-
--..----__-.-I_-__-
.- . - ___.. ----_-__
ELEC’TROH 1YSIOLOGY
__._.
Conduction Mock in the Inferior Vena Caval-Tricuspid Valve
Isthmus: Association With Outcome of Radiofrequency Ablation of
Type I Atria1 Flutter
DAVID
SCHWARTZMAN.
CHARLES
D. GO-I-l-LIEB.
mmcIs
E. MARCHLINSKL
MD, FACC. DAVID
MD.
J. CALLANS.
FACC. STEPHEN
M. DILLON.
MD, FACC.
PIID.
COLIN
MOVSOWITZ.
MD.
MD. FACC
--
.-.---
t&m?ives. We sought to I) correlate condurtion Murk in the
dmas
d the ri#l 8Wiua between Ibeiaferior vena cava aad the
tAcmsp&i aIlralus win tile eakacy d L!aaeter rblation d type I
8Wial flutter. and 2) cbaractcrlze Ibe ekts of ablative lesions on
be prnpertks d istbmns condta%on.
Eac@wad. Tbcre are few data oa the mecbsnism of persistent
sappressiou d Nd atrial flutter by catkter l blahn.
Mdhds. IWty-Rn
patkats with type 1 aMal flutter underwrit catlteter mlapping and ablation. Radlofkqurney
ksions WR
applied in tbe isham. Traasis~baus rwdactioa MIV aad after
the ksioas was assessed during atrial pacing in sinus rkythm
~IIBE the medial and lateral maq@s d the isthras at cycte
kngtbs d6W m ud 380 ms and the asthe Butter cycle length
lstbmrs comduetiun block was delld
using mvllipolrr rec&iq
techniques, Tbm uwv bee tmhnenl mps:
group I = radiofreqaeacy eaew applied duriq flutter, until termination (n =
14); gnmp 2 f radMhq#&eacy emay applkd daliag l trial~pacing
in sinus rhythm fmm lbe proaimal cunmary sinus al a cycle
kagIbd6fHms,
uncilistlmuscmdrctioeblockwmo4served
(II = 14); 8ad gruup 3 = radiofrequency energy applied ualil an
iak&l lhtter termlrahn,
after rvkkh further enrw was applied
daring atrial pacing in sinus rhythm until isthmus conduction
block was o&send (n = 7).
Ram&s. In gmup I. after the initial Ruttcr Ictvaination. isth-
mus conduclion block was obsened in 9 of the I4 patients. la each
of these nine patients, llutter could not be reinitiated. la each d
&e remaining five patknls. after the iniliai flutter Icrminrtion.
isthmus conduction was intact and atrial flutter rnuld be reiniliated. Ultimalely. successful ablation in each d these patients was
also associated with isthmus condtntion block In groups 2 and 3.
isthmus conduction block was achieved during ndidquency
energy application, and flutler could not subsequently be reinitiated Befog achieving conduction block marked conduction
slowing or intefmittent Mark. or both, was observed in some
patients. In sow patkn& isthmus conduction bIock was pacing
rate dependent. In addition, recovery brn coadactioa Mock was
~wmmuu b the laboralory and bad a varlahie lime come. Al a
mean follow-up inlcmai d IO months (rant I to 21). Ihe actuarial
incidence d freedom fmm type I llulter was 80% (rrcurtvm in
rbree paGents a( 7 lo I5 months).
Coa&Gas.
Isthmus conduction Mock is associated with tlaIrr ablalion success. Conduction slowing or intermittent biock, or
both. in the isthmus can occur before ashieviag persistent block.
Iecoveg
of conduction
after achieving block is common.
Fdlow-up has meakd a luw rate d flutter recurrence after
acbicviag isthmus conduction block, whether the block was
achieved in coqjunction with termination d flutter.
-
It is now accepted that the mcrhanism of tyn! I aerial tluttcr is
reentry. involving primarily the right atrium (1). It h3.r hccn
shown that hlth “ru)untcrcluck~ise”
and “cltxkwisc”
type 1
atrial flutter are critically dependent on conduction through
the isthmus of the right atrial myocardium hordercd by the
tricuspid annulus and the infcriar vena caval orincc (isthmus)
(2.3);~Several repo:tq have attested to the importance of the
isthmus by directing successful rath,cter or surgical ahlativc
From the Philadelphia tIcarc Institute. the Sidncp );%cl
Rcwxch Ccnw.
and the Clinical Elcctrophysiolop
Latwrato~
of the Allcghcn~ Univrrsity
School UC Ihc Health Skwzs
Philadelphia. Pennsylvania.
Manuscript rcccivcd Dcccm!wr
!1. IY95: rcviwd manuwipl
rcccivcd April
1. 1%. accepted July 10. lY%.
&ldrcss for c~~.~sgrg&~~:
Dr. David Schwrrizmw.
Alkghcnv Univrnify
Hwpilal. Easl Falk 3.W Henry Avenue. Philadclphir
Pcnn+&
IYl?J.
----
(j As
------I---~
Cdl
-___. __ __.-
t’anlid
I9%:28:15~~-JI)
------
clforta to this region. with the tinding that flutter termination
was associated with hiock of the activation wave front in the
isthmus (Z-6). However. few reports have been puhlishcd
regarding changes in atrial conduction in sinus rhythm rc?iulting from radiofrequenq
applications.
which culminate
in
flutter &rmination and ablation success. In recent studies. bty
ct al. (7) and Cauchemez ct al. (8) showed that acutely
successful catheter ablation US associated with marked glohal
changes in right atrial cocCuction during atrial pacing sinus
rhythm, suResttie of block of the activation H’BW front in the
isthmus. Given the necessity of isthmus conduction in support
of flutter. the purpose of this study was to cxaminc the state of
conductkm in the Ahmus in relation to the immediate and
long-term success of radiofrequency
catheter ablation. A second purpose for this study was to characterize the effects of
~lS20
SCJIWARIZMAR
ET AL
ISTHMUS CONDUCTION
BLOCK
AND
MLATIOS
OF ATRL4L
JACC Vol. ?R. No. b
Nowmtwr
IS. lush ILIV-31
FLUTER
-
Previous
(‘orona~
flcramidc.
qumidmr
arkrv _ dwrw
ddawd cardiomyopdrby
Vonc
Uuinidinr.
