J Cardiol 2007 Jul; 50（1）: 1 – 10

Role of a Novel Conduction Pattern
Around the Coronary Sinus in
Cavotricuspid Isthmus Dependent
Right Atrial Flutter
Yoshio YAMAGUCHI, MD
Hiroichi TSUGAWA, MD
Nakaba FUJIOKA, MD
Kenichi KASENO, MD
Michihiko KITAYAMA, MD
Kouji KAJINAMI, MD, FJCC
Abstract ─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────
Objectives. We tested our hypothesis that, in atrial flutter（AFL）
dependent on the cavotricuspid isthmus（CTI）, lower loop reentry is the common pathway route at the coronary sinus posterior site, and thus, dual
loop reentry is a common circular pattern.
Methods and Results. We studied 25 patients with CTI-dependent AFL, 16 with chronic counterclockwise atrial flutter（CCW-AFL）and 9 with clockwise atrial flutter（CW-AFL）and determined the precise
reentry circuitry, especially for conduction patterns around the coronary sinus orifice, using electroanatomical mapping. We measured post pacing interval and tachycardia cycle length during entrainment fromsites within the flutter circuit. The coronary sinus anterior pacing site was within the AFL circuit in 16 of
the 25 CCW-AFL patients, and in 6 of the 9 CW-AFL patients. Both the coronary sinus anterior and posterior sites were within the AFL circuit in 8 of 16 CCW-AFL and 8 of the 9 CW-AFL patients. Results of 3dimensional activation mapping suggest that all of these patients have a dual loop reentry circuit, and that
coronary sinus posterior conduction broke through the eustachian valve/ridge.
Conclusions. Coronary sinus posterior conduction consisted of the flutter circuit and appeared to be critical for maintaining AFL.
──────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────J Cardiol 2007 Jul; 50（1）: 1−10Key Words■ Atrial flutter■ Electrophysiology

INTRODUCTION
Atrial flutter（ AFL）, most often defined as
macroreentrant tachycardia, is maintained by thecircular movement of the activation wave front
around the tricuspid annulus.1,2）Dual loop reentry（DLR）uses the cavotricuspid isthmus（ CTI）andcompletes two broad competing loops with a common pathway in about 50% of cases of typical rightatrial（RA）counterclockwise flutter（CCW-AFL）.3）■ Reentry

In this pathway, the anterior loop is around the tricuspid annulus and the posterior loop is around theinferior vena cava（IVC）or the posterior block line.
This finding suggests that AFL is treatable by linear
ablation of the CTI.
A recent anatomical study 4）showed that theeustachian valve/ridge（EVR）had a muscular layer
running from the RA septal wall to the CTI, theEVR was not fused to the thebesian valve, and asmall flat area remained between the EVR and the──────────────────────────────────────────────
金沢医科大学 循環器内科 : 〒 920−0293 石川県河北郡内灘町大学 1−1
Department of Cardiology, Kanazawa Medical University School of Medicine, Ishikawa
Address for correspondence: YAMAGUCHI Y, MD, Department of Cardiology, Kanazawa Medical University School of Medicine,
Daigaku 1−1, Uchinada-machi, Kahoku-gun, Ishikawa 920−0293 ; E-mail : yoshio-y@kanazawa-med.ac.jp
Manuscript received February 20, 2007 ; revised March 24, 2007 ; accepted March 30, 2007

