rom the II. Medizinische Abteilung, Asklepios Klinik St. Georg, Hamburg, Germany.
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ACKGROUND The macroreentrant tachycardia that involves theeft atrium (LA) and the pulmonary veins (PVs) after atrial fibril-ation (AF) ablation has not been described.
BJECTIVE To clarify the mechanism and electrophysiologicalharacteristics of this tachycardia.
ETHODS AND RESULTS Eight patients presented with recurrentegular tachycardia after the initial procedure, which consisted ofwo circular linear lesions around the ipsilateral PVs. Clinicalachycardia with a cycle length of 297 � 38 ms presented asersistent in six and paroxysmal in two patients. During tachycar-ia, PV activation with one-to-one conduction from the LA to theV was found via recovered conduction gaps in the previousesions in all patients. Three-dimensional tachycardia mappinghowed a macroreentrant pattern in two and a focal pattern in sixatients. In two patients, mapping demonstrated an isthmusithin the left common PV in one patient and within the right-
ocal pattern, mapping demonstrated earliest atrial activationear the right-sided PV ostium in five patients and near theeft-sided PV in one patient. Entrainment mapping showed thathe LA and PVs were involved in the reentrant circuit with ansthmus between the two conduction gaps in all eight patients.he tachycardias were successfully terminated with a single radio-requency application. No AT recurred during follow-up (12 � 9onths) in all patients.
ONCLUSIONS The LA-PV macroreentrant tachycardia involveshe LA, PV, and the two conduction gaps in the previous lesions.ntrainment mapping is necessary to make the diagnosis. Ablationf this tachycardia can be facilitated by closing the conductionaps.
ided PVs in another patient. In the remaining six patients with rights reserved.
ntroductiont has been demonstrated that pulmonary veins (PVs) playn important role in the initiation and perpetuation of atrialbrillation (AF).1 This important finding has led to theevelopment of PV isolation in patients with AF with eithersmall and segmental lesion guided by a Lasso catheter2,3
r large and continuous circular lesions around ipsilateralVs guided by three-dimensional (3D) electroanatomicalapping and Lasso technique.4 Recent studies have dem-
nstrated that complete PV isolation with the circular le-ions has a better outcome in patients with paroxysmal andersistent AF.4,5 On the other hand, it may lead to iatrogeniceft atrial (LA) macroreentrant atrial tachycardia (AT),6–10
articularly if circumferential PV isolation is combined withinear lesions. The reentrant circuit of these left macroreen-
Dr. Kazuhiro Satomi is supported by grants from the Japan Heartoundation, the Japanese Society of Electrophysiology, St. Jude Medical,nd Fukuda Denshi. Address reprint requests and correspondence: Dr.eifan Ouyang, MD, II. Medizinische Abteilung, Asklepios Klinik St.eorg, Lohmühlenstraße 5, 20099 Hamburg, Germany. E-mail address:[email protected]. (Received July 18, 2007; accepted August 27,
rant ATs is dissociated from the PVs in the majority ofatients. However, mapping and ablation during a repeatedrocedure suggest that the myocardium within the PV isartially responsible for the mechanism in a few cases.9,10
n the present study, we describe a new type of LA-PVacroreentrant tachycardia after PV isolation related to two
aps in a previous circumferential line and investigate thelectrophysiological characteristics and catheter ablation ofhis type of macroreentrant AT.
ethodsatient populationetween January 2004 and August 2006, 850 patients witharoxysmal or persistent AF underwent complete PV isola-ion using our approach, which consists of only two con-inuous circular lesions around the ipsilateral PV guided byD mapping and Lasso catheter.4 Left macroreentrantachycardia was diagnosed in 45 patients after the initial PVsolation. In this study, there were eight consecutive patientssix male; age 56 � 12 years; range 35–74 years), whoresented with recurrent regular AT after the initial ablation
f AF and demonstrated LA-PV macroreentrant tachycardia
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44 Heart Rhythm, Vol 5, No 1, January 2008
uring a repeated procedure (Table 1). The ablation strategyuring the initial procedure was complete PV isolation us-ng only two continuous circular lesions around the ipsilat-ral PVs.4,5 In all eight patients, only AF was shown onurface electrocardiogram (ECG) and 24-hour Holter re-ordings. Six patients had paroxysmal AF, and two patientsad persistent AF. Clinical AT presented as a persistentattern in six patients and as a paroxysmal pattern in twoatients and occurred 23 � 17 days (range 8–50 days) afterhe initial procedure. Treatment with a mean of 1.9 � 0.4range 1–2) antiarrhythmic drugs including amiodarone wasneffective in all patients. Structural heart disease was di-gnosed in three patients (nonobstructive hypertrophic car-iomyopathy in two and coronary artery disease in one).he LA diameter measured by transthoracic echocardiogra-hy was 42 � 3 mm (range 38–48 mm).
