoodof other morbidities, like myocardial infarction,in patients with ischemic cardiomyopathy or

unnecessary ICD firing, with its attendantincreased mortality.16 These arrhythmias haveoften influenced the choice of ICD type in heartfailure patients (single ventricular chamber vsdual, atrial, and ventricular chambers) to facilitatesupraventricular tachycardia discrimination.17,18

In patients with cardiac resynchronization therapy,conducted ventricular beats due to AT and AFLreduce biventricular pacing that may reduce itsbenefit or cause deterioration in patients with priorresponse.19 If the percentage of biventricular pac-ing suddenly drops in-between evaluations, atrialtachyarrhythmias should be sought and it may beprudent to set up a lower detection or monitor-only zone to pick these up. In addition to these co-morbidities, the presence of AT and AF in heartfailure patients admitted for myocardial infarctionportends an almost 2-fold increase in 30-day mor-tality, more so if the ejection fraction is between25% and 35%.20 Lastly, the onset of AT and AFLmay be the first indicator of development of hyper-thyroidism, pulmonary embolism, or even progres-sion of the underlying myocardial disease.In addition to the direct effects of AT and AFL on

heart failure, there are several indirect effects. ATand AFL complicate the treatment of heart failurepatients by typically making them require higherdoses of nodal blocking agents, possibly withassociated hypotension, by increasing the needfor digoxin, anticoagulation, and antiarrhythmicagents along with their attendant risks.

WHAT IMPACT DOES HEART FAILURE HAVEON THE MANAGEMENT OF AT AND AFL?

The structural and neurohormonal changes inheart failure facilitate the development of AT andAFL, which in turn leads to further adverse remod-eling, which in turn predisposes patients to moreatrial tachyarrhythmias, thereby setting up a vi-cious cycle. By so doing, heart failure encouragesthe development of new atrial tachyarrhythmiaswhile increasing the burden of preexisting AT andAFL and encouraging recurrence.The presence of heart failure also influences

the treatment strategy of atrial tachyarrhythmias.Restoration of sinus rhythm is highly likely to be at-tempted given that AT and AFL can precipitate andperpetuate acute decompensation and hospitali-zations. In heart failure exacerbations, the authorsare inclined to promptly cardiovert patients ratherthan use nodal blocking agents. Cardioversion isuseful in AFL but has limited success in AT. Ifdeciding on a conservative strategy of using AVnodal blocking agents, choices are limited tob-blockers and digoxin. Nondihydropyridine cal-cium channel blockers, commonly used in the

Ablation of Atrial Tachycardia 505

general population, are negatively inotropic and,therefore, contraindicated in most patients withsystolic dysfunction. Given the high cathechola-minergic state of heart failure decompensation,digoxin is less desirable given its potentialmorbidity and mortality21 and reduced efficacy.22

Also, because of the high catecholaminergicstate of heart failure, higher than usual doses ofb- blockers may be needed—a challenge in a pop-ulation that may already have low blood pressurefrommultiple drugs andmay not be able to toleratehigher doses of b-blockers or may only be able totolerate them at the cost of reducing or discontinu-ing other medications, like angiotensin-convertingenzyme inhibitors. Not all acutely decompensatedpatients, however, may immediately be givenb-blockers because of pulmonary edema andthe risk of initial worsening.8 Having consideredall these factors, a combination of digoxin andb-blockers is often needed.23

Lastly, a conservative approach in treating ATand AFL in heart failure patients is more likely torequire antiarrhythmic medication, and there areessentially 2 choices with good safety profile inheart failure: amiodarone24 and dofetilide.25 Thislimitation is because commonly prescribed antiar-rhythmic class IC agents26 and sotalol27 are abso-lutely and relatively contraindicated in heart failure,respectively. Dronedarone, another widely useddrug in the general population, caused new heartfailure and death in patients with chronic atrial ar-rhythmias or decompensated heart failure, so itsuse is limited in patients with preexisting heartfailure.28

Multiple challenges, therefore, exist to a phar-macologic therapy of AT and AFL in heart failure.