None
Sonc
amrodlsronu
Ytimc
anen
Procamsmrdr
Ouinrdkrc.
prtx:din~mide
L.:Gnidine
cardromyop.lrhy
hcrr
Idropvrhrs ddarcd
f fyprrrcnsion
cardtomyupdrh!
Arrial sepral defecl
Ouinidine.
prorainamide
Coronary
Ouinidinc.
mcsilrtene.
ancr)
discaw
Hypertension
Procainamide
None
Atria1 sepral defect
Diiwpyramide.
artery disca*
Snnc
\alvular
wtnlolt
sntalnlt
None
Nun:
Diisopyramidc
None
Rcc,rinidr:
None
Ouinidinc.
None
Ouimdinc
unalol
Oumidinc.
qurnidinc.
dusopyramidc.
amiodaronz
Corriary
hknc
Procainamide
None
Nones
Ouinidinr.
Ouinidine.
f+pcrtcnsion
Nom
Nnnc
Idiopathic
Now
Procainamide
Amiodaronc
artery disersc
dilated cardiomyopathy
diisopyramide.
so~alol. amiodamne
niIalnl. amiodrrone
Coronary
xtery
diaau:
Coronary
artery disea.w
Coronary
Coronary
anery disease
artery discax
None
Flrcainidr
None
Amiodaronr
Amiodaronc
NIIIW
NIllW
Amiodaronc
.4r.ktaronr
None
Nom
Procaimrmidr
None
Ouinidinr
None
Prwainamide
None
prescribed
for suppression
of wxrrent
ventricular
radiofrequency energy applications on the properties of isthmus conduction.
Methods
Isthmus conduction was assessedby pacing the right atrium
during sinus rhythm before and after energy applications to the
isthmus. The study design comprised three treatment groups:
The first group assessed isthmus conduction after flutter
termination during radiofrequency energy application, to correlate the state of isthmus conduction with the ability to then.
reinitiate flutter. The second group tested whether the technique of energy application during pacing in sinus rhythm,
which resulted in elimination of isthmus conduction, was
correlated with an inability to reinitiate flutter. The third group
combined the approaches of the first and second groups by
Propafcnonc
Quinidine.
amiodamnc
Flecainidc
Ouinidine
Fkcainidc
None
Propafcnonx
None
NIIIW
.rmiodaronc
Procainamidc
Procainamidc
None
tSutalol
Sonc
Ndnc
Prtr.Gn.imidc
hcwr dirasc
None
None
‘Prmr ablation attempt.
male; R - parienr.
None
Nmrc
Rwrinrdc
Oumidinc. procainamrdc
Prtrainamide.
quinidine
Propafenorw
Procainamide.
cardurmyoparty
Sonc
sotalol. prclpafcnonc
Diisopyramide.
quinidinc
Ownidmr.
prtrrmamrdr
None
Idwparhrc dddkd
flywrension
wlalol
Amrarrhythmic
nlqr
ar study
Flrcanude.
dd&4
Now
Coronas
Pcgimrm
Ouinidine.
Idmparh~
None
(‘nronmn
fdmprrhic
Antixrhyrhmic
rachycardia.
None
$Amiodaronc
slopped
3 days hcfore proccdurc.
F = female; M =
assessingisthmus conduction after flutter termination and then
eliminating isthmus conduction using the technique of energy
application during pacing in sinus rhythm. Patients were not
randomly assigned to treatment groups.
This study organization enabled us to test whether isthmus
conduction block. defined during atrial pacing in sinus rhythm,
was mechanistically associated with ablation success,In addition, in the course of the study we were also able to gather
information on some of the properties of isthmus conduction,
including cycle length and pacing site. dependence.
Patients. The study group included 35 patients who had
experienced at least one spontaneousepisodc of type I attial
flutter (Table 1). Three patients had undergone a previous
radiofrequency catheter ablation procedure 3 to 11 months
before their entry into this study, during which energy applications to the isthmus were performed using a 4-mm long
JACC Vol. 2U. No. 6
rw%Cmhm I!?. lwtx1519-21
iSTHMlJS
CONMJC-IION
Flgm
athctcr posihna I& proxiiRbrr 1. Left anterior hlique mew d athet
mal (p) ammq
sinus (CS) catheter ekctnxk pair bordered
the
ostium, and rhe distal (d) coronarysinuselectrodepair bordered the
mitral annulus. The Halo catheter (Halo) was positioned in the isthmusand along the right atrial free wall.Thiscatheter
has radiopaquemarkers(opem-1
distal to electrodepair 1 (1)
and electrodepair 6 and proximalto electrodePair10(10). Amongthe
cohort, the position of Pair 10 varied.rangingbetweenthe alerisks.
The ablationcatheter(ABL) wasin the low la!cral right atrium, away
from the ablation zone. Dotted Ii- = cnnceptualmarginsof the
isthmus(seetext). IIRA = high right atrium: HB = His bundle.
posterolateral
electrode and were guided by activation and entrainment
mapping.
R#bl&hm rkctrophysioiogic evaluation. After informed
consent, each patient underwent the catheter mapping and
radiofrequency catheter ablation procedure described below.
which was approved by the Institutional Review Boards of the
Presbyterian Medical Center and the Allegheny University
Medical Center. By means of femoral, hrachial or internal
jugular venous approaches, a quadripolar catheter was placed
at the His position. A declpolar catheter was placed in the
coronary sinus and positioned such that the proximal eledrode
pair bordered the coronary sinus os (Fig. 1). A multipolar
catheter designed for mapping adjacent to the tricuspid annulus (Halo, Cordimebster Inc.) was placed in the right atrium.
