exploring atrial macroreentrant circuits

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688 Exploring Atrial Macroreentrant Circuits ETIENNE DELACRETAZ, M.D. From the Swiss Cardiovascular Center Berne, University Hospital, Berne, Switzerland Editorial Comment Late after surgical correction of congenital heart dis- ease (CHD), patients frequently develop atrial tachyarrhyth- mias that lead to significant morbidity. While antiarrhythmic agents have limited efficacy in the treatment of these arrhyth- mias, recent studies have demonstrated the feasibility of using radiofrequency (RF) ablation to treat them. 1-4 However, RF ablation may be challenging because of complex arrhythmia mechanisms. In operated CHD patients, the right atrium can support a variety of arrhythmia circuits referred to as macroreen- trant tachycardias (MRT) or intraatrial reentrant tachycardia (IART). 3-5 Isthmus-dependent atrial flutter may frequently occur. 6,7 Other arrhythmia mechanisms have been described, including reentry related to the lateral right atriotomy scar (or incisional atrial tachycardia), 2,8 and less commonly, lower- loop or higher-loop atrial flutter (around the inferior or su- perior vena cava), reentry around a septal patch or linked to the coronary sinus, and left atrial flutter. 4 Tachycardias with an apparently focal origin have also been described. The availability of three-dimensional mapping techniques has greatly improved our understanding of these arrhythmia mechanisms. 9,10 In this issue of the Journal, the study by Magnin-Poull et al. 11 confirms that isthmus-dependent flutter is the most common ensuing reentry mechanism in patients late after sur- gical repair of an atrium septal defect. 6 Using extensive three- dimensional electroanatomic mapping data acquired during sinus rhythm and tachycardia, the authors relate lines of dou- ble potentials to sites of conduction block and depict patterns of wavefront propagation within the right atrium. The posi- tions of these lines of block match the location of the surgical incisions made parallel to the intercaval line. In a majority of patients, there is a relatively narrow isthmus between the atriotomy scar and the inferior vena cava, which is a suitable target for RF ablation if this low pivot point is critical for the maintenance of a periatriotomy reentry. In a few patients, the atriotomy scar had two segments separated by an isthmus of conducting myocardium, while in some other patients, there were two parallel intercaval lines of block, outlining an ad- ditional potential corridor for reentry. These findings reflect the diversity of the arrhythmia substrates in CHD patients. Magnin-Poull et al. 11 claim that 70% of patients with IART late after surgical closure of an atrial septum defect have J Cardiovasc Electrophysiol, Vol. 16, pp. 688-689, July 2005. Etienne Delacretaz is supported by a grant from the Swiss National Foun- dation for Scientific Research. Address for correspondence: Etienne Delacretaz, M.D., F.E.S.C., Swiss Cardiovascular Center Berne, University Hospital, CH-3010 Berne, Switzerland. Fax: +41 31 632 14 14; E-mail: [email protected] doi: 10.1111/j.1540-8167.2005.50121.x double-loop reentrant circuits, mainly based on the visualiza- tion of lines of conduction block and high-density activation maps. When confronted with figure-eight reentrant circuits, it is essential to determine whether the “second loop” is a codominant or a nondominant loop, which will keep rotating once the first loop is abolished by RF ablation, or whether it is a dead-end pathway, an “innocent” bystander that will not re- quire additional treatment. This issue cannot be addressed by activation mapping alone. The problem is relevant, since the common isthmus of double-loop atrial circuits (contrasting with that of ventricular circuits) is usually not a vulnerable site and cannot easily be transected with a short line of RF ablation (see below). Figure-eight reentry was first described by El-Sherif in epicardial mapping studies of postinfarction dog models. 12 Figure-eight circuits were then demonstrated to be frequent in scar-related ventricular tachycardia in humans, and func- tional classification of the circuit sites using entrainment map- ping was shown to be essential to facilitate RF ablation. 13 In the right atrium, most of the reentry circuits have a single- loop pattern. 4 CHD patients often have more than one circuit, but the circuits do not rotate simultaneously. 4,7,14,15 How- ever, more complex reentry patterns have been inferred by a number of electrophysiologists who had to grapple over the transformation of tachycardia during RF ablation of IART. Shah et al. 16 were the first investigators to delineate an entire circuit of dual-loop atrial reentry in 5 patients late after surgi- cal closure of an atrial septum defect. Although double-loop activation circuits may have been overlooked in some series, they appear to be uncommon. In a series of 36 CHD patients with IART, dual-loop atrial reentry was present in only 3 pa- tients (8%). 17 This is in contradiction with Magnin-Poull’s assertion. The term “double-loop” or “dual-loop” reentry should be reserved to those circuits in which there is a functional sec- ond loop that is either a codominant or nondominant loop, according to the terminology defined for ventricular tachy- cardia circuits. The second loop will continue to rotate after disconnection of the first tachycardia limb and needs to be addressed with ablation. The term should not be used for circuits with an “innocent” dead-end pathway. The absolute demonstration of a double-loop reentry requires transforma- tion of the tachycardia into a different tachycardia, without a pause in between, with some change in F-wave morphology or intracardiac activation pattern (as in the case illustrated in Figure 5 of Magnin-Poull’s article). Tachycardia changes are most often associated with a sudden change of tachycardia cycle length, although this is not essential for the diagnosis of double-loop reentry. Sudden slowing of tachycardia during RF current application may also be due to the creation of slow conduction within the reentry isthmus being neutralized. What is the best approach if a double-loop reentry is suspected? Entrainment mapping is an important complement to three-dimensional activation mapping in the exploration of