CONSIDERATIONS FOR THE ABLATION OF ATAND AFL IN HEART FAILURE PATIENTS

There is a need for definitive therapy for AT andAFL in heart failure patients, particularly given thehigh efficacy of catheter ablation in the generalpopulation, with 85% to 90% success in AT and90% to 93% in AFL.29–31 Moreover, approximately10% of patients with atrial tachyarrhythmias inheart failure, after elimination of the arrhythmia,may be essentially cured of heart failure, leadingto a retrospective diagnosis of tachycardia-related cardiomyopathy.15 In essence, heart failureadds an urgency to the treatment of AT and AFL aswell as the need for early consideration of defini-tive therapy.

A caveat to ablation is that its potential compli-cations may be higher in this population, withmore comorbidities, impacts of polypharmacy,propensity for renal insufficiency, drug-drug

interactions, and other factors. These factorsrequire meticulous preprocedural planning in pa-tients with heart failure, who may initially be toosick for the procedure. Under these circum-stances, cardioversion may be a useful tempo-rizing measure. Besides influencing the timing ofprocedure, the presence of heart failure has animpact on periablation management. Ablation ofcomplex left-sided AT and AFLmay last for severalhours, a serious challenge in those with preexist-ing orthopnea and paroxysmal nocturnal dyspnea.This may require preprocedural aggressivediuresis sometimes at the cost of an acceptabletemporary worsening of renal function. When thisis inadequate, an early evaluation by anesthesiastaff may be helpful in planning the procedure.

Other considerations include the presence ofICD and cardiac resynchronization therapy de-vices in an increasing proportion of heart failurepatients, introducing the risk of lead dislodgement.This may inform the choice of diagnostic cathetersand the choice of electroanatomic mapping sys-tems. For example, a bulky catheter, like a Halocatheter, which encircles the tricuspid annulus,may not be elected to be used a patients withmultiple leads, or a decision may be made to avoidinserting a diagnostic catheter into the coronarysinus of patients with left ventricular leads. Be-cause coronary sinus activation is often used asan intracardiac timing reference, its unavailabilityrequires an alternative reference site or eventechnology.

The presence of heart failure may also influencethe choice of ablation catheters, especially with re-gards to open irrigation catheters, which add tothe periprocedural fluid input. This additional fluidload should carefully assessed so that intraproce-dure or postprocedure additional diuretics may begiven as needed.

Once these scenarios and the peculiarities of ATand AFL in heart failure patients have been ad-dressed, there should be few differences betweenablation of these arrhythmias in patients with heartfailure compared with those without.

ABLATION OF AT

Success in the ablation of AT depends on an un-derstanding of the arrhythmia mechanism. ATshave been localized to several predictable areasof the atria and surrounding structures with thefollowing frequencies (Table 1).32

Rarely, ATs have also been localized to the non-coronary aortic cusp,33 superior vena cava(SVC),34 or the ligament of Marshall.35 These ATfoci are typically 2 cm2 or less in area, and theaim of catheter ablation is to identify the site of

Table 1Distribution of the anatomic locations of foci ofatrial tachycardias in both atria

Right Atrium Distribution

Crista terminalis 31%

Tricuspid annulus 22%

Perinodal tissue 11%

Coronary sinus os 8%

Interatrial septum <1%

Right atrial appendage <1%

Total 73%

Left Atrium Distribution

Pulmonary veins 19%

Superior mitral annulus 4%

Coronary sinus body 2%

Interatrial septum <1%

Left atrial appendage <1%

Roof <1%

Total 27%

Bamimore & Mounsey506

earliest atrial activation, apply radiofrequencyenergy, and eliminate them.

Localizing Atrial Tachycardias

The surface P-wave morphology of the AT may behelpful in predicting the site of origin and hencehelp in planning the procedure using algorithmsthat have been developed. Fig. 3 shows an adapt-ed and simplified algorithm that partially summa-rizes the elegant work of Kalman and colleagues.32

There are exceptions to the rule and that mostalgorithms are developed in patients with clearisoelectric baselines, resulting in undistorted Pwaves and mostly normal hearts, so extrapolationto patients with structural abnormalities withdistortion from chamber enlargement may renderECG prediction less reliable.