1

2

Yamaguchi, Tsugawa, Fujioka et al

coronary sinus（CS）orifice in 44% of necropsied
normal human hearts（ n ＝ 80）. Therefore, mostcases of RA clockwise flutter（CW-AFL）are supported by a reentrant circuit around the IVC or afigure-of-eight DLR involving both the IVC and tricuspid annulus. 3,5−8）Although DLR may circle
both the IVC and tricuspid annulus, the potential
role of conduction around the CS orifice in maintaining AFL remains unclear.
Based on these considerations, we hypothesizedthat lower loop reentry was the common pathway
route at the CS posterior site in CTI-dependent
AFL,5,7）so that DLR had a common circular pattern. To test this hypothesis, we studied patientswith CTI-dependent AFL, and investigated the precise reentry circuitry, especially for conduction patterns around the CS orifice, using high-density 3dimensional（3D）mapping.9）
SUBJECTS AND METHODS
Study population
The subjects were 25 patients who underwent
mapping and ablation of CTI-dependent chronic
CCW-AFL（n ＝ 16）and CW-AFL（n ＝ 9）. All
patients had suffered from tachyarrhythmic eventsfor 33.5 ± 55.7 months（ mean ± SD, range 3 to180）, had a history of more than one hospitalization, and were unresponsive to a mean 2.4 ± 1.2
antiarrhythmic drugs（range 1 to 4）. To ensure visualization of F-waves, inverted F-waves were documented for leads Ⅱ, Ⅲ, and a ⅤF in 16 patientswith CCW-AFL, and positive or isoelectric Fwaves were observed in inferior leads in another 9
patients with CW-AFL. All antiarrhythmic medications were discontinued for at least 5 half-lives
before the procedure. All patients gave written
informed consent and the research protocol wasapproved by the ethics committee of Kanazawa
Medical University.
Electrophysiological study
In all patients, venous accesses were obtainedwith 7F and 8F sheaths in the right internal jugularvein and femoral veins. A 20-pole catheter（HaloXP20, Biosense-Webster Inc.）was placed counterclockwise along the tricuspid annulus with the distal tip at the lateral entrance point to the isthmus
between the CTI and IVC and the proximal electrode at the high interatrial septum. A 10-pole
catheter was positioned in the CS（Response CSL,
St. Jude Medical Inc.）with electrode spacing 2-8-

2 mm ; and a built-in 0.025 inch lumen with theproximal, bipolar electrode positioned 1 cm distal
to the CS orifice as determined in the left anterior
oblique（LAO）projection. A quadripolar catheter
was positioned to record His bundle electrocardiography. Atrial activation was also recorded at theanterior septum and CS. The 12-lead surface electrocardiography and intracardiac signals wererecorded, and programmed stimulation was delivered through a programmable stimulator（ EP
WorkMate, EP MedSystems Inc.）.
Activation and voltage mapping were performed
in 16 of the 25 patients with 3D electroanatomical
mapping（ Biosense-Webster Inc.）. RA mapping
points totaled 194 ± 56
（range 138 to 254 points）.
A 7F navi-star catheter（4-mm tip, 2 bipolar electrode pairs, interelectrode distance 2 mm ; Biosense-Webster Inc.）was used as the mapping/ablation catheter. The catheter was dragged over theendocardial surface to record electrograms at different sites. Complete RA endocardial maps wereobtained for all patients to ensure reconstruction ofa detailed activation 3D map.7−9）This catheter was
also used for entrainment pacing at the RA.7,10,11）
Intracardiac signals were filtered with low and highcutoff frequencies of 30 and 500 Hz, with a sampling frequency of 〜 1,000 Hz.
The cycle length of the AFL was measured as thetachycardia cycle length（ TCL）and entrainment
was done at pacing cycle lengths 10, 20, and 30
msec shorter than the TCL.5,10）Pacing was done attwice the local capture threshold determined during
pacing at a faster rate than the TCL. Entrainment
pacing used overdrive pacing at multiple atrial sites
in all patients（Fig. 1）. The postpacing interval（PPI）
was defined as the time interval from the last pacing artifact to the first local electrogram recorded at
the pacing site.3,5,10）The pacing site was considered
to be within the reentrant circuit when the difference between the PPI and the TCL was within 30
msec.5, 6）
Anatomical findings
An angiography series of the coronary artery,
RA, and CS was obtained for all patients. The CTI
was localized at roughly the 6 o clock position in
the LAO projection. The EVR was attached medially to the orifice of the IVC along the CS orifice.
This site was at 4 : 00 to 6 : 30 in the LAO projection. The CS orifice was located at the junction of
the great cardiac vein and the origin of the CS, theJ Cardiol 2007 Jul; 50（1）: 1 – 10