All patients had been on oral anticoagulants before ab-ation. Transesophageal echocardiography was performedo rule out LA thrombi in all patients. Oral anticoagulantsere stopped at admission and replaced by intravenouseparin to maintain partial thromboplastin time at two tohree times the control value. This was stopped 6–8 hoursefore ablation for transseptal puncture.11 All patients gaveritten informed consent.
lectrophysiological studyhe ablation procedure was performed on the previous
neffective antiarrhythmic drugs and under deep sedationith a continuous infusion of propofol. Two standard cath-
ters were positioned: a 6-Fr catheter (Biosense-Webster,iamond Bar, CA) at the His bundle region via a femoralein and a multipolar electrode 6-Fr catheter in the coronaryinus (CS) via the left subclavian vein. Three 8-Fr SL1heaths (St. Jude Medical, Minnetonka, MN) were ad-anced to the LA via the patent previously punctured site ory use of a modified Brockenbrough technique. After trans-eptal catheterization, intravenous heparin was administeredo maintain an activated clotting time of 250–300 seconds.
n addition, continuous infusions with heparinized saline a
ere connected to the transseptal sheaths (flow rate of 10L/hour) to avoid thrombus formation or air embolism.
lectroanatomical mappinghe reconstruction of the LA was performed with a 3.5-mmlectrode tip (Navistar Thermo-Cool, Biosense Webster) vian SL1 sheath. Activation mapping was performed relativeo the timing reference from the catheter inside the CS.etailed mapping was carried out in the areas around theVs and in electrically silent areas, which presented with notrial potential distinguishable from noise and were dis-layed in gray or along continuous lines of double potentialseparated by an isoelectric interval of �50 ms.8,12
After LA reconstruction, selective PV angiography with7-Fr multiple-purpose catheter (Biosense-Webster) was
erformed to evaluate all PV ostia. Each angiographic PVstium was tagged on the electroanatomical map. Subse-uently, two decapolar Lasso catheters (Biosense-Webster)ere placed within the ipsilateral superior and inferior PVsr within the superior and inferior branches of a commonV to confirm whether recovered PV conduction was re-overed.13
After tagging the PV ostia on the 3D mapping, thentrainment maneuver was performed in multiple sites todentify the tachycardia reentrant circuit. Pacing sites with aostpacing interval (PPI) that did not exceed the tachycardiaycle length (TCL) by more than 30 ms were consideredart of the circuit. In addition, the conduction gaps weredentified in the 3D mapping. The location of the conduc-ion gaps was defined as the roof, anterosuperior, anteroin-erior, inferior, posteroinferior, or posterosuperior region ofhe previous circular lesions.11
atheter ablationhe 3.5-mm-tip catheter (Navistar Thermo-Cool; Biosenseebstar) was used for ablation. Irrigated radiofrequency
RF) energy was delivered as previously described with aarget temperature of 45°C, a maximal power limit of 30 W,nd an infusion rate of 17 mL/min.11 RF energy was applied
t the critical sites of the reentrant circuit. After tachycardia
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45Satomi et al LA-PV Macroreentrant Tachycardia after PV Isolation
ermination, all conduction gaps in the previous circularesions were closed.