Induction and Mapping of ATs

Mapping of a focal AT entails recording electro-grams from various parts of the atrial endocar-dium, with the aim of localizing the earliest pointof activation, which is consistent with the point oforigin. This point usually precedes the surface Pwave by 38 � 7 ms in duration.36

At the time of EPS, if tachycardia is not present,then it may have to be induced by pacing rapidly inthe atrium (burst pacing) or programmed extrastimuli. Isoproterenol or other sympathomimeticagents may need to be given in addition to theseprotocols to induce tachycardia. Antiarrhythmicagents should be discontinued at least 5 half-

lives before EPS when possible and limitingsedation as much as possible may also facilitatetachycardia initiation.Multielectrode diagnostic catheters are placed

in the heart, which can simultaneously record sig-nals from different regions of the heart to give ageneral idea of the activation sequence. Forexample, a 20-electrode catheter (Halo) can bewrapped along the lateral wall of the right atriumpartly overlapping the crista terminalis. Propaga-tion along this Halo catheter enables determiningif the lateral wall is activated before the septumor determining if the activation sequence proceedsfrom a superior to inferior direction or vice versa. Acatheter with between 4 and 10 electrodes is usu-ally placed in the coronary sinus, which interro-gates the proximal portion of the os all the wayto the area around the mitral annulus on the leftside. Coronary sinus propagation enables deter-mining if AT activation is from left atrium to rightatrium or vice versa. Once the chamber of originof the tachycardia is known, a roving cathetercan then be used to interrogate the area of interestin detail until the earliest point of activation isfound. This area of earliest activation may alsodemonstrate low and multicomponent voltageindicative of an abnormal focus. Radiofrequencyablation (RFA) is applied at a power of 30 W to50 W for approximately 30 to 60 seconds. Termi-nation of tachycardia and an inability to reinitiateit approximately 30 minutes after the last RFAapplication is a good indicator of success.Other forms of mapping include 3-D electroana-

tomic mapping (Fig. 4), which involves reconstruc-tion of the shell of the atria on which the activationsequence of the tachycardia is superimposed toidentify and target the area of earliest activationfor RFA.37

Finally, if the tachycardia cannot be reproducedin an electrophysiology laboratory in a patient withpreviously documented AT, the ECG can be usedto initially predict the area of origin and then a rov-ing catheter can be moved around the large initialarea of interest with intermittent atrial pacing untilP-wave morphologies similar to that of the clinicaltachycardia (pace mapping) are reproduced. Thisarea is then targeted for ablation.38

ABLATION OF ATRIAL FLUTTER

Ablation of macroreentrant atrial tachyarrhythmiadiffers from AT in that there is no discrete focusto be identified and targeted for RFA but rather acritical isthmus that permits sustenance of thetachycardia, which can be interrupted with a lineof RFA lesions. Ablation of AFL is thus targeted tothe precise circuit along which the wave front of

Fig. 3. (A) A modified and simplified algorithm showing how ECG P-wave morphology (PWM) can be used topredict the anatomic site of origin of ATs. This partially summarizes the work of Kistler and colleagues.32 (B) Atable with visual representation of different P-wave morphologies. CT, Crista terminalis; LAT, left atrial tachy-cardia; LUPV, left upper pulmonary vein; MA, Mitral annulus; RAA, right atrial appendage; RAT, right atrial tachy-cardia; RPV, right pulmonary vein.

Ablation of Atrial Tachycardia 507

the tachycardia conducts (Figs. 5–7). The bound-aries of such circuits are typically formed by re-gions of functional or anatomic conduction block.Multiple circuits have been described in the rightand left atria, with the most common in the rightatrium and responsible for the initiation of typicalAFL. AFLs are classified into the following2:

1. Counterclockwise cavotricuspid isthmus (CTI)–dependent right AFL (typical flutter)

2. Clockwise CTI–dependent right AFL (reversetypical flutter)

3. Lesion macroreentrant AT (scar-related AFL)4. Left atrial macroreentrant tachycardia (left AFL)

The circuit along which typical flutter travels in-volves the crista terminalis as it runs along thelateral wall of the right atrium, extending from the

