933

Nature of Rapid Pulmonary Vein Tachycardias: Reentryor Not Reentry?

MICHAEL A.E. SCHNEIDER, M.D.

From the Department of Cardiology, Center of Cardiovascular Medicine, Bad Neustadt, Germany

Editorial Comment

Ongoing discussions about ablation strategies of atrial fib-rillation and different reports about long-term success rateshave increased the interest in the mechanisms of initiationand perpetuation of this arrhythmia. For the most part, pul-monary vein ectopy has been considered responsible for in-duction of paroxysmal atrial fibrillation1,2; furthermore, theleft atrium seems capable of maintaining it.3,4 Although,there is some evidence for the role of nonpulmonary veinrelated focal ectopy in atrial fibrillation patients,5 it seemsthat ectopic activity with even longer coupling intervals gen-erated by pulmonary veins is more likely to induce atrialfibrillation.6

Regarding the anatomic substrate, earlier studies had al-ready demonstrated atrial myocardial tissue extending assleeves into pulmonary veins.7,8 After the introduction ofcatheter ablation to abolish trigger arrhythmias by electri-cal isolation of pulmonary veins,1,2 additional efforts weremade to assess the anatomy more precisely and to clarifyrelated electrical pathophysiology. Initial reports showed fo-cal activity responsible for initiation of paroxysmal atrialfibrillation and targeted it by radiofrequency catheter abla-tion.1 Interestingly, no related pacemaker or nodal-like cellstructures could be convincingly identified.9 Recent anatomicstudies confirmed degenerative changes in human myocardialsleeves with increased connective tissue depositions betweenmuscle groups and canine pulmonary vein tissue structure,with connexin distribution showing a circumferential my-ocyte orientation.9,10 Both findings suggest a substrate forrapid pulmonary vein reentry. On the other hand, increasedtissue anisotropy may facilitate the propagation of ectopicactivity to the surrounding tissue.11 Finally, another experi-mental study demonstrated the arrhythmogenic substrate ofpulmonary veins by high-resolution optical mapping.12 Theauthors showed rapid reentrant loops with a mean cycle lengthof 155 msec, as well as isoproterenol-mediated slower focalectopy. Stimulation maneuvers revealed anisotropic conduc-tion and repolarization heterogeneity with induction of reen-try. Burst stimulation was partially necessary to induce thefocal ectopy that seemed to be suppressible by faster atrialrates.12

Recently, during the last NASPE meeting, Weerasooriyaet al.13 reported that postablation dissociated pulmonary veinfoci may discharge repetitively. The authors support the hy-pothesis that, at least in some patients, a focal pulmonary veinactivity can maintain atrial fibrillation.13

J Cardiovasc Electrophysiol, Vol. 14, pp. 933-934, September 2003.

Address for correspondence: Michael Schneider, M.D., Herz-und Gefaß-Klinik Bad Neustadt, Kardiologie, An der Salzburger Leite 1, 97616 BadNeustadt/Saale, Germany. Fax: 49-89-36192293; E-mail: MAE.Schneider@t-online.de

The nature of atrial fibrillation onset is still a controversialissue. There are arguments in favor of reentry, but there alsois evidence for an impact of focal ectopy.