This catheter had Itl electrode pairs with a 2-19-2 mm
interelectrode spacing. The distal electrode pair of the Halo
catheter was designated as Halo pair I. and the remaining pairs
were numbered 2 through 10 in sequence. The catheter was
positioned so that pair I lay just outside of the coronary sinus
ostium (Fig. 1 and 2). This resulted in the remaining pairs lying
in the isthmus and along the lateral right atrial free wall. The
catheter was maintained in a plane approximately parallrl to
the tricuspid annulus, and in proximity to the annulus. A
separate quadripolar catheter was used for pacing from multiple atrial sites (see later). For the purposes of, this study the
isthmus was defined as having medial and lateral margins (Fig.
1). With the catheters positioned as described ah&e. this
placed the proximal coronary sinus electrode pair on the
medial isthmus margin, and Halo electrode pair 4 or 5
(depending on the size of the inferior right atrium) on the
RLO(‘K
AND
.ARLATlON
SWWARTZMAN
0F ATRIAL
ET A:..
FLL’TTER
IS21
Figure2. Schematicleft anterior oblique view of the atria, sectioned at
the tricuspidand mitral valveannuli.OriBcruof the inferior venacava
(NC) and superiorvenaEva (SK). aswell asthe coronarysinus.are
shown.The approximatepositionsof Halo pairs 1 to 10 and pacing
sites I and 2 are shown. Halo electrodepair 1 was adjamnt lu the
coronary sinus orifice. The range of radiofrequency
ahlation
sites
among Ibc a)hort was from just outsidethe coronarysinusnstiumto
Halo electrodepair 3. C!%d= &tal coronarysinus:Csp = proximal
coronarysinus;HB = His bundle.
lateral isthmus margin. Approximately 4 to o cm of atrial
endocaidium was enclosed by thex margins. Bipolar electrograms from each endocardial si:c were acquired simultaneously (1 kHz) by a commercial digital acquisition system.
filtered at 30 to 500 Hz and stored on an optical disk for
subsequent analysis.
Isthmus conduction was assessedduring pacing in sinus
rhythm from two different right atrial sites and at a variety of
pacing cycle lengths. Atrial tissue stimulation on both sides of
the projected site of the radiofrequency lesionswas performed
to investigate any directional differences in conduction through
the isthmus. Pacingwas performed at a pulse width of 2 ms and
an amplitude that was the minimum necessary to achieve
consistent atrial capture. We used a variety of pacing cycle
lengths to reveal any ratedepcndent conduction characteristics. The first pacing site (site 1) was the low septal right atrium
adjacent to or just inside the coronary sinus OS(Fig. 2). The
second pacing site (site 2) was at the low lateral right atrium
adjacent to the tricuspid annulus. just lateral to Halo pair 4 or
5. Pacingwas performed from each site at four different pacing
cycle lengths: 600.400 and 300 ms and the native flutter cycle
length. Flutter was then initiated by programmed atrial stimulation (one to three extrastimuli; at least one drive cycle
length) or incremental pacing (cycle lengths 400 to 150 ms), or
both, from sites 1 and 2 or the high right atrium. Flutter was
defined electrocardiographically as counterclockwise or clockwise. In cases of counterclockwise flutter, the isthmus was
presumed to be an integral limb based on the classicsurface
electrocardiographic (ECG) p wave configuration, combined’
with a counterclockwise pattern of right atrial activation recorded by the Halo catheter (Fig. 3). In casesof clockwise
flutter, the isthmus was defined as an integral limb hy the
demonstration of a clockwise pattern of right atrial activation
recorded, by the Halo catheter (Fig. 4) and by the demonstration of concealed entrainment during pacing from the isthmus.
Demonstration of concealed entrainment entailed atrial pacing from within the isthmus during flutter at a pacing cycle
length 20 to 50 ms less than the tachycardia cycle length.
Ia
-9
=&I
Figure 3. Alrisl activation
during cnuntrrcluckwikc flutter. The Halo :Icc!rodcs
activated
sequcntiali>
in ;I counlcrclockwi\c
Jircction,
ctnsidcrinf
the tricuspid
aenL:us
as a clockface.
Activation
proceeded
through the isthmus in a
lateral-to-medial
direction.
Halo rlectrodc
pair
numbers
are shown.
Abbreviations
as in Figurc I.
-1
2
3
4
5
6
7
6
9
10
Concealed
entrainment was defined by a right atrial activation
Halo and His bundle electrodes). which
reproduced the flutter activation pattern among leads orthodromic to the pacing site. and by a postpacing interval (interval
between the pacing artifact preceding the last entrained cycle
and the first spontaneous atrial activation
recorded on the
proximal pair of the pacing catheter). which was within 10 ms
of lhe flutter cycle length (3).
Catheter ablation technique. A quadripolar catheter with
an &mm long distal electrode was used for energy applications.
The catheter was posirioned through a Mullins sheath, which
was pared to decrease its curvature. Radiofrequency
energy
was applied using a commercial generator. Power output was
pattern
(including
continuously adjusted (10 to 45 W) to maintain the impedance
-5 r>hrns below baseline (defined at 5 W). Beginning at the
atrial aspect of the tricuspid annulus in an area of the medial
isthmus. ranging from Just beneath the coronary sinus ostium
to Halo pair 3. the ablation electrode was slowly dragged
posteriorly toward the orifice of the inferior vcna cava during
continuous power delivery. In 29 patients, energy applications
were performed without moving the Halo catheter, such that
!he ablation ticctrode coursed beneath this catheter in direct
contact with the floor of the atrium. In these patients, Halo
position was monitored Ruoroscopically throughout the procedure. In Cdch of the six patients in whom the Halo catheter was
removed during crizrgy applications.
it was replaced in a
Figure 1. Atrial adivalion
during clockwise
Ruttcr. The Halo clectrxlcs
activated
sequrntially
in
a clockwise
directIon.
Activatlun
proceeded
through
the isthmus in a medial-to-lateral
dircclion. Abhrrviations
as in Figure I.
---
d&/----
----b---------
---b-
-.-- --
JACC Vol. 28. No. b
hklvcm~r
IS. lwb:ISl%JI
KI-HMUS
cDNDt’0-lON
BLOCK
AND
ABi4TIDN
SCHWARRMAN
OF ATRIAL
ET AL.
FLLi?ER
1523
Firr
5. Baseline atria1 activation during
pacing at site I at a cycle length of tiNI ms.