SVC superiorly to the inferior vena cava (IVC) infe-riorly. Its continuation inferiorly blends with theanterior lip of the IVC and the eustachian ridge,which extendsmedially from the IVC toward the in-teratrial septum, all forming a single continuousunit that in turn forms the posterior limit of whatis known as the CTI. The anterior limit of the CTIis the annulus of the tricuspid valve. The wave frontof typical flutter ascends in a counterclockwisefashion caudocranially along the interatrial septumto the roof of the right atrium and courses anteriorto the crista terminalis to descend along the rightatrial lateral wall. Its path is then funneled intothe CTI, which is the narrowest portion of the cir-cuit and is also the area of slow conduction thatpermits the wavelength of the arrhythmia to fitinto the fixed circuit and still have an excitable

Fig. 4. Electroanatomic map of the left atrium showing the activation pattern of a left AT with a radial spreadfrom the anterior wall of the atrium. Point of earliest activation is the white spot followed by the region inred, then orange, then yellow, and so on. Blue indicates the latest activated regions. LAA, left atrial appendage;LLPV, left lower pulmonary vein; LUPV, left upper pulmonary vein; RLPV, right lower pulmonary vein; RUPV, rightupper pulmonary vein.

Bamimore & Mounsey508

gap that perpetuates the arrhythmia.39 In cases ofthe reverse typical flutter, the wave front moves ina clockwise fashion caudocranially along thelateral wall of the right atrium, crosses the roof,and descends along the interatrial septum fromwhere it is funneled into the CTI. Ablation of typicalflutter is essentially ablation along the CTI from itsanterior to its posterior limit40 with the aim of cre-ation of a line of bidirectional block.41

Lesion macroreentrant atrial tachyarrhythmiasare those with circuits around anatomic scars inthe atrium. Commonly these scars are from atriot-omies, septal patches for ASD repairs, suturelines, and scar formed by previous ablation. Inthese scenarios, the goal of EPS is to identify thecircuit, delineate the narrowest portion, and thenattempt to create a line of RFA lesions along thisnarrow isthmus in such a way that one connectsat both ends to nonconducting structures. Forexample, a line of RFA lesions may be createdfrom the anatomic line of scar to the SVC, theIVC, or the tricuspid annulus.Several other described flutters include a lower

loop reentry flutter, which rotates around the IVC,traversing the CTI anteriorly and the low posteriorright atrium posteriorly. This is a variant of typicalflutter and can be ablated along the CTI. An upperloop reentry flutter rotates around the SVC. Mixedvariants (double loop or figure of 8) are essentiallya combination.2

Left-sided AFLs also exist and these are com-mon in patients who have had catheter or surgicalAF therapy. These have been arbitrarily classifiedas peripulmonary vein reentry (roof-dependent)flutters, perimitral annular (mitral isthmus–depen-dent) flutters, and periseptal flutters (see Fig. 7).Ablating these flutters requires mapping andapplying RFA lesions along narrowest and/ormost accessible portion of the circuit.42

ALTERNATIVES TO ABLATION OF AT/AFL:ABLATION OF THE AV NODE

“Ablate and pace” is an old strategy that involvedAV nodal ablation with implantation of a dual-chamber permanent pacemaker and was reservedfor patients refractory to all medications. It pro-duced excellent relief of symptoms43 but hasbeen largely overtaken by the advent of catheterablation. In the current state of electrophysiology,few patients who are intolerant of or allergic tomultiple medications and also not amenable tocatheter ablation may qualify for it. With increasingknowledge of the deleterious effects of chronicright ventricular pacing, however, particularly inpatients with cardiomyopathies,44 biventricularpacemaker implantation has become the pre-ferred mode because it prevents worsening ofheart failure and reduces hospitalization.45

Fig. 5. (A) Electroanatomic map of the right atrium showing the activation pattern of a typical counterclockwiseflutter circuit, an upper loop reentry, and a lower loop reentry flutter circuit. The reverse typical flutter runs clock-wise instead of counterclockwise along the same circuit. The blue spheres represent RFA lesions created along theCTI. Halo, Halo catheter hugging crista terminalis. (B) Surface ECG of a patient showing typical counterclockwise(CTI-dependent) flutter.

Ablation of Atrial Tachycardia 509

Fig. 6. (A) Electroanatomic mapping of the right atrium showing the activation pattern of a scar-related AFLalong the lateral wall. Point of earliest activation is the region in red followed by yellow, then green, thenblue, and purple. There is a gap of excitable tissue (gray) between the head and the tail of the arrow, indicatingthe head and tail, respectively, of the arrhythmia wave front. The line of red dots represents the area of scar inthis instance made by prior RFA lesions. (B) A surface ECG of a patient showing atypical flutter secondary to aright atriotomy scar. The arrows point to positive flutter waves in lead III.