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688

Exploring Atrial Macroreentrant CircuitsETIENNE DELACRETAZ, M.D.

From the Swiss Cardiovascular Center Berne, University Hospital, Berne, Switzerland

Editorial Comment

Late after surgical correction of congenital heart dis-ease (CHD), patients frequently develop atrial tachyarrhyth-mias that lead to significant morbidity. While antiarrhythmicagents have limited efficacy in the treatment of these arrhyth-mias, recent studies have demonstrated the feasibility of usingradiofrequency (RF) ablation to treat them.1-4 However, RFablation may be challenging because of complex arrhythmiamechanisms.

In operated CHD patients, the right atrium can supporta variety of arrhythmia circuits referred to as macroreen-trant tachycardias (MRT) or intraatrial reentrant tachycardia(IART).3-5 Isthmus-dependent atrial flutter may frequentlyoccur.6,7 Other arrhythmia mechanisms have been described,including reentry related to the lateral right atriotomy scar (orincisional atrial tachycardia),2,8 and less commonly, lower-loop or higher-loop atrial flutter (around the inferior or su-perior vena cava), reentry around a septal patch or linkedto the coronary sinus, and left atrial flutter.4 Tachycardiaswith an apparently focal origin have also been described.The availability of three-dimensional mapping techniqueshas greatly improved our understanding of these arrhythmiamechanisms.9,10

In this issue of the Journal, the study by Magnin-Poullet al.11 confirms that isthmus-dependent flutter is the mostcommon ensuing reentry mechanism in patients late after sur-gical repair of an atrium septal defect.6 Using extensive three-dimensional electroanatomic mapping data acquired duringsinus rhythm and tachycardia, the authors relate lines of dou-ble potentials to sites of conduction block and depict patternsof wavefront propagation within the right atrium. The posi-tions of these lines of block match the location of the surgicalincisions made parallel to the intercaval line. In a majorityof patients, there is a relatively narrow isthmus between theatriotomy scar and the inferior vena cava, which is a suitabletarget for RF ablation if this low pivot point is critical for themaintenance of a periatriotomy reentry. In a few patients, theatriotomy scar had two segments separated by an isthmus ofconducting myocardium, while in some other patients, therewere two parallel intercaval lines of block, outlining an ad-ditional potential corridor for reentry. These findings reflectthe diversity of the arrhythmia substrates in CHD patients.