Coronary Sinus Conduction in Isthmus-Dependent Atrial Flutter

3

RESULTS
Patient profiles
The baseline characteristics of the study group of
25 patients were not significantly different（sex,age, underlying heart disease, used antiarrhythmic
drugs, cardiothoracic ratio, flutter cycle length）,
excluding the conduction pattern around the coronary sinus（Tables 1, 2）.
Fifteen of the 25 subjects had structurally normal
hearts, of whom 6 had coronary artery disease, and4 cardiomyopathy. All patients who underwent
entrainment pacing and radiofrequency energy
were determined to have AFL originating from theCTI, so ablation was successful in all patients.1,2,12）Fig. 1 Entrainment pace mapping points
CS-3 ＝ coronary sinus（CS）orifice at 3 : 00 in the rightanterior oblique projection ; CS-6 ＝ coronary sinus orifice at 6 : 00 in the right anterior oblique projection ;CS-9 ＝ coronary sinus orifice at 9 : 00 in the right anterior oblique projection ; iTA ＝ cavotricuspid isthmus（CTI）near the tricuspid annulus ; iCS ＝ cavotricuspid
isthmus near the coronary sinus orifice ; iIVC ＝
cavotricuspid isthmus near the inferior vena cava ;RAS ＝ right atrium（RA）lower septal site ; RAL ＝
right atrium lower lateral site ; RAA ＝ right atrium
lower anterior site ; SRA ＝ superior right atrium ;TA12 ＝ superior tricuspid annulus ; IVC ＝ inferior
vena cava ; SVC ＝ superior vena cava ; TA ＝ tricuspid
annulus.

thebesian valve, and the EVR. The site was at 4 :00 to 5 : 00 in the right anterior oblique（RAO）
projection. The CS-3 was at 3 : 00 for the CS orifice in
the RAO projection（Fig. 1）. The CS-9 was at 9 :00 for the CS orifice in the RAO projection. The
anatomical structure and catheter positioning were
reinforced by 3D electroanatomical mapping information and biplane mobile fluoroscopy.
Coronary sinus pacing site
The pacing catheter was placed into the CS andpulled outside the CS orifice. The CS-3 pacing site
was positioned between CS-3 and tricuspid annulus, and similarly, the CS-9 pacing site was locatedbetween CS-9 and IVC close to the EVR（Fig. 1）.
Statistical analysis
All continuous variables are expressed asmean ± SD. Statistical comparisons within thegroup were made using a paired t-test. p ＜ 0.05
was considered statistically significant.
J Cardiol 2007 Jul; 50（1）: 1 – 10

PPI-TCL for coronary sinus orificeDuring entrainment from sites（Fig. 1）within the
flutter circuit, the mean PPI-TCL interval was ＜− 30
msec for all pacing rates regardless of the AFL
direction. The CS orifice pacing site was within the
AFL circuit in all patients（Fig. 2）. The CS-3 waswithin the AFL circuit in 19 of 25 patients（76% :mean PPI-TCL ＝ 16.2 msec）and outside the circuitin 6 patients（ mean PPI-TCL ＝ 53.2 msec, p ＜0.05）. The CS-9 was within the AFL circuit in 16
of 25 patients（64% : mean PPI-TCL ＝ 15.3 msec）,
outside the AFL circuit in 9 patients（mean PPITCL ＝ 52.8 msec, p ＜ 0.05）, and within the AFL
circuit for both the CS anterior and posterior in 10
of 25 patients（40%）.
CCW-AFL was confirmed in 16 of 25 patients.
The CS-3 pacing site was within the circuit in 13
patients（81% : mean PPI-TCL ＝ 17.3 msec）and
outside the AFL circuit in 3 patients（mean PPITCL ＝ 69.7 msec, p ＜ 0.05）. CW-AFL was confirmed in 9 of 25 patients. The CS-3 pacing site waswithin the AFL circuit in 6 of 9 patients（67% :mean PPI-TCL ＝ 13.4 msec）, and outside the circuit in 3 patients（mean PPI-TCL ＝ 36.7 msec, p ＝0.15）. Pacing sites were within the AFL circuit
both for the CS-3 site and CS-9 sites in 9 of 16
CCW-AFL patients（56%）and in 8 of 9 CW-AFL
patients（89%）（Figs. 3, 4）.
Macroreentrant circuits in CCW-AFL and CWAFL
Entrainment mapping results indicated that the
RA lower portion of the quarterly divisions（anterior, lateral, septal, and CTI near IVC）, tricuspid annulus superior, and RA superior（Fig. 1）were4