Bamimore & Mounsey510

WHEN AFL IS REALLY AF

In patients with atypical AFL, in particular arisingfrom the left atrium after a prior AF ablation, map-ping not uncommonly reveals a much disorga-nized rhythm, which is actually AF rather than

AFL. Redo AF ablation may be scheduled insuch patients with the understanding that thesuccess of catheter ablation in heart failurepatients with recurrent persistent AF is at bestmodest. More extensive ablation is usually

Fig. 7. (A) Electroanatomic anatomic map of the anterior and posterior surfaces of the left atrium showing someof the possible multiple paths/circuits of a left AFL. LAA, left atrial appendage; LLPV, left lower pulmonary vein;LUPV, left upper pulmonary vein; RLPV, right lower pulmonary vein; RUPV, right upper pulmonary vein. (B) A sur-face ECG of a patient showing atypical flutter, which in this case was a left AFL. The arrows point to positiveflutter waves in lead III.

Ablation of Atrial Tachycardia 511

required in such patients and a hybrid epicardial-endocardial catheter ablation may offer anincreased efficacy, particularly when performedsimultaneously rather than in a staged fashion.The largest cohort that underwent this strategy

to date was reported by Gehi and colleagues.46

They reported a 66% rate of freedom fromarrhythmia 12 months post–single hybrid proce-dure in spite of an average left atrial size of5.1 cm. This is a promising result.

Bamimore & Mounsey512

ABLATION OF AT AND AFL IN CHALLENGINGSITUATIONS

AT and typical AFL have been reported as themostcommon supraventricular arrhythmias occurringlate after cardiac transplantation. Typical AFLstend to occur in the donor heart whereas the ATscommonly originate from the recipient atria or peri-suture areas. Ablations have been successfullyperformed by delivering RFA to CTI in cases ofAFL and by ablation of atrioatrial electrical connec-tions across anastomotic suture lines or ablation ofthe foci of origin in either the donor or recipient atriawithout prohibitive complications.47 Similarly, AToriginating from the anastomotic pulmonary veinsof donors propagating across suture lines intothe atria of lung transplant recipients have been re-ported and ablated by pulmonary vein isolation.48

Patients with congenital heart diseases andheart failure commonly develop atrial tachyar-rhythmias. The challenges in these cases includeunderstanding of the congenital heart diseaseand its hemodynamic consequences and of thealtered anatomy that may render certain areasinaccessible. Ablation in this cohort requiresextensive planning and a multidisciplinary ap-proach. Concomitant corrective surgeries andarrhythmia substrate ablation may be useful inthis cohort as may be preemptive techniques dur-ing surgery, such as extension of surgical cuts toareas of anatomic and physiologic barriers toprevent future arrhythmias. Success of catheterablation is in the range of 80% to 90%49 in suchpatients, with a 10% to 25% risk for recurrence.50

Finally, to show the breadth of patient popula-tion that may benefit from catheter ablation, AFLablation has been performed successfully andwithout complications even in patients on leftventricular assist devices.51

SUMMARY

AT and AFL are common tachyarrhythmias in theheart failure population. They commonly lead to,exacerbate, and increase the morbidity and mor-tality associated with heart failure and, thereby,warrant urgent and early definitive therapy in theform of catheter ablation. Catheter ablation re-quires careful patient stabilization and extensivepreprocedural planning, particularly with regardsto anesthesia, strategy, catheter choice, mappingsystem, and fluid balance, to increase efficacyand limit adverse effects. Heart failure may limitthe success of catheter ablation with higher re-ported recurrence rates52 and, in selected pa-tients, a hybrid epicardial-endocardial ablationcan be considered.

REFERENCES

1. Markides V, Peters NS. Mechanisms underlying the

development of atrial arrhythmias in heart failure.

Heart Fail Rev 2002;7:243–53.