Activationproceededsequentiallythrough the
isthmusin a medial-to-lateral direction. beginning with Halo pair 1. Note that Halo pairs 0
and 10 activated out of sequence, consistent
with activation in this region by a wave front
that did not traverse the isthmus. The STOWbeads at the top of the figure representthe
moment of the pacing stimulus artifact. Abbreviations ti in Figure I.
similar fluoroscopic position as at baseline for rhe postablation
assessment.Three treatment groups were defined.
Group I (n = 14). All energy applications were performed
during atrial flutter. An ongoing application was completed
even if flutter terminated before the point at which the
ablation ckttorle reached the orifice of the inferior vena cava.
After each flutter termination, pacing from sites 1 and 2 was
repeated. Atria1 stimulation, including extrastimuli and turst
pacing at rl atrial site was then performed. Specifically, this
included the stimulation method and the site with which flutter
was initiated in the baseline state. Patients in whom flutter
could not be reinitiated were observed for at least 30 min,
during which time repclitive pacing and atria1 stimulation were
performed. Ablation successwas defined as termination of
flutter during energy application and the inability to reinitiate
one or more clockwise or counterclockwise flutter cycles. In
three patients, the Halo catheter position was temporarily
altered at the end of a successful ablation procedure to
examine inti*ra!rial septal activation in greater detail during
pacing from site 2. The catheter was positIoned such that
electrode pairs lay along the interatrial septum, extending
cranimudally from His lo the coronary sinus ostium parallel
snd adjacent to the tricuspid annulus.
G10up 2 (n = 14). Al1 energy applications were performed
during atrial pacing in sinus rhythm from the proximal coronary sinus at a cycle length of 600 ms. After isthmus conduction
block was achieved (refer to Definitiolis), pacing from sites 1
and 2 was repeated, and repetiiie atrisl stimulation was
performed. patients in whom flutter could not be reinitiated
were observed in the laboratory for at least 30 min, during
which time rGpetitive pacing and atrial stimulation were performed. Ablation success was defined as the inability to
reinitistc one or more flutter cycles,
C;roup 3 (n = 7). In each patient, energy application during
flutter resulted in a single tachycardia termination. Afterward,
intact isthmus conduction at all pacing cycle lengths was then
revealed during pacing from site 1 in each patient. Further
energy applications were then performed during atrial pacing
in sinus rhythm at 600 ms from the proximal coronary sinus.
After isthmus conduction block was achieved, pacing from sites
I and 2 was repeated. and repetitive atrial stimulation was
performed for at least 30 min. SWXXSof the ablation procedure was defined by .the inability to reinitiate oue or moie
flutter cycles.
De6nitioas. Local atrial activation was defined by the peak
of the largest electrogram deflection. If a double potential that
was not present at baseline was observed in the energy
application region, then the timing of the later potential was
defined as the moment of “distal” wave front act%:ion a: :ha:
site.
Before ablation, pacing at site 1 resulted in sequential
activation of Halo pairs 1 to 5 in all patients (Fig. 5). Atrial
activation in the region of Halo pairs 6 to 10 appeared to be
due to continuation of the wave front that had traversed the
isthmus, as well as a separate wave front. This aciiration
pattern was minimally a&ted by the pacing cycle length. We
defined irthmus cot&&on Mock during pacing at site 1 as a
reversal in the activation sequence of those Halo pairs 1 to 5
that were distal 10 the ablation zone--that is, on the opposite
side of the lesion area hrn site 1. Our definition of isthmus
conduction block was limited to those Halo pairs that were
located in the isthmus, despite the almost uniform finding that
electrodes outside of the isthmus (pairs 6 lo 10) also show+ a
reversal in their activation sequence in association with isthmus conduction block.
Before ablation, pacing at site 2 resltlted in Activation of
1924
SCHWA’tTZMAN
ET AL.
ISTHML’!; CONDUCTION
BLOCK
AND
ABiATION
OF ATRIAL
Novcmkr
FLUITER
JACC Vol. 28. Nn. h
15. IYYfclSlY-31
Figure
6. Basclincatrial activation during
pacingfrom site2 at a gclr length of 600 ma.
Aclivation
of the isthmus proceeded
scquentially in a lateral-to-medial
direction.
beginning with Halo pair 5. In additlgn. lateral right
atrial free wal! activation
proceededcranio-
caudally.The coronarysinusostiumactivated
before both fhc His bundle and distal coronary sinus.
Halo pairs S lo 1 in sequence (Fig. 6). Activation at the
coronav sinus ostium followed activation of Halo pair 1 and
preceded activl;rion of His in all patients (mean [‘SD] 20 ?
7 ms). This activation pattern was minimally affected by the
pacing cycle length. Because of the medial Iocacationof most
isthmus lesions.w could not define isthmus conduction block
during pacing at site 2 using electrodes positioned in the
isthmus. Rather. isthmus conduction block during pacing at
site 2 was dcfincd as an reversal of the sequence of activation
at the coronary sinus ostium and Ha. with His preceding
activation at the coronary sinus ostium (mean 40 + 10 ms at
the end of the ablation procedure).
Follow-up. Patients were questioned hy telephone or in
person for symptoms suggestive of an arrhythmia recurrence
after hospital discharge. In seven patients who developed
recurrent palpitation or documented atrial tachycardia with
regular atrinl activity. or both, a repeat invasive electrophysiologic evaluation was performed.
Analydcal methods. Arrhythmia cycle lengths and atria1
activation times presented herein represent the mean va!ue
?SD of 10 consecutivecyclesmeasured during a stable period
of flutter or atrial pacing. Fluoroscopy and procedure times arc
presented as the mean value ?SD. Significancebetween paired
data sets was assessedusing the Student I test; a p value ~0.05
was considered significant. Analysis of flutter recurrence was
performed using the Kaplan-Meier method.
Results
Group 1 (n = ,141. In accordance with the protocol, all
radiofrequency applicatidns were performed during flutter.