Yamaguchi, Tsugawa, Fujioka et al

Table 1 Patient characteristics in CS-3 and CS-9 groups
CS-3

CS-9

p value＊

CS-3 and -9

p value＊＊

n

9（36）

6（24）

NS

10（40）

NS

Male

8（89）

5（83）

NS

8（80）

NS

Age（yr）

73±8

61±19

NS

67±17

NS

Hypertension
Ischemic heart disease

6（67）

4（67）

NS

4（40）

NS

3（33）

1（17）

NS

4（40）

NS

Cardiomyopathy

1（11）

0

NS

3（30）

NS

Ia

5（56）

4（67）

NS

6（60）

NS

Ic

3（33）

2（33）

NS

2（2）

NS

CTR
（%）

51±4

50±4

NS

51±4

NS

CCW

8（89）

3（50）

NS

5（50）

NS

253±33252−42NS

254±46

NS

iTA

23±20

25±13

NS

21±20

NS

iCS

25±20

18±10

NS

14±16

NS

iIVC

48±17

7±4

0.028

17±13

0.008

CS-3

22± 9

53±21

0.027

9± 6

0.021

CS-9

53±11

16±9

0.028

16±10

0.008

FCL（msec）
PPI-FCL（msec）

Continuous values are mean±SD.（ ）: %.
CS-3 vs CS-9, ＊＊CS-3 vs CS-3 and -9.
Ia＝Vaughan-Williams Ia group drug ; Ic＝Vaughan-Williams Ic group ; CTR＝cardiothoracic ratio on chest
radiography ; CCW＝counterclockwise ; FCL＝flutter cycle length ; PPI＝post pacing interval. Other
abbreviations as in Fig. 1.
＊

Table 2 Patient characteristics in CW-AFL and CCWAFL groups
CW-AFL（n＝9）

CCW-AFL（n＝16）

p value

6（67）

15（94）NS

Age（yr）

65±17

69±17

NS

Hypertension

6（67）

8（50）

NS

Ischemic heart disease

4（44）

4（25）

NS

Cardiomyopathy

2（22）

2（13）

NS

Ia

5（56）

10（63）

NS

Ic

3（33）

4（25）

NS

CTR
（%）

51±3

51±5

NS

FCL
（msec）

257±45251±37

NS

iTA

21±12

24±21

NS

iCS

21±16

18±18

NS

iIVC

16±14

31±24

0.032

CS-3

20±14

27±24

NS

CS-9

18±13

35±22

0.007

Male

PPI-FCL（msec）

Continuous values are mean±SD.（ ）: %.
CW＝clockwise ; AFL＝atrial flutter. Other abbreviations as inFig. 1, Table 1.

part of the reentrant circuit because the PPI-TCL
was within 30 msec of the TCL. The tricuspid
annulus superior site at roughly 11 : 00 to 12 : 00 in
the LAO projection was outside the AFL circuit in
6 of 25 patients（mean PPI-TCL ＝ 42 msec）. The
superior RA site was within the AFL circuit in 5
patients（mean PPI-TCL ＝ 16.2 msec）. Lower loop
reentry（LLR）,5,6）demonstrated in the posterior andseptal regions of the lower RA along the IVC, waswithin the AFL circuit in 17 patients. Only the LLR
circuit was within the AFL circuit in 3 patients, 1
with CCW-AFL and 2 with CW-AFL.
3D activation mapping in 10 of these 14 patients
showed identical revolution times around the IVC
and tricuspid annulus（Figs 3, 4）. Typical AFL witha single reentrant loop around the tricupid annulus
was confirmed in 6 patients, all of whom had
CCW-AFL. Activation wave fronts collided at the
septum where a substantial conduction delay was
noted（Fig. 5）at the CS-3 site in patients with CS
posterior conduction breakthrough and only LLR
circuit.
DISCUSSION
Our major finding was that most CTI-dependent
J Cardiol 2007 Jul; 50（1）: 1 – 10

Coronary Sinus Conduction in Isthmus-Dependent Atrial Flutter

5

Fig. 2 Post pacing interval-flutter cycle length（PPI-FCL）
Subjects were divided into three groups based on atrial flutter circuit patients at the coronary sinus orifice,CS-3 and CS-9 and cavotricuspid isthmus .
CS-3 ＜ 30 msec group : PPI-TCL ＜ 30 msec at both the CS-3 and near the tricuspid annulus sites.
CS-9 ＜ 30 msec group : PPI-TCL ＜ 30 msec at both the CS-9 and near the inferior vena cava sites.
CS-3 and -9 ＜ 30 msec group : PPI-TCL ＜ 30 msec at both CS-3 and CS-9.
Mean PPI-FCL from two points was compared, and p is shown. Values are numbers of cases or mean ±SD. Statistical comparisons within the group were made using a paired t-test. p ＜ 0.05 was considered statistically significant.
Abbreviations as in Fig. 1, Tables 1, 2.