Magnin-Poull et al.11 claim that 70% of patients withIART late after surgical closure of an atrial septum defect have

J Cardiovasc Electrophysiol, Vol. 16, pp. 688-689, July 2005.

Etienne Delacretaz is supported by a grant from the Swiss National Foun-dation for Scientific Research.

Address for correspondence: Etienne Delacretaz, M.D., F.E.S.C., SwissCardiovascular Center Berne, University Hospital, CH-3010 Berne,Switzerland. Fax: +41 31 632 14 14; E-mail: [email protected]

doi: 10.1111/j.1540-8167.2005.50121.x

double-loop reentrant circuits, mainly based on the visualiza-tion of lines of conduction block and high-density activationmaps. When confronted with figure-eight reentrant circuits,it is essential to determine whether the “second loop” is acodominant or a nondominant loop, which will keep rotatingonce the first loop is abolished by RF ablation, or whether it isa dead-end pathway, an “innocent” bystander that will not re-quire additional treatment. This issue cannot be addressed byactivation mapping alone. The problem is relevant, since thecommon isthmus of double-loop atrial circuits (contrastingwith that of ventricular circuits) is usually not a vulnerablesite and cannot easily be transected with a short line of RFablation (see below).

Figure-eight reentry was first described by El-Sherif inepicardial mapping studies of postinfarction dog models.12

Figure-eight circuits were then demonstrated to be frequentin scar-related ventricular tachycardia in humans, and func-tional classification of the circuit sites using entrainment map-ping was shown to be essential to facilitate RF ablation.13 Inthe right atrium, most of the reentry circuits have a single-loop pattern.4 CHD patients often have more than one circuit,but the circuits do not rotate simultaneously.4,7,14,15 How-ever, more complex reentry patterns have been inferred by anumber of electrophysiologists who had to grapple over thetransformation of tachycardia during RF ablation of IART.Shah et al.16 were the first investigators to delineate an entirecircuit of dual-loop atrial reentry in 5 patients late after surgi-cal closure of an atrial septum defect. Although double-loopactivation circuits may have been overlooked in some series,they appear to be uncommon. In a series of 36 CHD patientswith IART, dual-loop atrial reentry was present in only 3 pa-tients (8%).17 This is in contradiction with Magnin-Poull’sassertion.

The term “double-loop” or “dual-loop” reentry should bereserved to those circuits in which there is a functional sec-ond loop that is either a codominant or nondominant loop,according to the terminology defined for ventricular tachy-cardia circuits. The second loop will continue to rotate afterdisconnection of the first tachycardia limb and needs to beaddressed with ablation. The term should not be used forcircuits with an “innocent” dead-end pathway. The absolutedemonstration of a double-loop reentry requires transforma-tion of the tachycardia into a different tachycardia, without apause in between, with some change in F-wave morphologyor intracardiac activation pattern (as in the case illustrated inFigure 5 of Magnin-Poull’s article). Tachycardia changes aremost often associated with a sudden change of tachycardiacycle length, although this is not essential for the diagnosis ofdouble-loop reentry. Sudden slowing of tachycardia duringRF current application may also be due to the creation of slowconduction within the reentry isthmus being neutralized.

What is the best approach if a double-loop reentry issuspected?

Entrainment mapping is an important complement tothree-dimensional activation mapping in the exploration of