2. Saoudi N, Cosio F, Waldo A, et al. Classification of

atrial flutter and regular atrial tachycardia accord-

ing to electrophysiologic mechanism and anatomic

bases: a statement from a joint expert group from

the Working Group of Arrhythmias of the European

Society of Cardiology and the North American

Society of Pacing and Electrophysiology. J Cardio-

vasc Electrophysiol 2001;12:852–66.

3. Poutiainen AM, Koistinen MJ, Airaksinen KE, et al.

Prevalence and natural course of ectopic atrial

tachycardia. Eur Heart J 1999;20:694–700.

4. Granada J, Uribe W, Chyou PH, et al. Incidence

and predictors of atrial flutter in the general popu-

lation. J Am Coll Cardiol 2000;36:2242–6.

5. Fuster V, Ryden LE, Cannom DS, et al, American

College of Cardiology, American Heart Association

Task Force, European Society of Cardiology Com-

mittee for Practice Guidelines, European Heart

Rhythm Association, Heart Rhythm Society. ACC/

AHA/ESC 2006 guidelines for the management of

patients with atrial fibrillation: full text: a report of

the American College of Cardiology/American

Heart Association Task Force on practice guide-

lines and the European Society of Cardiology Com-

mittee for Practice Guidelines (Writing Committee

to Revise the 2001 guidelines for the management

of patients with atrial fibrillation) developed in

collaboration with the European Heart Rhythm As-

sociation and the Heart Rhythm Society. Europace

2006;8:651–745.

6. Liberthson RR, Salisbury KW, Hutter AM, et al.

Atrial tachyarrhythmias in acute myocardial infarc-

tion. Am J Med 1976;60:956–60.

7. Savelieva I, Camm AJ. Atrial fibrillation and heart

failure: natural history and pharmacological treat-

ment. Europace 2003;5:S5–19.

8. Hunt SA, Abraham WT, Chin MH, et al, American

College of Cardiology, American Heart Association

Task Force on Practice Guidelines, American Col-

lege of Chest Physicians, International Society for

Heart and Lung Transplantation, Heart Rhythm So-

ciety. ACC/AHA 2005 Guideline Update for the

Diagnosis and Management of Chronic Heart Fail-

ure in the Adult: a report of the American College of

Cardiology/American Heart Association Task Force

on Practice Guidelines (Writing Committee to Up-

date the 2001 Guidelines for the Evaluation and

Management of Heart Failure): developed in

collaboration with the American College of Chest

Physicians and the International Society for Heart

and Lung Transplantation: endorsed by the Heart

Rhythm Society. Circulation 2005;112:154–235.

Ablation of Atrial Tachycardia 513

9. Kannel WB, Wolf PA, Benjamin EJ, et al. Preva-

lence, incidence, prognosis, and predisposing

conditions for atrial fibrillation: population-based

estimates. Am J Cardiol 1998;82:2N–9N.

10. Wyndham CR, Arnsdorf MF, Levitsky S. Successful

surgical excision of focal paroxysmal atrial tachy-

cardia. Observations in vivo and in vitro. Circulation

1980;62:1365–72.

11. Josephson ME, Spear JF, Harken AH, et al. Surgi-

cal excision of automatic atrial tachycardia:

anatomic and electrophysiologic correlates. Am

Heart J 1982;104:1076–85.

12. Gossage AM, Braxton Hicks JA. On auricular fibril-

lation. QJM 1913;6:435–40.

13. Whipple GH, Sheffield LT, Woodman EG, et al.

Reversible congestive heart failure due to rapid

stimulation of the normal heart. Proc New Engl Car-

diovasc Soc 1961–1962;20:39–40.

14. Jeong YH, Choi KJ, Song JM, et al. Diagnostic

approach and treatment strategy in tachycardia-

induced cardiomyopathy. Clin Cardiol 2008;31:

72–8.

15. Medi C, Kalman JM, Haqqani H, et al. Tachycardia-

mediated cardiomyopathy secondary to focal atrial

tachycardia: long-term outcome after catheter

ablation. J Am Coll Cardiol 2009;53:1791–7.

16. Poole JE, Johnson GW, Hellkamp AS, et al. Prog-

nostic importance of defibrillator shocks in pa-

tients with heart failure. N Engl J Med 2008;359:

1009–17.