Recordings from the Halo catheter showed that termination of
both counterclockwise and clockwise flutter was preceded by
conduction block in the area of the isthmus to which energy
Abhreviarions
as in Figure
1.
was applied. However? despite the appearance of conduction
block during flutter. intact isthmus conduction was subsequent!y demonstrated in some patients during pacing in sinus
rhythm. Nine patients had isihmus conduction block during
pacing from sites 1 and 2 after the initial flutter termination.
Flutter could not be reinitiated in these patients (Table 2).
Figures 7 and 8 illustrate the typical appearance of isthmus
conduction block during pacing at site 1. with reversal of the
activation sequence in the isthmus relative 10 the preablation
sequence and a counterclockwise Halo activation sequence.
The typical appearance of isthmus block during pacing at site
2 is illustrated in Figure 9, which shows the inverted sequence
of activation relative to baseline at the coronary sinus ostium
and the His electrodes.
By contrast, in the remaining five patients in group 1 in
whom flutter could be reinitiaied after the initial termination,
intact isthmus conduction was present during pacing at all cycle
lengths. Subsequent energy applications during flutter resulted
in one to three additional tachycardia terminations per patient.
In each patient. the ability to reinitiate flutter after termination
was associa:cdsi:h intact isthmus conduction. The inability to
reinitiate flutter was associatedwith isthmus conduction block
from both sites 1 and 2.
In most patients isthmus conduction block was manifest at
a pacing cycle length of 600 ms, whereas in othc~s conduction
block occurred only at shorter cycle lengths (Table 2). Thesedata show that even when energy application resulted in ‘the
termination of flutter, it was still possible to reinitiate flutter in
some patients. In addition. the effectiveness of the ablation
‘procedure ‘&as directly related to the rate with which the
isthmus could support impulse conduction: Thus, when isthmus conduction remained intact at all pacing cycle lengths it
was possible to reinitiate flutter. In contrast, when isthmus
conduction block occurred during pacing in sinus rhythm at
JACC Vul. 2X. No. 6
Novcmbcr
15. IWfr1510~31
ISTHMUS
CWNDL’CIION
RLOCK
AND
ARL..iTlON
SCHWARTZMAN
OF ATRIAL
ET AL.
FLUTIER
Table 2. Procedural and Follow-Up Data
-.Isthmus Bkrk
Flutter Type
Pt.
No.:
Group
I
2
3
4
53
1
2
I
(cylc length
in m.s$)
No. ai
Drugs
cc (250 i 3)
cc (26s + II))
5
I#
?I
5
5
4
R
cc (220 z 2)
C(2.5 “ 3)
I
i
cc (220 I 3)
Sh
6
1
C(lW_c
I)
cc (220 .r 2)
7
2
cc
Xa
3
-
c (2.40 c 1)
Xh
9
(Zllc, 2 3)
No. of Flutter
Tcrminations#
Sift 1
Pacing (ms)
Cyclr Lqth
Site-?
Pacing (ms)
Drug Rqimcn’
Follow-Up
(mo)
DrU3
Indication
I
13
None
-
-I
1-t
1.1
Flccainidc
None
-
2
1
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None
-
0.5
lb
None
km
-
2
16
None
-
1
I6
None
-
I
I.5
IS
None
None
-
-
-
4
-
-
1
I
cc (24s _c I)
cc (XII + III)
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v
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None
-
lob
lla
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None
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IS
None
-
cc (245 -c- 2)
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None
I
cc (250)
;
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None
-
S
IY
0
Flccainidc
2
Propafcnonc
2
s
6
:
Quinidinc
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P:!@J”O:!lr
1
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llb
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13
14
-
(240)
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cc
~~(230)
IS
2
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cc (310)
5
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I6
3
cc (220)
4
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I7
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CC (265)
3
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IX
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cc
(295)
5
20
I
cc (27tl)
c (289)
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21a
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C (275 t 10)
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2lb
22
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cc (3ou 2 7)
cc (23112 5)
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23a
I
cc (240 c 2)
1
24a
24h
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cc (240 L 4)
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cc (300 + N)
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cc (220 + 5)
cc (ai) 2 3)
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None
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8
7
None
Propafcnonc
1
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None
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-
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None
-
Pnlrainamidc
N
-
Amiodxonc
N
2
-
1
I
-
0.3
-.1:
1
-
0,s
3.0
Propdfcnonc
2
-
2.0
Amiodaronc
1
-
5
I
Propafenonc
Flccainide
I
I
-
1
Amiudaronc
-
2
I
4
None
3
-
I
Flccainidc
I
-
-
-
-
32
2
cc (220 1- 5)
3
-
1
33
2
cc (240 r 4)
2
-
3
Procainamidc
34
3s
2
cc (2sO)
cc (alI 2: 2)
3
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-
3
4
Amicnlaronc
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-
-
Rccurrcncc’
1
103
2. 15)
t_ I)
1x3
I
1
-
l indication rcfcrx to the specific reason for ihcrapy: 1 = continuation of preahlation regimen. started for Episodes of atrial fibrillation: _7 = started after the ablation
fur episodes of atrial fibrillation or atrial tachycardia: 3 = continuation
of prcahlation regimen. started fkr recurrent ventricular
tachycardia. rln parients who have
undergone rcpcat elcctrophysiologic
study. -a” refers to the first procr\iurc,
“b” to the scxond procedure. *Data are prcscntcd as mean value -SD. #Toral number of
flutter terminations obsctvcd during cnrr~
application. By definition. in group 3 patients. one termination was observed. and in group 2 patients. no terminations were
observed. i/Yes = rccurrcnce
of type I atrial flutter; No = no rccurrcncc
of flutter. 1Recurrcncc
of nontargcted atrial tachycardia. AFL = mean native Ruttcr cycle
length: C = clockwise; CC
countcrclochwisc:
N = none.
cycl;: lengths greater than or equal to the native flutter cycle
length, flutter could not be reinitiated.
After achieving isthmus conduction block in three patients,
the Halo catheter was repositioned on the interatrial septum to
further investigate its activation sequence during pacing from a
site lateral, to the radiofrequency appliition zone. In each
patient, pacing from site 2 results in a craniocaudal septal
activation sequence, in association with the reversal in the
coronary sinus ostium-His activation sequence.