AFL involved a reentrant circuit around the CS-9
site in both CCW-AFL and CW-AFL cases.
Entrainment pacing at the CS-9 site along the EVRor the posterior septum revealed that PPIs werecomparable to the TCL in 16 of 25 patients. CS-9
conduction traversed between the IVC and CS orifice in 13 of these 16 patients. 3D activation
sequence mapping showed an activation wave front
circulating around the IVC or the RA superior, withevidence of slow conduction in 6 of the 25 patients.
Activation wave fronts collided at the internal septum at the CS-3 site in patients with CS posterior
conduction breakthrough and only LLR circuit（Fig. 5）.
Conduction breakthrough the EVR in CTIdependent AFL
The musculature of the CS has been implicatedin a variety of arrhythmias, including those mediated by accessory pathways, and focal 13,14） andmacroreentrant atrial tachycardia.7,15）This musculature has a consistent but morphologically variable
left atrial CS myocardial connection 2,5,9,16,17）andJ Cardiol 2007 Jul; 50（1）: 1 – 10

RA of CTI in the tricuspid trabecular muscle. A
recent anatomical study4）reported that the EVR
had a small flat area remaining between the EVR
and CS orifice in 44% of necropsied normal humanhearts（n ＝ 80）. Our study provides the first evidence that almost all CTI-dependent AFL may beoccur through the CS posterior wall. In short, the
EVR and circuit pattern and both CCW and CW
did not differ in patients without prior atriotomy.
Recent studies suggested that conduction throughthe EVR was highly possible. 2,5,6,11,16,17）During
early conduction breakthrough in the lower RA, theactivation wave front collided in the high lateral RA
or the septum, and conduction through the CTI wasdemonstrated by activation sequence mapping or
3D electroanatomical mapping in 6 CCW-AFL
6）
patients（spontaneously in 3）
and in 11 of 12 CW11）
AFL patients. Analysis of 36 episodes of sustained atypical right AFL found LLR in 24（67%）,
13（54%）episodes had early breakthrough at thelower lateral tricuspid annulus, and 9（38%）
episodes showed multiple annular breaks.5）A pattern of posterior breakthrough from the EVR to the6

Yamaguchi, Tsugawa, Fujioka et al

A

B

Fig. 3 Representative case with counterclockwise atrial flutter（CCW-AFL）
A : In the 3-dimensional-activation map（center）, blue dots represent double potential and fragment electrograms. Red dots areradiofrequency points. Black dots and area are ＜ 0.1 mV. Reference electrograms were recorded within the coronary sinus.
Activation proceeded in a complete CCW loop from red to purple around the TA and IVC. Entrainment pace mapping sites, CTI（iTA and iIVC）, and coronary sinus orifices（CS-3 and CS-9）to measure PPI are shown by red arrows. Entrainment pacing fromthe iTA and iIVC revealed a PPI of 320 and 315 msec, which indicated that the iTA and iIVC are part of the reentrant circuit.
Similarly, entrainment pacing from CS-3 and CS-9 revealed PPI for both of 310 msec, indicating that CS-3 and CS-9 may bepart of the reentrant circuit. The iIVC electrogram sequence seems to be different from the other site of T1-2 and ABL-d. The
iIVC pacing site is slightly in the RA lower free wall direction, so the multielectrode catheter T1-2 and ABL-d are closer.
B : Entrainment pace mapping sites, superior TA（TA-12）and around IVC, are shown by red arrows. Entrainment pacing from
TA-12, RA lower free wall, lower posterior wall, and lower septal wall revealed PPI of 310, 320, 320, and 310 msec, respectively, which indicates that both the superior TA and around the IVC are part of the reentrant circuit. These results may suggest that
activation from the CTI to CS-3 and CS-9 traversed the eustachian ridge/valve, and circulated around the TA and lower RA.
ABL-d, ABL-p ＝ radiofrequency ablation catheter distal and proximal bipolar electrogram ; CS-d, CS-p ＝ coronary sinus distaland proximal electrogram ; HBE ＝ His bundle electrogram ; T17-18, T13-14, T9-10, T5-6, T1-2 ＝ bipolar electrograms recorded from decapolar catheter placed around TA. Other abbreviations as in Fig. 1, Tables 1, 2.