17. Dorian P, Philippon F, Thibault B, et al. Randomized

controlled study of detection enhancements versus

rate-only detection to prevent inappropriate ther-

apy in a dual-chamber implantable cardioverter-

defibrillator. Heart Rhythm 2004;1:540–7.

18. Friedman PA, McClelland RL, Bamlet WR, et al.

Dual-chamber versus single-chamber detection

enhancements for implantable defibrillator rhythm

diagnosis: the detect supraventricular tachycardia

study. Circulation 2006;113:2871–9.

19. Gasparini M, Galimberti P, Ceriotti C. The impor-

tance of increased percentage of biventricular

pacing to improve clinical outcomes in patients

receiving cardiac resynchronization therapy. Curr

Opin Cardiol 2013;28:50–4.

20. Pedersen OD, Bagger H, Køber L, et al, TRACE

Study Group. Impact of congestive heart failure

and left ventricular systolic function on the prog-

nostic significance of atrial fibrillation and atrial

flutter following acute myocardial infarction. Int J

Cardiol 2005;100:65–71.

21. The effect of digoxin on mortality and morbidity in

patients with heart failure. The Digitalis Investiga-

tion Group. N Engl J Med 1997;336:525–33.

22. Sarter BH, Marchlinski FE. Redefining the role of

digoxin in the treatment of atrial fibrillation. Am J

Cardiol 1992;69:71G–81G.

23. Khand AU, Rankin AC, Martin W, et al. Carvedi-

lol alone or in combination with digoxin for the

management of atrial fibrillation in patients

with heart failure? J Am Coll Cardiol 2003;42:

1944–51.

24. Singh S, Fletcher RD, Fisher S, et al. Congestive

heart failure: survival trial of antiarrhythmic therapy

(CHF STAT). The CHF STAT Investigators. Control

Clin Trials 1992;13:339–50.

25. Møller M, Torp-Pedersen CT, Køber L. Dofetilide

in patients with congestive heart failure and

left ventricular dysfunction: safety aspects and ef-

fect on atrial fibrillation. The Danish Investigators

of Arrhythmia and Mortality on Dofetilide

(DIAMOND) Study Group. Congest Heart Fail

2001;7:146–50.

26. Preliminary report: effect of encainide and flecai-

nide on mortality in a randomized trial of arrhythmia

suppression after myocardial infarction. The Car-

diac Arrhythmia Suppression Trial (CAST) Investi-

gators. N Engl J Med 1989;10:406–12.

27. Pratt CM, Camm AJ, Cooper W, et al. Mortality in

the survival with ORal D-sotalol (SWORD) trial:

why did patients die? Am J Cardiol 1998;81:

869–76.

28. Connolly SJ, Camm AJ, Halperin JL, et al. Drone-

darone in high-risk permanent atrial fibrillation.

N Engl J Med 2011;365:268–76.

29. Xia Y, Ju WZ, Chen ML, et al. Catheter ablation of

focal atrial tachycardia: the topographic distribu-

tion and long-term outcome. Zhonghua Xin Xue

Guan Bing Za Zhi 2012;40:231–6 [in Chinese].

30. Perez FJ, Schubert CM, Parvez B, et al. Long-term

outcomes after catheter ablation of cavo-tricuspid

isthmus dependent atrial flutter: a meta-analysis.

Circ Arrhythm Electrophysiol 2009;2:393–401.

31. Lee G, Sanders P, Kalman JM. Catheter ablation of

atrial arrhythmias: state of the art. Lancet 2012;380:

1509–19.

32. Kistler PM, Roberts-Thomson KC, Haqqani HM,

et al. P-wave morphology in focal atrial tachy-

cardia: development of an algorithm to predict

the anatomic site of origin. J Am Coll Cardiol

2006;48:1010–7.

33. Ouyang F, Ma J, Ho SY, et al. Focal atrial tachy-

cardia originating from the non-coronary aortic

sinus: electrophysiological characteristics and

catheter ablation. J Am Coll Cardiol 2006;48:

122–31.

34. Dong J, Schreieck J, Ndrepepa G, et al. Ectopic

tachycardia originating from the superior vena

cava. J Cardiovasc Electrophysiol 2002;13:620–4.