Crimp 2 (ir 7. 14). Isthmus’cond~rction in these patients
was continuously monitored during pacing at a 6o(j-ms cycle
length from the proximal coronary sinus during radiofrequency
applications. The progress of lesion development was indicated
by a gradual prolongation of ‘the isthmus com!uction time
1526
SCHWARTZMAN
ET AL.
WHMUS
CONDUCTION
BLOCK
AND
ABLATION
OF ATRIAL
FLZ!TTER
JACC Vol. 28 Nn. b
Novemhcr
IS. 1996:1519-31
Figure
7. Pacing at site 1 after a radiofrequency energy application.
In this patient radiofrequenq
energy
had been applied
between Halo 1 and the coronary
sinus osrium.
Isthmus
conduction
block was demonstrated
by inversionof the activationsequencpof Halo
Plectrode pairs 1 to 5 relative to baseline. The
activation
time at Halo electrode
pair 1, adjacent to the stimulationsite,was 190ms. Abbreviations
as in Figure 1.
acrossthe lesion zone in all patients during these applications.
Eventually, this culminated in isthmus conduction block (Fig.
10). Immediately after isthmus conduction block was observed,
the Mock was also demonstrable during pacing at all cycle
lengths at both sites 1 and 2. When isthmus conduction block
was demonstrable. flutter could not be reinitiated.
Group 3 (n = 7). A single termination of flutter was
observed during radiofrequency application in eac3 patient.
Subsequently, intact isthmus conduction during pacing at site 1
was demonstrable at all pacing cycle lengths. In three natients,
atrial stimulation was repeated. and flutter xas reinitiated. In
the other four patients, atrial stimulation was not :epeated. In
each patient in this group. subsequent energy applications
were performed during pacing from the coroaary sinus at a
cyclelength of 600 ms. As observed in group 2 patients. energy
applications caused a gradual prolongation in conduction time
acrossthe lesion zone, which culminated in isthmus conduction
block. After isthmus conduction block was observed, block was
also demonstrable during pacing at sites 1 and 2 at all pacing
cycle lengths.
Additional
intraprocedural
obsenatioas.
In several patients in whom block occurred at pacing cycle lengths ~600 ms.
variable or markedly slowed conduction was observed in the
isthmus at pacing cycle lengths greater than the complete block
cycle length (Fig. 10). Also, time-dependent recovery of isthmus conduction was common. as observed in seven patients. In
--.-_.--__
--
--
Figure E. Pacing a~ sit: I after a radiofrequency
energy application.
In this pxient
the application was near Halo elet !ndc
pair 3. Isthmus
conduction
block was demonstrated
by an inverted
activation
sequenx
of Halo electrode
pairs 3 lo 5. A double potential
(armwheads)
is
recorded
on Halo eleclro5e
pair 3. with the
timing of each of the potentials
cy)rres*‘2 .nding to
the terminus
of a separate
activation
\rave front:’
Abbreviations
as in Figure
1.
JA~C Vol. LX. No. 6
Ncw~mbcr IS, IW6:1S19-31
ISl’HMLYS
CONDUCIION
BLOCK
AND
ABLATIOS
SCHWARTZMAN
OF AT&U
ET AL
FLUTTER
1527
w
li)
csp
csd
F&WV 9. Pacing at site 2 after a radicfrequcnc)
energy application.
Isthmus
conduction
block
was demonstrated
by the reversal of the Lctivation sequence at the coronary
sinus ostium and
His bundle (HB). with His preceding the prox-
-
1
2
3
imal coronary sinus (CS,) by longer than 10 ms.
Note also that activation at the distal coronav
sinus
(Cs,)
was essentially
simu!;aneous
with
activation of the proximal coronav sinus.
‘tie patients, we observed tsta! resolution of isthmus block,
which had been demonstrable during pacing from either site at
a cycle length of 600 ms early after a radiofrequency application; this was associatedwith the ability to reinitiate sustained
flutter. In two other patients, recovery was shown by a decrease
in the pacing cycle length at which isthmus conduction block
was observed (600 to 400 ms in one patient, 400 to 300 ms in
one patient). The time course of recovery was >60 min after a
radiofrequency application in two patients and lessthan 15 min
after the last radiofrequency application in five patients. The
rate of recovery from conduction block appeared equivalent
when defined by pacing at site 1 versus site 2.
Figure
IO. Atrial
activation
sequence
during
pacing from the proximal coronary sinus (Cs,)
at a cycle length of 600 ms in a patient from
group 3. A, Atrial pacing at baseiine from the
proximal
coronary
600 ms after the
Isthmus
conduction
sinus at a cycle length of
initial flutter
termination.
was intact. except that it
was slowed relative to baseline (not shown),
with wave front collision
in the lateral right
atrium. B, Continued pacing from the proximal
coronary sinus during further radiofrequency
energy applicatiop. Marked conduction slowing
in the isthmus is now obszrved, with collision in
the isthmus shown as essentially simultaneous
activation of electrode pairs in the lateral and
medial isthmus. C,,ln the next cycle, isthmus
conduction block was observed. associated with
fully counterclockwise
activatign
sequence
of
the Halo. HB = .His bundle: Cs, = distal
coronary sinqs.
At the end of the procedure, the pacing cycle length at
which isthmus conduction
block was observed
during pacing
from sites 1 and 2 was equal in all patients except patient 12. in
whom isthmus conduction block was observed during pacing at
site 1 at a cycle length of 300 ms and during pacing from site
2 at a cycle length of 400 ms (Table 2).
The mean procedure and fluoroscopy times were 5.6 2
1.1 h and 114 2 45 min. respective!y.
Follow-up.