Coronary Sinus Conduction in Isthmus-Dependent Atrial Flutter

A

B

Fig. 4 Representative case with clockwise atrial flutter（CW-AFL）
A : In the 3-dimensional-activation map（center）, blue dots represent double potentials and fragments. Red
dots are radiofrequency ablation points. Activation proceeded in a complete CW loop from red to purple
around the TA and IVC. Entrainment pace mapping sites to measure the PPI are shown by red arrows.
Entrainment pacing from the iTA and iIVC, CS-3, CS-9 revealed PPI of 240, 240, 240, and 245 msec,
respectively, which may suggest that all of the CTI（iTA and iIVC）, CS-3, and CS-9 are part of the reentrant circuit.
B : Entrainment pacing from the TA-12, RA lower free wall, and lower septal wall revealed PPI of 230,
245, and 250 msec, respectively, which also indicates that all of the superior TA, RA lower free wall, andlower septal wall were part of the reentrant circuit. These mapping results consisted of the conduction fromCS-3 and CS-9 to CTI.
Abbreviations as in Figs. 1, 3, Tables 1, 2.

J Cardiol 2007 Jul; 50（1）: 1 – 107

8

Yamaguchi, Tsugawa, Fujioka et al

Fig. 5 Lower loop reentry in clockwise atrial flutter in left lateral view
Left : The RA posterior wall and septal wall（included the coronary sinus area）are forward sites. 3-dimensional electroanatomical map of baseline in lower loop reentry（LLR）. Blue dots : double potential. Yellow
dots : fractionated potential. Red dots : ablation point. Activation proceeds in a complete CW loop from red
to purple around the IVC. The CTI is activated from posteromedial to anterolateral as in CW-AFL.
Right : CW-AFL propagation during tachycardia showed the activation wave front around the IVC. The redzone indicates propagation of the activation wave front and the blue zone regions recovering from previous
excitation. Green arrows represent the earliest wave front of CW-AFL around the coronary sinus orifice. In
this map, the collision of wave fronts is shown at mid-septum（white bar）in the lower septum, so the circuit
around the tricuspid annulus blocked conduction. Separate from this conduction, another conduction circled
around IVC and formed the second reentrant circuit, LLR. In this CW-AFL case, LLR consisted of conduction that broke through the eustachian ridge/valve.
Abbreviations as in Figs. 1, 3, Tables 1, 2.

septum was observed in 4（ 14%）of 28 patients.
None of these studies conducted high-density
entrainment mapping to determine the CS orifice
position or included atypical conduction pattern
CCW-AFL patients. In common AFL, the LLR circuit is considered to be the flutter activation front,
which circles along the IVC, through the CS-3 site,and curves in the mid RA septum.3,6,11）In atypical
AFL patients, the lower loop activation wavefront
could break EVR directly. 5,11）In our study, thelower loop activation front was defined through theCS-9 or CS-3, and formed a LLR circuit in both
CW-AFL and CCW-AFL patients.
Reentry circuits in CTI-dependent AFL
Postoperative macroreentrant AFL includes DLR
and figure-of-eight loops. These AFLs circulate
around postoperative scars, which could slow theconduction zone formed in injured myocardialmuscles adjacent to operative scars or anatomicalbarriers.7,8）DLR was defined in 6 of 12 CCW-AFL
patients who had no cardiotomy. 3）Entrainment
mapping was conducted to evaluate atrial electro-

grams from the tricuspid annulus and the posterior
RA with paradoxical delayed capture and foundthat the posterior line of the block did not extend to
the superior vena cava. DLR in 4 of 12 CW-AFL
patients after applying 3D anatomical mapping
found that 4 tachycardia episodes involved a CW
loop around the tricuspid annulus and showed reentrant tachycardia around the IVC, with the activation wave front propagating from the septal to thelateral aspect of the CTI.11）
Study limitations
Our study has certain limitations. Our analysis of
PPI was limited to sites at which entrainment pacing had a measurable effect on RA conduction.
Pacing of the entire EVR would have made it very
difficult to compare electrograms at the same
recording site in all patients. Application of intracardiac echocardiography, a technique to visualize
various intra-atrial structures that are not visualizedon fluoroscopy, may allow precise localization of
the intracardiac catheters relative to these anatomic
structures.18）Some of the flutter involved was relaJ Cardiol 2007 Jul; 50（1）: 1 – 10