The endpoint of the ablation was defined as no inducibleT after ablation by programmed stimulation and the ab-
ence of all PV spikes documented with the two Lassoatheters within the ipsilateral PVs at least 30 minutes aftersolation during sinus rhythm (SR).
ollow-upfter the procedure, intravenous heparin was administered
or 3 days, followed by warfarin for at least 3 months in allatients. All patients continued the previously ineffectiventiarrhythmic drugs for 1 month after the ablation. A sur-ace ECG, transthoracic echocardiography, and 24-hourolter recording were performed 1 day after the procedure
nd repeated after 3 and 6 months by the referring physicianr in the ablation center.
tatistical analysisalues are given as mean � standard deviation or median as
ppropriate.
esultslectrophysiological testhe clinical and electrophysiological characteristics arehown in Tables 1 and 2. During the procedure, the clinicalachycardia with a CL of 297 � 38 ms (240–370 ms) wasersistent in six patients and paroxysmal in the other twoatients. The P-wave morphology on the surface ECGhowed positive in V1 during tachycardia in all eight pa-ients. In the two patients with paroxysmal AT, the clinicalachycardias were reproducibly induced by burst pacingrom the CS. During the tachycardias, recovered PV con-uction was confirmed with one or two Lasso catheters.uring tachycardia, there was one-to-one conduction into
he involved PV along the previous circular lesions in allatients. After exclusion of right AT, entrainment mappingas initially performed within the proximal part of the CS.fused intracardiac activation with a PPI-TCL �30 ms was
emonstrated in all patients. Subsequently, 3D electroana-omical mapping with mapping points of 99 � 7 (range
LPV � left pulmonary veins; RCPV � right common pulmonary vein; RPV � r
4–105) in the LA presented as macroreentrant tachycardian two patients and focal pattern in six patients.
acroreentrant pattern during tachycardian two patients presenting with a macroreentrant pattern, thearliest site of atrial activation during mapping was poste-ior to the left common PV (LCPV) and the latest atrialctivation anterosuperior to the LCPV with an isthmushrough the LCPV (Figure 1A) in patient 1 and the earliesttrial activation anterosuperior to the right superior PVRSPV) and the latest atrial activation posterior to the right-ided PVs in patient 2 (Figure 1B). Tachycardia mappingemonstrated mapped CLs of 317 and 211 ms, which were80% of the TCL (370 and 240 ms, respectively). Entrain-ent mapping within the PV demonstrated that the LCPVas part of the circuit in patient 1 (Figure 2) and part of the
ight-sided PVs in patient 2. Captured PV activation duringntrainment mapping demonstrated a P-wave morphologydentical to that during tachycardia. Furthermore, entrain-ent at the posterior LA demonstrated that atrial myocar-
ium was also part of the reentrant circuit (Figure 3). On theasis of the entrainment, both tachycardias were diagnoseds macroreentrant tachycardia with a tachycardia isthmusithin the LCPV in patient 1 and in the right PVs in patient. A single irrigated RF application was delivered at the exitite with the earliest atrial activation and resulted in tachy-ardia termination in both patients. Recovered PV conduc-ion with the same PV activation sequence was shownuring tachycardia and SR after tachycardia termination.apping during SR revealed that one remaining conduction
ap was located at the entrance with the latest atrial activa-ion during tachycardia and was closed by one to tworrigated RF applications during SR.
ocal pattern during 3D mappingn the six patients with a focal pattern (Figure 4), the earliesttrial activation was located in the LA near the right-sidedV ostia in five patients and near the left-sided PV ostia inne patient during tachycardia. In the six patients, the localtrial electrogram at the site with earliest atrial activationresented as a low amplitude with fragmented component in
our patients and with double potentials in two patients.hese findings indicated that the site with the earliest atrialctivation was located in the previous circular lesions. Thearliest atrial activation was located in the roof of therevious right circular lesions in four patients, in the pos-erosuperior part of the right circular lesions in one patient,nd in the posterosuperior part of the previous left circularesions in one patient. The mean mapped CL of the tachy-ardia was 144 � 39 ms, which was 49% of the mean TCLf 294 � 18 ms (range 265–320 ms). Entrainment mappingithin the PVs and in the LA confirmed that both the PVyocardium and the LA participated in the tachycardia
ircuit. Furthermore, captured PV activation during entrain-ent demonstrated P-wave morphology identical to that
uring tachycardia. In three patients, irrigated RF applica-ions were delivered at the site with earliest atrial activation,hich indicated the exit of the LA-PV macroreentrant
achycardia. A single RF application successfully termi- t
ated the tachycardia in these three patients (Figure 4B). Inhe remaining three patients, irrigated RF applications wereelivered at the entrance of the macroreentrant tachycardiaharacterized by the shortest LA-PV activation time (Figure). The tachycardia was also terminated with a single irri-ated RF application (Figure 6).