Delacretaz Editorial Comment 689

arrhythmias in CHD patients.7,18 It has also proved useful toinvestigate double-loop circuits, but entrainment data need tobe carefully interpreted.19 For example, if the revolution timeof both circuits is different (>20-second difference), entrain-ment mapping at sites within the nondominant (slower) loopshows long postpacing intervals and classifies the sites as“out of the circuit.” On the other hand, entrainment mappingis useful to examine the effect of RF ablation: comparisonof entrainment mapping before and after elimination of afirst conduction isthmus allows one to demonstrate whethera limb of the circuit has been successfully disconnected fromthe remaining circuit.19 In most cases of double-loop reentrycircuits described to date, the common isthmus is situatedbetween the lateral aspect of the tricuspid annulus and a rightatrial lateral longitudinal scar. Stabilization of the ablationcatheter may be difficult in this location. Moreover, the corri-dor between the atriotomy scar and the tricuspid annulus maybe broad, as observed in the study of Magnin-Poull11 (on av-erage 41 mm). Thus, ablation of two separate isthmuses isusually preferred to an attempt to transect the common isth-mus. During RF ablation, detecting an abrupt change of theactivation pattern or cycle length is crucial, and remappingafter this change may be necessary.

Reoccurring arrhythmias requiring repeat ablation proce-dures were frequent (54%) in Dr. Magnin-Poull’s series, eventhough conduction block was documented following abla-tion. A possible interpretation is that conventional cathetersmay not allow the creation of adequate RF lesions. Maximalpower delivered during RF current application is sometimeslimited due to insufficient electrode cooling in some atrialrecesses with low blood flow, and the depth of the lesion maynot be sufficient to create a transmural scar after the heal-ing process. Several studies suggest that using irrigated-tipcatheters may be helpful in patients with CHD.17,20 Anothernoteworthy point is that CHD patients who underwent suc-cessful ablation of one circuit may develop new arrhythmiacircuits over a longer follow-up period. Thus, RF ablation inthese patients should not be considered to be curative beforelong-term follow-up is available.

In conclusion, the treatment of arrhythmias by catheterablation in the CHD population offers unique challengesthat inspires further investigation. The interesting article byMagnin-Poull brings to our attention the variability and com-plexity of arrhythmia substrates in patients late after sur-gical repair of CHD. Double-loop reentry circuits are apotential cause for ablation failure and should be routinelyinvestigated. Although there are several approaches to studyarrhythmia circuits, entrainment mapping at a few key lo-cations rapidly delivers important information. Entrainmentmapping should be viewed as an invaluable opportunity to ex-plore the fascinating physiology of complex reentry circuitsbefore “burning.” But ultimately, we should not be embar-rassed by “learning by burning,” at least as far as the ablationof complex reentry circuits is concerned.

References

1. Triedman JK, Saul JP, Weindling SN, Walsh EP: Radiofrequency ab-lation of intra-atrial reentrant tachycardia after surgical palliation ofcongenital heart disease. Circulation 1995;91:707-714.

2. Kalman JM, VanHare GF, Olgin JE, Saxon LA, Stark SI, Lesh MD: Ab-lation of ‘incisional’ reentrant atrial tachycardia complicating surgery

for congenital heart disease. Use of entrainment to define a critical isth-mus of conduction. Circulation 1996;93:502-512.

3. Walsh EP: Arrhythmias in patients with congenital heart disease. CardElectrophysiol Rev 2002;6:422-430.

4. Cosio FG, Martin-Penato A, Pastor A, Nunez A, Goicolea A: Atypicalflutter: A review. Pacing Clin Electrophysiol 2003;26:2157-2169.

5. Saoudi N, Cosio FG, Waldo A, Chen SA, Iesaka Y, Lesh MD, SaksenaS, Salerno J, Schoels W: Classification of atrial flutter and regular atrialtachycardia according to electrophysiologic mechanism and anatomicbases: A statement from a Joint Expert Group from the Working Groupof Arrhythmias of the European Society of Cardiology and the NorthAmerican Society of Pacing and Electrophysiology. J Cardiovasc Elec-trophysiol 2001;12:852-866.

6. Chan DP, Van Hare GF, Mackall JA, Carlson MM, Waldo AL: Im-portance of atrial flutter isthmus in postoperative intra-atrial reentranttachycardia. Circulation 2000;102:1283-1289.