During a follow-up period ranging from 1 to 2 1
months (mean 10). recurrence of type I flutter uas observed in
three patients, for an actuarial flutter-free incidence of 80%
(Fig. 11). Patients currently taking an an!iarrhythmic
drug (n =
15%
SCHWARTZMAN
ET AL
ISI-HWJS
CONDUCTION
JAW
BLOCK
ASD
ABLATION
OF ATRIAL
Novcmtw
FLlXTER
Vol. ?R. No. 6
IS. lW6:1510-31
Figure 11. Prop&on of patients without flu!!cr
rccurrcnce.Numbers at bottom renresent cohort
4
16 [Ih%]) continued their preablation antiarrhythmic drug
regimen f,)r episodic atrial fibrillation (n = 9) or for ventricular
tachycardia (n = 1). or started a new regimen for episodic
atrial tachyarrhythmias. Type I flutter has recurred spontaneously ir. patients 10. 11 and 21 at 9, IS and 7 months,
respectively. In two of these three patients. the flutter cycle
length at the time of recurrence was significantly longer than at
baseline (Table 2). In each patient, at the time of repeat study,
isthmus conduction had recovered and was intact at all pacing
cycle lengths, albeit significantly slowed relative to baseline
during pacing in sinus rhythm at all cycle lengths and during
Putter. Additional radiofrequency applications to the same
isthmus zone resulted in isthmus conduction block at all pacing
cycle lengths, associatedwith ablation success.
Four other patients who developed recurrent palpitation
and documented tachycardia with regular atrial activity underwent a repeat electrophysiologic evaluation, but none of these
patients underwent further ablation. Patient 5 underwent
repeat .study at 14 days after the ablation procedure for
assessmentof episodes of a regular atria1 tachycardia in which
thz surface ECG p wave configura!ion and cycle length were
different than the clinical flutter targeted at the ablation
procedure. Isthmus conduction block was demonstrable at all
‘pacing cycle lengths in this patient, unchanged from the
immediate postablation result, and type I flutter could not be
reinitiated. In patient 8, a regular atrial tachycardia resembling
type 1 flutter targeted at the ablation procedure was observed
at 6 weeks.This patient was studied 1 week later, at which time
no fIutter could be initiated. Isthmus conduction block was
seen at pacing cycle lengths of 400 ms or less,unchanged from
the immediate postablation result. Patient 23 underwent a
repeat study 10 days after tht: ablation procedure for asessment of spontaneous episodes ot 3 regular atrial tachycardia in
which the surface ECG p wave configuration and cycle length
were different from the flutter targeted at the ablation procedure. Isthmus conduction block was demonstrable at all pacing
cycle lengths in this patient, unchanged from the immediate
postablation result. Type I flutter could not be reinitiated.
Patient 24 underwent a repeat study 14 days after the ablation
procedure for assessmentof what appeared to be coarse atrial
I
fibrillation with a regular ventricular response. Isthmus conduction block w:. demonstrable at all pacing cycle lengths.
unchanged from the immediate postablation result. Type 1
flutter could not be reinitiated.
Discussion
The central finding of this study was the association between the successof radiofrequency catheter ablation of type I
atria1 flutter and isthmus conduction block, defined during
pacing in sinus rhythm from either margin of the isthmus at
cycle lengths ranging from the native flutter cycle length to
600 ms. Several observations served to establish this association: 1) Isthmus conduction was mtxt in each of the three
study patients who had flutter recurrence after ablation using a
4.mm long electrode, as well as in each of the three additional
patients with flutter recurrence after block had been documented. 2) During the ablation procedure the absenceof block
was associated with the ability to reinitiate flutter, even in
those patients in whom the flutter terminated during radiofrequency application. 3) In several patients recovery of isthmus
conduction during the procedure preceded our ability to
reinitiate flutter. Finally, successful ablation could be performed completely in sinus rhythm, utilizing only isthmus
conduction block as the procedural end point.
In the course of this study we also characterized the effects
of radiofrequency energy applications on the properties of
isthmus conduction.
Importance of intact isthmus conduction for pcrpetuatiuo
of flutter. Alterations in right atrial activation associatedwith
ablation in the isthmus has recently been reported in an animal
model and in humans. Tabuchi et al. (9) studied a canine
model of flutter previously developed by Frame et al. (24), in
which a Y-shaped incision ,was placed in the posterior ‘right,
&al free wall. These investigators (24) demonstrated that
flutter iermination was preceded by block of the activation.
wave front in the isthmus during mechanical (ligature) or
radiofrequency catheter ablation. The inability to reinitiate
flutter subsequently was associated with isthmus conduction
block during pacing in sinus rhythm from the left atrium at a
JACX Vol. 24. No. h
Ncwmhcr
IS. Ivyh:ISIU-31
ISTHMlX
CONDUCTION
fixed cycle length of 300 ms. which resulted in reversal relative
to baseline of the atrialactivation sequence around the right
atria1 incision lines. In some animals new double potentials,
similar to those seen in some of our .patients (Fig. 8). were
‘observed in the ablation zone. These were due to activation of
the zone hy two different wave fronts proceeding in opposite
directions. In humans. Poty et al. (7) used multipolar catheters
to assessthe right atrial activation sequence before and after
catheter ablation of type I flutter. Successful ablation was
associatedwith conduction block in the isthmus, as manifest by
reversal of the isthmus activation sequence during pacing in
sinus rhythm from the proximal coronary sinus. Similarly,
Cauchemez et al. (8) reported that successfulcatheter ablation
of type I flutter was associated with isthmus conduction block
at a pacing cycle length approximating the flutter cycle length
in 19 of 20 patients. The present study confirms several key
observations made oy each of these investigators. First, termination of flutter during radiofrequency application was not
tantamount to ablation success.Second, there was an association between the abi!ity to reinitiate flutter and the presence of
isthmus conduction. Third, intact isthmus conduction was a
uniform finding in patients who experienced flutter recurrence.
Changes in atrial cxmhcth
tier ablation in the isthmus.