35. Polymeropoulos KP, Rodriguez LM, Timmermans C,

et al. Images in cardiovascular medicine. Radio-

frequency ablation of a focal atrial tachycardia

originating from the Marshall ligament as a trigger

for atrial fibrillation. Circulation 2002;105:2112–3.

Bamimore & Mounsey514

36. Chen SA, Chiang CE, Yang CJ, et al. Radiofre-

quency catheter ablation of sustained intra-atrial

reentrant tachycardia in adult patients. Identifica-

tion of electrophysiological characteristics and

endocardial mapping techniques. Circulation

1993;88:578–87.

37. Natale A, Breeding L, Tomassoni G, et al. Ablation

of right and left ectopic atrial tachycardias using a

three-dimensional non fluoroscopic mapping sys-

tem. Am J Cardiol 1998;82:989–92.

38. Singh B, Sapra R, Gupta RK, et al. Pace mapping

for the localization of focal atrial tachycardia

arising near the mitral annulus. Indian Heart J

2004;56:58–60.

39. Feld GK, Fleck RP, Chen PS, et al. Radiofrequency

catheter ablation for the treatment of human type 1

atrial flutter. Identification of a critical zone in the

reentrant circuit by endocardial mapping tech-

niques. Circulation 1992;86:1233–40.

40. Fischer B, Haissaguerre M, Garrigues S, et al. Ra-

diofrequency catheter ablation of common atrial

flutter in 80 patients. J Am Coll Cardiol 1995;25:

1365–72.

41. Moreira JM, Alessi SR, Rezende AG, et al. Catheter

ablation of atrial flutter. Electrophysiological char-

acterization of posterior and septal isthmus block.

Arq Bras Cardiol 1998;71:37–47 [in Portuguese].

42. Jaıs P, Shah DC, Haıssaguerre M, et al. Mapping

and ablation of left atrial flutters. Circulation 2000;

101:2928–34.

43. Kay GN, Ellenbogen KA, Giudici M, et al. Ablate

and Pace Trial: a prospective study of catheter

ablation of the AV conduction system and perma-

nent pacemaker implantation for treatment of atrial

fibrillation. APT Investigators. J Interv Card Electro-

physiol 1998;2:121–35.

44. Wilkoff BL, Dual Chamber and VVI Implantable

Defibrillator Trial Investigators. The Dual Chamber

and VVI Implantable Defibrillator (DAVID) Trial:

rationale, design, results, clinical implications and

lessons for future trials. Card Electrophysiol Rev

2003;7:468–72.

45. Brignole M, Botto G, Mont L, et al. Cardiac re-

synchronization therapy in patients undergoing

atrioventricular junction ablation for permanent

atrial fibrillation: a randomized trial. Eur Heart J

2011;32:2420–9.

46. Gehi AK, Mounsey JP, Pursell I, et al. Hybrid

epicardial-endocardial ablation using a pericardio-

scopic technique for the treatment of atrial fibrilla-

tion. Heart Rhythm 2013;10:22–8.

47. Li YG, Gronefeld G, Israel C, et al. Radiofrequency

catheter ablation in patients with symptomatic atrial

flutter/tachycardia after orthotopic heart transplan-

tation. Chin Med J (Engl) 2006;119:2036–41.

48. Nazmul M, Munger TM, Powell BD. Atrial tachy-

cardia originating from a donor pulmonary vein in

a lung transplant recipient. Circulation 2011;124:

1288–9.

49. Lam W, Friedman RA. Electrophysiology issues in

adult congenital heart disease. Methodist Debakey

Cardiovasc J 2011;7:13–7.

50. Akar JG, Kok LC, Haines DE, et al. Coexistance of

type I atrial flutter and intra-atrial re-entrant tachy-

cardia in patients with surgically corrected

congenital heart disease. J Am Coll Cardiol 2001;

38:377–84.

51. Maury P, Delmas C, Trouillet C, et al. First experi-

ence of percutaneous radio-frequency ablation

for atrial flutter and atrial fibrillation in a patient

with HeartMate II left ventricular assist device.

J Interv Card Electrophysiol 2010;29:63–7.

52. Landolina M, Cantu F, De Ferrari GM, et al. The role

of invasive electrophysiology in the management of

patients with chronic heart failure. Heart Fail Monit

2002;3:49–59.