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Focal Atrial Tachycardia I: Clinical Features, Diagnosis,

Focal Atrial Tachycardia I: Clinical Features, Diagnosis,

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Focal Atrial Tachycardia I:
Clinical Features, Diagnosis,Mechanisms, and Anatomic Location
From the Department of Cardiology, Royal Melbourne Hospital and the Department of Medicine, University of Melbourne, Melbourne, Australia
Atrial tachycardia (AT) may be focal or macroreentrant. In this review we will concentrate on focal AT.The diagnosis of focal AT may be made from a standard electrocardiogram (ECG); however, in some casesdifferentiation from other forms of supraventricular tachycardia may be difficult. Focal AT may be dueto several different mechanisms, including abnormal automaticity, triggered activity, and microreentry.Focal AT does not occur randomly throughout the atria but has a characteristic anatomic distribution. Inthis review, we particularly focus on the clinical features, diagnosis, mechanisms, and anatomic locationof focal AT. (PACE 2006; 29:643–652)
 focal atrial tachycardia
Focalatrialtachycardia(AT)isarelativelyun-common arrhythmia. In this review, we will con-centrate on the clinical features, diagnosis, mech-anisms, and anatomic locations of focal AT. FocalATisoftenrelatedtoanatomicalstructuresandhasdiffering arrhythmia mechanisms. These mecha-nismsincludeabnormalautomaticity,triggeredac-tivity, and reentry.
Definition of Focal AT
In2001,theJointExpertGroupfromtheWork-ing Group of Arrhythmias of the European Societyof Cardiology and the North American Society of PacingandElectrophysiologyclassifiedregularATaccordingtoelectrophysiologicalmechanismsandanatomical structures.
Regular AT may be classi-fied as focal or macroreentrant. Focal AT was de-fined as atrial activation starting rhythmically at asmall area (focus) from which it spreads out cen-trifugally and without endocardial activation oversignificant portions of the cycle length. The maintenet of this definition is that atrial activity origi-nates from a point source. In contrast, macroreen-trant activation is conventionally defined as acircuit with a diameter of greater than 2 cm indiameter and frequently occurs around a centralobstacle.
Nonsustained AT is commonly found onHolter recordings and is seldom associated with
Address for reprints: Jonathan M. Kalman, M.B.B.S., Ph.D.,F.A.C.C., Department of Cardiology, Royal Melbourne Hospi-tal, Melbourne, Australia 3050. Fax: 61 3 9347 2808; e-mail:jon.kalman@mh.org.auDr. Kurt Roberts-Thomson and Dr. Peter Kistler are the recipi-ents of a Postgraduate Research Scholarship from the NationalHealth and Medical Research Council of Australia.Received June 27, 2005; revised September 21, 2005; acceptedOctober 12, 2005.
symptoms. However, sustained AT is relativelyrare. AT accounts for 5–15% of adults undergo-ing electrophysiological studies for paroxysmalSVT,
with higher rates in children. Poutiainenet al.
investigated the prevalence of AT in asymp-tomatic young individuals and in patients attend-inganarrhythmiaclinic.Theprevalenceinasymp-tomatic young individuals was calculated to be0.34%,withaprevalenceof0.46%ofsymptomaticpatients. In contrast to other supraventriculartachycardias,malesandfemalesappearequallyaf-fected.
Kammeraad et al.
described a group of patients with nonautomatic AT and reported thattheyoccurredpredominantlyinwomen.However,no gender difference was noted by Chen et al.
In general, automatic AT tends to be a conditionwhich affects the young, whereas AT due to mi-croreentry is more common in older populations,althoughmanyexceptionstothisoccur.
Olderpa-tients are also more likely to have right-sided ATand multiple AT.
Clinical Features
The atrial rate during focal AT usually ranges between130and250beats/min,butmaybeaslowas 100 beats/min or as high as 300 beats/min. Ingeneral, younger patients tend to have faster AT,with rates up to 340 beats/min described in in-fants.