Coronary Sinus Conduction in Isthmus-Dependent Atrial Flutter

tively slow, suggesting that an antiarrhythmic drug
effect may have persisted.
We did not determine the potential influence ofthe crista terminalis, an elongated muscular prominence between the SVC and IVC in the posterolateral wall of the RA.3,18）The crista terminalis andsinus venosa were demonstrated to be the line of
the conduction block during typical AFL. However,most crista terminalis conduction gaps using noncontact mapping are functional and only appeared
when upper loop reentry was done to evaluate
transverse conduction across the crista terminalis
during typical AFL, and pacing from the CS and
low anteriolateral RA found no transverse crista
terminalis gap conduction during typical AFL.19）
We evaluated only the crista terminalis lower position（RA lower lateral position）and superior crista
terminalis（RA superior position）
using entrainment
pace mapping, so we did not evaluate the crista terminalis gap and CS pacing or posterior block line
in detail.
The present study performed entrainment pacing
outside around CS orifice, IVC, superior RA andobtained PPI-FCL within 30 msec in almost all
CTI-dependent AFL patients. However, we did not
use the multi-electrode catheter location for the RA
要

posterior wall 3,11）and simultaneously measured
paradoxical delayed capture of both tricuspid annulus and IVC or superior RA site. Therefore, to confirm dual loop reentry circuit, this issue should betaken into consideration in future studies. In addition, the validity of our criteria for the position on
the AFL circuit, PPI-FCL of shorter than 30 msec,
should be confirmed by future studies.
CONCLUSIONS
We have demonstrated that almost all flutter
patients had a CS anatomical barrier, although CS-3
and CS-9 muscular conductions were separated by
the CTI trabecular muscle layer. CS-9 conduction
may extend from the lower RA to the anterior RA
through the CTI, and consist of a flutter circuit,which may be critical for maintaining AFL. Most
AFL was propagated in a broad-band flutter wave
front pattern from the RA post-septal wall to the
CTI or vice versa, through CS orifice conduction,
so radiofrequency ablation should be performed
closely along the complete bidirectional block linein the CTI. Therefore, in an incomplete isthmus
block line or recurrence of CTI-dependent AFL,
analysis of CS orifice conduction may be useful for
obtaining a complete bidirectional block line.
約

三尖弁輪−下大静脈間峡部依存性心房粗動における冠状静脈洞周囲伝導の役割

目

山口

善央

津川

博一

藤 岡

央

野

健一

北山

道彦

梶波

康二

的 : 三尖弁輪−下大静脈間峡部依存性心房粗動において，冠状静脈洞後壁を伝播する旋回路が存在し，それが lower loop reentry を形成し，それによって dual loop reentry が形成されるのではな
いかと仮定した．
方

法 : 対象は慢性心房粗動連続 25 例の通常型心房粗動（CCW-AFL）16 例と非通常型心房粗動（CW-AFL）9 例である．冠状静脈洞周囲で entrainment pace mapping を施行し，post pacing interval（PPI）と tachycardia cycle length（TCL）を計測し，旋回路が冠状静脈洞の三尖弁輪側か下大静脈側のどちらを旋回するのかを検討した．また，併せて electroanatomical mapping を施行した．
結

果 : PPI-TCL の結果からは，CCW-AFL16 例中 13 例と CW-AFL9 例中 6 例が冠状静脈洞の三尖

弁輪側を通過すると考えられた．さらに CCW-AFL8 例と CW-AFL8 例が冠状静脈洞の三尖弁輪側も下大静脈側も同様に通過すると考えられた．Electroanatomical mapping の結果では，それらは dual
loop reentry を形成している可能性が示された．
結論: 冠状静脈洞下大静脈側を伝播する心房粗動の興奮波は，三尖弁輪−下大静脈間峡部依存性心房粗動の成立・維持に関連しているものと推察された．

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10Yamaguchi, Tsugawa, Fujioka et al

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