After the tachycardia termination, two Lasso cathetersithin the ipsilateral PV showed a discrete PV electrogram
n all six patients during SR. In the three patients withblation at the tachycardia exit, the PV activation was iden-ical during tachycardia and during SR (Figure 4B), whereasn the other three patients with ablation at the tachycardiantrance (Figure 5), the PV activation during SR was dif-erent from that during tachycardia (Figure 6). Mappinguring SR demonstrated the second conduction gaps locatedn the previous circular lesions around these PVs, whichere successfully abolished with one to four RF applica-
Figure 1 A: The 3D reconstructionof the LA in the postanterior (PA)view in patient 1 is shown. The PVostium is tagged in white. The activa-tion propagates from the posterior re-gion of the left PV to the LA and backto the anterior region of the left PV ina figure-of-8. The green dots indicatethe site with a PPI identical to that oftachycardia. The site with a brown dotlocated in the left posterior-inferior re-gion along the PV ostium indicates theregion of tachycardia termination, andanother brown dot in the anterior-su-perior region of PV indicates isolationof the right PVs. B: The 3D recon-struction of the LA in the right anterioroblique (RAO; left panel) and rightlateral (RL; right panel) view in pa-tient 2 is shown. The activation prop-agates from the superior region of theright PV to the LA and returns to theposterior-inferior region of the PV.The site with a brown dot located inthe right anterior-superior region alongthe PV ostium indicates the ablationregion with tachycardia termination,and another brown dot in the posterior-inferior region of PV indicates the iso-lation of the right PVs.
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47Satomi et al LA-PV Macroreentrant Tachycardia after PV Isolation
ther datahe tachycardia reentrant circuit in all eight patients isisplayed in Figure 7, which is based on the mapping andblation data. In addition, the locations of two conductionaps and the distance between the two gaps (35 � 4 mm;ange 28–40 mm) are also shown in Figure 7. After thesolation of the tachycardia-involved PVs, recovered PV
igure 2 Tracings are surface ECGeads and intracardiac recordings fromn ablation catheter (Mp) inside theV and diagnostic catheters inside theuperior and inferior branches of theCPV (LSPV, LIPV) and CS in pa-
ient 1. Asterisks indicate PV poten-ials, and arrows indicate LA poten-ial. Note that pacing inside the PVenerates the same P-wave morphol-gy as the tachycardia and that the PPIs almost equal to the TCL.
onduction was also found in the contralateral PVs in sevenut of the eight patients. All conduction gaps were success-ully closed. After isolation of all PVs, no tachycardia wasnduced in any patients.
The mean fluoroscopic and procedure times were 24 � 9inutes and 168 � 51 minutes, respectively. No complica-
ions were observed during or after the procedures. During
Figure 3 Tracings are surface ECGleads and intracardiac recordings froman ablation catheter (Mp) at the poste-rior wall of the LA and a diagnosticcatheter inside the left superior branchof LCPV (LSPV), CS, and His region(His) in patient 1. Note that pacing atthe LA posterior wall generates thesame P-wave morphology and activa-tion sequence as the tachycardia andthat the PPI is almost equal to theTCL.
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48 Heart Rhythm, Vol 5, No 1, January 2008
median of 12 � 9 months (range 3–27 months) of follow-p, all patients were free of AT. However, paroxysmal AFnfrequently recurred in patient 7 with persistent AF beforeV isolation.
iscussionhe present study describes LA-PV macroreentrant tachy-ardia as a novel type of man-made reentrant tachycardiafter circumferential PV isolation and the electrophysiolog-cal characteristics and catheter ablation for this tachycardia.