In a study reported in this issue of the Journal, Takahashiet al.14 assume that rapid reentrant tachycardias can occurin some isolated pulmonary veins and reentry may be oneof the arrhythmogenic mechanisms in pulmonary veins. Thefindings of Takahashi et al. regarding the disputable opinionson potential pulmonary vein arrhythmia genesis are interest-ing. However, several issues of the study should be consid-ered. The study was conducted in patients with establisheddrug-refractory atrial fibrillation. It is known that rapid atrialstimulation and fibrillation results in alterations of histologicand electrophysiologic tissue properties. Thus, it is not clearif modified tissue properties lead to the observed phenomenaof rapid tachycardias or if rapid pulmonary vein tachycar-dias had an earlier contribution to the induction/maintenanceof atrial fibrillation. The authors consistently support theirthesis about a reentrant mechanism of the tachycardias bydescribing (1) decremental conduction properties with shortrefractory periods; (2) induction and termination by stimula-tion; and (3) by performing entrainment maneuvers.15,16 Theauthors demonstrated decremental conduction properties byrapid burst stimulation at the pulmonary veins (Fig. 1 andTable 1). Programmed stimulation with extrastimulus tech-nique would have added even more value to assess effectiverefractory periods and to describe decremental conductionproperties. The ability to induce and terminate some of therapid tachycardias by burst pacing supports the hypothesisthat rapid reentrant tachycardias can occur in isolated pul-monary veins. It probably is difficult to perform a perfectentrainment maneuver with fusion of activation and resump-tion of the clinical tachycardia on cessation of pacing at cyclelengths <180 msec.16,17 Thus, Figure 4 shows only fusionof activation, and the authors assume that the tachycardiamechanism may be a reentry. The authors pointed out dou-ble potentials at “Lasso” electrode recordings (Fig. 5) andindicate properly a local conduction block in the pulmonaryvein. However, an ablation line may also cause such a localblock. As a consequence, it may be part of postablation reen-trant tachycardia instead of being a reentrant component of anintact pulmonary vein. A further analysis of pulmonary vein-related fractionated electrograms and electrogram durationsduring different cycle lengths before and after ablation couldclarify evidence for a reentrant substrate.18 Furthermore, incontrast to Takahashi et al., other authors relate an observedpostablation dissociated slow pulmonary vein activity to ec-topy rather than to reentry.13

It must be emphasized that, in this study, regular and ir-regular sustained tachycardias could only be induced in <3%of the studied vessels and in <7% of patients. It is ques-tionable if the described mechanism plays a major role inthe genesis of atrial fibrillation. In contrast to experimental

934 Journal of Cardiovascular Electrophysiology Vol. 14, No. 9, September 2003

studies supporting the reentry theory,12,19 the clinical evi-dence of pulmonary vein reentry as a basis for atrial fibrilla-tion remains difficult because of the high velocity of propa-gation and the complexity of anatomy and tissue structure.

The question about the true nature of observed pulmonaryvein tachycardias—focal ectopy or reentry—is still open.Nonetheless, Takahashi et al. provide clinical evidence sup-porting the reentrant theory, at least in some patients. Regard-ing the clinical relevance to date, interruption of the electricalinput from a pulmonary vein into the left atrium should abol-ish both potential focal and induced reentrant arrhythmias.Thus, further experimental and clinical studies are requiredto clarify if patients stratified according to different atrialfibrillation onset mechanisms would benefit from other ade-quately modified ablation approaches and therapies.

References

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2. Haissaguerre M, Shah DC, Jais P, Hocini M, Yamane T, Deisenhofer II,Garrigue S, Clementy J: Mapping-guided ablation of pulmonary veinsto cure atrial fibrillation. Am J Cardiol 2000;86:K9-K19.

3. Wu TJ, Ong JJ, Chang CM, Doshi RN, Yashima M, Huang HL,Fishbein MC, Ting CT, Karagueuzian HS, Chen PS: Pulmonary veinsand ligament of marshall as sources of rapid activations in a caninemodel of sustained atrial fibrillation. Circulation 2001;103:1157-1163.

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thoracic veins in human beings and dogs. Am J Cardiol 1972;30:844-854.

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17. MacLean WA, Plumb VJ, Waldo AL: Transient entrainment andinterruption of ventricular tachycardia. Pacing Clin Electrophysiol1981;4:358-366.

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19. Hocini M, Ho SY, Kawara T, Linnenbank AC, Potse M, Shah D, JaisP, Janse MJ, Haissaguerre M, de Bakker JM: Electrical conduction incanine pulmonary veins: Electrophysiological and anatomic correlation.Circulation 2002;105:2442-2448.