The properties of the atrial focus may besimilar to that of the sinus node in that they areresponsive to changes in activity and autonomictone.Ratesduringsleepmaybeupto40beats/minless than those during waking hours.
Patients may experience a spectrum of symp-toms, from being asymptomatic to complete inca-pacitation. Symptoms include palpitations, dizzi-ness, chest pain, dyspnea, fatigue, and syncope.Feeding problems, vomiting, and tachypnea may be seen in young children. The onset of symptomsmay occur at any age, from birth through to oldage. Rodriguez et al.
investigated the age of on-set in both adults and children and showed that
2006, The Authors. Journal compilation
2006, Blackwell Publishing, Inc.
PACE, Vol. 29
June 2006 643
the majority of patients had their first arrhythmicevent between the ages of 10 and 39 years.
Spontaneous Remission of AT
A study by Poutiainen et al.
demonstratedthat a follow-up ECG on patients diagnosed withAT 3–16 years earlier showed that 26% of patientscontinued to have an ectopic atrial rhythm. Only22% of patients were taking antiarrhythmic med-ication. Some patients had P-wave morphologychanges consistent with fusion of sinus and ec-topicrhythms.Thisledtheauthorstoproposethatthe AT foci gradually degenerate and slow withtime. Spontaneous remission has been reported in24–63%ofbothadultsandchildrenfollowingces-sation of medical therapy.
Klersy et al.
in-vestigated factors that predicted spontaneous re-mission. They found that the age of onset of thearrhythmia, heart rate during tachycardia, pres-ence of cardiomyopathy and clinical presentation(paroxysmal vs permanent) predicted remissionon univariate analysis. However, following logis-tic regression analysis, the only independent pre-dictor was the age of onset of the arrhythmia. Infact, the AT disappeared in 55% of patients underthe age of 25, compared to 14% of patients aged26 or older. This has been attributed to regressionof automatic AT, the most common mechanism inyounger patients.
The outlook of the majority of patients withfocal AT is benign. However, patients with in-cessant AT may develop tachycardia-induced car-diomyopathy.
analyzedtheliteratureup until 1997, and reported that 63% of patientswith focal AT had left ventricular dysfunction.Ofthese,73%hadtachycardia-inducedcardiomy-opathy.Tachycardiainducedcardiomyopathywascaused by AT due to abnormal automaticity in80% of cases. Patients with faster heart rates seemmore likely to develop cardiomyopathy. However,it remains unclear why some patients develop car-diomyopathyandothersmaintainnormalleftven-tricular function. The cardiomyopathy usually re-verses spontaneously following correction of thetachycardia, with the majority of patients achiev-ing normal or near-normal left ventricular func-tion.
There have been rare reports of embolicevents in patients with AT.
Diagnosis of Focal AT
Detection of AT is usually straightforward.Most patients can be diagnosed by a routine ECG(Fig. 1), although those with paroxysmal AT mayrequireHoltermonitoringoralooprecorder.How-ever, the differentiation of focal AT from other
Figure 1.
Twelve-lead ECG of incessant atrial tachy-cardia arising from the right septum. Note the P-wavemorphology in V 
which is inconsistent with a sinusmechanism.BiphasicP-wavesin
,whicharenegative- positive as in this case, usually indicate a tachycardiaoriginating from the left or right side of the septum or  from the superior mitral annulus.
forms of SVT or from macroreentrant AT may bedifficult.
Sinus Tachycardia versus AT
Differentiating AT from sinus tachycardia onthe ECG can at times be difficult, particularly fortachycardias originating at the superior crista ter-minalis. Although the P-wave in AT usually hasa different morphology to the sinus P-wave, inAT from the superior crista terminalis these differ-encesmaybesubtle(Fig.2).Frequentspontaneousectopic activity or nonsustained bursts of tachy-cardia may allow a direct comparison if the tachy-cardia P-wave is visible. Like sinus rhythm, focalATmayhavealongR-Pinterval,definedasgreaterthan50%oftheR-Rinterval,butatveryrapidrateswith AV nodal conduction delay the apparent R-Pmay be short. An abrupt onset and termination of the tachycardia or warm-up and cool-down over3–4 beats favors AT (Fig. 3), whereas sinus tachy-cardia gradually increases and decreases in rateoverapproximately30secondstoseveralminutes.In the electrophysiological laboratory, the ad-ministration of isoproterenol can differentiate si-nustachycardiafromAT.InfocalAT,isoproterenolwill increase the rate of the AT but the location of earliest atrial activation will not change. The ori-gin of earliest activation in sinus tachycardia willmove superiorly up the crista terminalis with iso-proterenol.