acroreentrant AT after PV isolationegular AT can develop late after PV isolation. The inci-ence of these tachycardias was reported to be 4%–40%
fter PV isolation.7,14,15 The incidence depends on the type c
f AF, LA diameter, and ablation technique. These ATs areostly due to a macroreentrant mechanism, which uses
egions of incomplete or recovered ablation lesions or ana-omical isthmuses to sustain the arrhythmia.15 Mapping andblation have demonstrated that the most common macro-eentrant AT after PV isolation is AT around the mitralnnulus.7 In the present study, these tachycardias developedithin 1 month after the initial circumferential PV isolation,hich is similar to previous findings that these macroreen-
rant ATs generally develop 1–2 months after ablation.owever, their reentrant circuit included myocardiumithin the PV and the LA via two conduction gaps in therevious circular lesions, which were widely separated by aean distance of 35 mm. On the basis of these findings, we
Figure 4 A: A 3D reconstructionof the LA in the anterior-posterior(AP) and posterior-anterior (PA)view in patient 4 is shown. The right-sided PV ostium is tagged in white.The activation sequence shows thepropagation from the anterior-supe-rior region of the right PV to the LA(as focal activity). The site with abrown dot located in the right ante-rior-superior region along the PV os-tium indicates the ablation region oftachycardia termination, and anotherbrown dot in the inferior region ofthe PV indicates isolation of the rightPVs. B: Tracings are surface ECGleads I, II, V1, and intracardiac re-cordings from an ablation catheter(Mp) at a superior-anterior site of theLA and diagnostic catheters insidethe right common PV (RCPV) andCS at the termination of tachycardiain patient 4. Asterisks indicate PVpotential. Note that (1) ablation per-formed at the anterior-superior re-gion of right PV leads to terminationof tachycardia and that (2) the lastbeat has the signal of LA and PV inRCPV during SR just after termina-tion of tachycardia, indicating thatthe PV still conducted with signifi-cant delay (arrow). The sequence ofRCPV activation during SR exhib-ited by the Lasso catheter was iden-tical to that of the tachycardia.
oncluded that these tachycardias were macroreentrant
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49Satomi et al LA-PV Macroreentrant Tachycardia after PV Isolation
achycardia and different from the previous clinical reports.nterestingly, Merino16 has recently hypothesized the pos-ibility of this type of reentrant circuit after AF ablation, buto far it has not been clinically reported in the literature. Tohe best of our knowledge, this is the first description ofA-PV macroreentrant tachycardia that presented as a cir-uit with a critical isthmus within the PV and LA myocar-ium via two conduction gaps in the previous circular le-ions.
lectrophysiological characteristics of LA-PVacroreentrant tachycardia
n the present study, all patients presented with a regularachycardia with a constant CL. Three-dimensional electro-natomical mapping demonstrated a macroreentrant patternn two patients and a focal pattern in six patients. In twoatients with macroreentrant pattern, activation and entrain-ent mapping clearly demonstrated that the tachycardia
resented as dual-loop reentry that propagated through theV with a critical isthmus located between two conductionaps in the previous circular lesions. Mapping demonstratedhat one conduction gap was the entrance and the other washe exit during tachycardia. Interestingly, in the other sixatients with a focal pattern on 3D mapping, entrainmentapping at the LA and inside the PV exhibited an identical
igure 5 The mapping catheter positions at the ablation site in the rightn the left panel. In the right panel, tracings are surface ECG leads I, II,atheters inside the right superior PV (RSPV), right inferior PV (RIPV), ahat the LA potential recorded by an ablation catheter at the posterior-suctivation of PV.
trial activation sequence and P-wave morphology. This d
mportant information confirmed that the tachycardia circuitnvolved both the PV and the LA. These findings were veryimilar to a previous report that a focal mechanism wasesponsible for recurrent AT after segmental or circumfer-ntial PV isolation. On the basis of the 3D mapping only,his tachycardia could potentially be misdiagnosed as focalT without entrainment guided by Lasso catheter within
he PV.