7. Delacretaz E, Ganz LI, Soejima K, Friedman PL, Walsh EP, TriedmanJK, Sloss LJ, Landzberg MJ, Stevenson WG: Multi atrial macro-re-entrycircuits in adults with repaired congenital heart disease: Entrainmentmapping combined with three-dimensional electroanatomic mapping.J Am Coll Cardiol 2001;37:1665-1676.

8. Lesh MD, Kalman JM, Saxon LA, Dorostkar PC: Electrophysiologyof “incisional” reentrant atrial tachycardia complicating surgery forcongenital heart disease. Pacing Clin Electrophysiol 1997;20:2107-2111.

9. Dorostkar PC, Cheng J, Scheinman MM: Electroanatomical mappingand ablation of the substrate supporting intraatrial reentrant tachycar-dia after palliation for complex congenital heart disease. Pacing ClinElectrophysiol 1998;21:1810-1819.

10. Nakagawa H, Shah N, Matsudaira K, Overholt E, Chandrasekaran K,Beckman KJ, Spector P, Calame JD, Rao A, Hasdemir C, Otomo K,Wang Z, Lazzara R, Jackman WM: Characterization of reentrant cir-cuit in macroreentrant right atrial tachycardia after surgical repair ofcongenital heart disease: Isolated channels between scars allow “focal”ablation. Circulation 2001;103:699-709.

11. Magnin-Poull I, de Chillou C, Miljoen H, Andronache A, Aliot E: Mech-anisms of right atrial tachycardia occurring late after surgical closureof atrial septal defects. J Cardiovasc Electrophysiol 2005;16:681–687.

12. El-Sherif N, Smith RA, Evans K: Canine ventricular arrhythmias in thelate myocardial infarction period. 8. Epicardial mapping of reentrantcircuits. Circ Res 1981;49:255-265.

13. Stevenson WG, Khan H, Sager P, Saxon LA, Middlekauff HR, Natter-son PD, Wiener I: Identification of reentry circuit sites during cathetermapping and radiofrequency ablation of ventricular tachycardia lateafter myocardial infarction. Circulation 1993;88:1647-1670.

14. Triedman JK, Jenkins KJ, Colan SD, Saul JP, Walsh EP: Intra-atrialreentrant tachycardia after palliation of congenital heart disease: Char-acterization of multiple macroreentrant circuits using fluoroscopicallybased three-dimensional endocardial mapping. J Cardiovasc Electro-physiol 1997;8:259-270.

15. Akar JG, Kok LC, Haines DE, DiMarco JP, Mounsey JP: Coexistenceof type I atrial flutter and intra-atrial re-entrant tachycardia in patientswith surgically corrected congenital heart disease. J Am Coll Cardiol2001;38:377-384.

16. Shah D, Jais P, Takahashi A, Hocini M, Peng JT, Clementy J, Hais-saguerre M: Dual-loop intra-atrial reentry in humans. Circulation2000;101:631-639.

17. Tanner H, Lukac P, Schwick N, Fuhrer J, Pedersen AK, HansenPS, Delacretaz E: Electroanatomic mapping and irrigated-tip catheterablation of intra-atrial reentrant tachycardia in patients aftersurgery of congenital heart disease. Heart Rhythm 2004;3:268-275.

18. Triedman JK, Alexander ME, Berul CI, Bevilacqua LM, Walsh EP:Electroanatomic mapping of entrained and exit zones in patients withrepaired congenital heart disease and intra-atrial reentrant tachycardia.Circulation 2001;103:2060-2065.

19. Irtel TA, Delacretaz E: Intra-atrial reentry tachycardia with ambiguousdata from activation mapping—What to do next? Heart Rhythm 2005;Inpress.

20. Triedman JK, Alexander ME, Love BA, Collins KK, Berul CI, Bevilac-qua LM, Walsh EP: Influence of patient factors and ablative technolo-gies on outcomes of radiofrequency ablation of intra-atrial re-entranttachycardia in patients with congenital heart disease. J Am Coll Cardiol2002;39:1827-1835.