The most important differentiating factoron ECG between AT and atrioventricular nodal644 June 2006
PACE, Vol. 29
Figure 2.
Sinus P-wave and a P-wave from an atrial tachycardia arising from the medial extent of the highcrista terminalis in the same patient. This demonstratesthe similar P-wave morphology between sinus rhythmand atrial tachycardia from this region. In this case,tachycardia could be induced and terminate with pro-grammed stimulation.
reentrant tachycardia (AVNRT) and atrioventric-ular reentrant tachycardia (AVRT) is the R-P re-lationship. Both typical AVNRT and AVRT havea short R-P interval, which does not vary (the for-mersuperimposedontheQRSandthelatterintheST segment) and the P-wave morphology usuallycannot be clearly discerned. Although most com-monly associated with a long R-P interval, AT canoccur with either a short R-P interval or a long R-P interval depending on the tachycardia rate andthe speed of AV nodal conduction. It can there-fore mimic either AVNRT or AVRT. The ability todemonstrate “unhooking” or variability of the R toP relationship invariably indicates AT. In AT theR-P relationship is incidental and hence possiblyvariable. In AVRT and AVNRT this relationshipwill be constant as it is integral to the tachycar-dia mechanism, although the presence of multiplepathways or a pathway with decremental proper-ties may cause variation in the R-P interval. In ad-dition, there may be variation in the R-P intervalat the onset of AVNRT. Another clue to the diag-nosis is the presence of an inferior P-wave axis.This suggests an origin high in the atrium, exclud-ing AVNRT. A superiorly directed P-wave vector
Figure 3.
Twleve-lead ECG of a burst of atrial tachycar-dia from the superior crista terminalis. Note the sponta-neous onset and termination. While these tachycardiasmay be responsive to isoproterenol for induction in theEP laboratory they are not inducible with programmed extrastimulation.
mayindicateAVRTorAVNRToranATfocusorig-inating from the coronary sinus (CS) ostium or an-nular structures. Of note, atypical AVNRT and aconcealedaccessorypathwaywithslowretrogradeconduction may have long R-P intervals but haveconstant R-P intervals and a superior P-wave axis.Automatic AT may also manifest with recurrentself-limiting bursts of tachycardia, which can ex-hibit warm-up and cool-down phases.Several studies have proposed a variety of tachycardia features and pacing maneuvers to dif-ferentiate AT from AVNRT and AVRT in the elec-trophysiological laboratory.
In perhaps themost definitive paper on this subject, Knightet al.
investigated the diagnostic value of thesefeatures and pacing maneuvers in 196 patientswith supraventricular tachycardia, of whom 25had AT. Multiple baseline observations and tachy-cardia features were evaluated. Pacing maneuversassessed included atrial pacing during SVT just below the tachycardia cycle length; atrial pacingduring SVT at the longest cycle length that re-sulted in AV block; ventricular pacing during SVTjust below the tachycardia cycle length; burst ven-tricular pacing for 3–6 beats at a cycle length of 200–250 ms; and scanning diastole with a prema-ture ventricular extrastimulus.AT was unable to be identified by any sin-gle feature or maneuver, however, certain featureswere useful: AT required isoproterenol for induc-tionmoreoftenthanAVNRTorAVRT,althoughthepredictive value was poor. Importantly, the pres-ence of AV block with persistent tachycardia didnot discriminate between AVNRT and AT. How-ever, spontaneous termination of tachycardia with
June 2006 645

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