iagnosis and ablation of LA-PV macroreentrantachycardia after AF ablationn the basis of our results of mapping and ablation, Figure 8
hows the underlying mechanisms of the tachycardia. Weropose the following criteria for diagnosis of the LA-PVacroreentrant tachycardia: (1) recovered PV conductionith one-to-one LA-PV or PV-LA conduction during tachy-
ardia; (2) identification of sites with perfect entrainmentithin the PVs and the LA near the involved PVs; (3)
ntrainment within the PVs with identical P-wave morphol-gy as during tachycardia; (4) identification of two conduc-ion gaps in the previous circular lesions: one conductionap presented as the entrance with earliest PV activationnd one presented as the exit with earliest atrial activation;5) termination of the tachycardia by RF delivery at eitherhe entrance or the exit site. The PV activation sequence
t anterior oblique fluoroscopic views (RAO, LAO) in patient 8 are shownd intracardiac recordings from an ablation catheter (Mp) and diagnostict the termination of tachycardia. Asterisks indicate the PV potential. Noteegion demonstrated double potential during tachycardia with the earliest
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50 Heart Rhythm, Vol 5, No 1, January 2008
as delivered at the exit site. On the other hand, the PVctivation sequence was different between tachycardia andR when RF energy was delivered at the entrance site.
tudy limitationhere are two limitations to this study: (1) the incidence of
his tachycardia is unknown from our study due to a parox-smal pattern of this tachycardia in some patients. Also, it
igure 7 Schematic diagram ofonduction gaps around the ispilateralVs. Black contours indicate the cir-ular lesions. Black arrows indicatehe location of conduction gaps as thentrance and exit to the PV.
as very difficult to evaluate whether there was a recur-ence of AF only or recurrence of both arrhythmias after PVsolation in patients with only documented recurrent AFecause tachycardia induction was not performed in patientsith recovered PV conduction during the repeated proce-ure. (2) In our practice, the PV was generally not mappedo better visualize the reconstructed LA anatomy and abla-
Figure 6 The tracings are surfaceECG leads I, II, V1, and intracardiacrecordings from a ablation catheter(Mp) and diagnostic catheters insidethe right superior PV (RSPV), rightinferior PV (RIPV), and CS at the ter-mination of tachycardia. Note that (1)the tachycardia terminated by the ap-plication at the posterior-superior re-gion of the RSPV; (2) the tachycardiaterminated just after the LA potentialwith the conduction block from LA toPV by RF application (arrow); thisshows that the ablation catheter waslocated at the entrance site of PV; and(3) PV conduction with significant de-lay (asterisk) was still present aftertermination of the tachycardia. Theearliest activation site of PV is RSPV1-2 during tachycardia. After the ter-mination of tachycardia, the earliestsite of PV activation moved fromRSPV 1-2 to RIPV 3-4. This phenom-enon indicates different entrance sitesto the right PV (assumed conductiongaps in previous circular lesions) dur-ing tachycardia and SR.
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51Satomi et al LA-PV Macroreentrant Tachycardia after PV Isolation
ion catheter13; this resulted in a focal pattern on the 3Dapping in six out of eight patients with LA-PV macro-
eentrant tachycardia because the slow conduction betweenhe two conduction gaps was not mapped. However, usinghe entrainment technique from the LA and the PVs, theA-PV macroreentrant tachycardia with an isthmus through
wo widely separated conduction gaps in the previous cir-ular lesions could be shown.
onclusions
he LA-PV macroreentrant tachycardia can occur after cir-umferential PV isolation and presents as a novel type ofan-made macroreentrant tachycardia, which involves theA, PV, and two conduction gaps in the previous circular
esions. Entrainment mapping within the LA and the PV isecessary to make the diagnosis.
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S, Le Mouroux A, Le Metayer P, Clementy J. Spontaneous initiation of atrialfibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med1998;339:659–666.
2. Haissaguerre M, Shah DC, Jais P, Hocini M, Yamane T, Deisenhofer I, ChauvinM, Garrigue S, Clementy J. Electrophysiological breakthroughs from the leftatrium to the pulmonary veins. Circulation 2000;102:2463–2465.
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igure 8 The scheme of the activa-ion around the PVs during the tachy-ardia and SR after termination of theachycardia. The reentrant circuit is as-umed to enter the PV at one site andxit at another site, thus including bothhe PV and LA, which are connectedy two conduction gaps between theV and LA. This tachycardia can be
erminated by RF delivery at either thentrance or the exit site. The PV acti-ation sequence during tachycardiand SR was the same when RF energyas delivered at the exit site (A).owever, the PV activation sequenceas different between tachycardia andR when RF energy was delivered at
he entrance site (B).
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