Following a uniform protocol, we examined isthmus conduction at four different pacing cyclelengths from both margins of
the isthmus. In six patients, a clear pattern of rate-dependent
isthmus conduction block was observed (Table 2). In patients
demonstrating this pattern. variable isthmus conduction was
not uncommon during pacing at cycle lengths greater than the
cycle length at which there was consistent block. Cauchemez et
al. (8) also reported this phenomenon in some patients,
althL+h no cycle lengths were specified. In contrast to our
findings, they found that rate-dependent isthmus conduction
block could be a unidirectional phenomena,,:. alwaysoccurring
in the medial-to-lateral direction. We also systematicauy e.aiuated the right atrial activation pattern associated with pacing
from the lateral isthmus margin (site 2). A reversal in the
sequence of activation of electrodes located at the coronary
sinus ostium and His bundle was correlated with isthmus
conduction block defined during pacing from the medial
isthmus margin (site 1) and was associated with cranioraudal
activation of the interatrial septum. With one exception. the
pacing cycle length at which isthmus Lunduction block occurred during pacing from each site was the same. In contrast,
Cauchemez et al. (8) reported some patients in whom isthmus
block could be unidirectional, with conduction intact during
pacing in cycle lengths as short as the baseline flutter cycle.
length.
We have. documented the ,phenomenon of recovery, of’
isthmus conduction after radiofrequency application. This
could ti shown by a decrease in the pacing cycle length
necessaryfor persistent isthmus conduction block. or by recovery of intact conduction after conduction block had been
demonstrable at all pacing cycle lengths. The time course of
recovery varied, ranging from minutes to longer than 1 h.
Transient isthmus conduction block was also reported in four
BLOCK
ABD’kATlON
SCHWARTZMAN
OF ATRIAL
iiT AL
FLUTTER
’
1529
patients by Calichemez et al. (8). ail occurrirrg within 30 min of
the last radiofrequency lesion.
We have demonstrated that successfulablation of-flutter
can be performed completely in sinus rhythm. using isthmus ’
conduction block during pacing at the proximal coronary sinus
as the procedural end point. Block was observed after progressive slowing of conduction in the radiofrequency energy application zone. The ability to document isthmus conduction block
during sinus rhythm may be particularly useful in certain
patients, such as those who tolerate flutter poorly or those in
whom flutter tends to degenerate into atrial fibrillation. in
addition, in certain patients sinus rhythm may permit improved
mechanical stability of the ahlation electrode in the isthmus
relative to flutter, enhancing the ethcacy of lesion formation.
The preliminary experience of Poty et al. (10) supports this
experience.
Finally, we have had the opportunity to reevaluate seven
patients who had undergone successful ablation resulting in
isthmus conduction block 1 week to Y months after the
procedure. Each of the three patients in whom type I flutter
recurrence was observed had intact isthmus conduction. Interestingly, in two of these three patients the recurrent flutter
cycle length was significantly longer than before the ablation.
associated with conduction slowing in the isthmus during
pacing in sinus rhythm or during flutter. In patient 8. although
a tachyarrhythmia resembling the targeted flutter was observed
6 weeks after the ablation procedure, at repeat study I week
later no flutter could be initiated and there was no change in
the pacing cyclelength at which isthmus conduction block cycle
was observed. She has had no further tachyarrhythmic episodes
at a follow-up interval of 1 I months, and she is not receiving
antianhythmic drug therapy. It is conceivable that the recurrent tachyarrhythmia in this patient was tvpe I flutter and that
the isthmus conduction block was ir,ie.i;;ittent or delayed after
initial recovery. It is also possible that the rhythm was an atrial
tachycardia originating near the ablation zone, possiblyresulting from abnormal automaticity related ;o ablation injury (11).
In each of the three other patients who we have reevaluated at
a postablation interwal of 2 weeks to 3 months, the recurrent
ECG tachycardia appearance was distinctly different from the
targeted flutter. In these patients, the targeted flutter could not
be reinitiated, and the pacing cycle length at which isthmus
conduction biock was demonstrated was unchanged.
Reeurrenee of flutter. The ablation technique reported
here is an extension of previously reported ;bation techniques
that focused Qn an anatomic target--the isthmus (1213). The
ability’to document isthmus conduction block may provide a
framework for understanding and addressing the issue of
flutter recurrence.. First, we have documented the phenomcnon of recovery of isthmus conduction. Factors associatedwith
recovery may include inadequate tissue heating or transient
effects nf radiofrequency energy application on perfusion or
innervation of isthmus myocardium. Although we conceptualized that isthmus conduction block was associated with a
continuous lesion extending from the !ricuspid annulus to the
inferior vena caval orifice, the pathologic result of our radio-
1530
SCHWARRMAN
ET AL
ISTHMUS CONDUCTION
BLOCli
AND
ABLATION
OF ATRIAL
frequency applications is unknown. It is possible that inctsmplete lesions could result in true conduction
block (14).
Second, in one of the three patients,(patient
1Oj in whom type
! flutter recurrence tias observed. the.pacing cycle length at
which block was demonstrable
was limited to rapid pacing
cycle lengths. It is possible that flutter recurrence will be
minimized
by ensuring isthmus conduction
block at long
pacing cycle lengths. Reports by Cauchemez et al. (8) and Poty
et al. (IS) support this hypothesis. However. we have also
shown that conduction block at even long pacing cycle lengths
will be an end point insufficient to prevent all recurrences. It is
of interest that the recurrence of flutter in our study was
relatively late, ranging from 7 to 15 months. Although previous
reports have documented some late recurrences of flutter after
radiofrequency
ablation. most patients have had recurrences
within 6 months (16). It is possible that the lesion created in
our patients was more substantial and thus slower to recover.
However. owing to a lack of longitudinal data on the state of
isthmus conduction in our patients, and in view of the paroxysmal nature of flutter. the validity of this concept is unknown.
Our data thus far suggest that among patients in whom the
ablation proccdurc is performed in sinus rhythm. !he recurrence rate is not significantly higher than in those in whom
termination of flutter is documented during radiofrequency
application.
Study limitations.
The present study has several limitations: 1) The prerise position of the Halo catheter varied
among the cohort. However, in this study we did not base our
IDSUIIS on changes in activation time which could be suscep
tihle to minor changes in catheter position, but instead on
changes in activation pattern. The changes in activation pattern demonstrated in this study could have only been due to a
global change in right atrial activation. and would have been
apparent despite differences in apical-to-basal
or medial-tolateral Halo placement within the isthmus. In addition, the
Halo activation sequence changes were corroborated
by activation sequence changes among independent
(His bundle,
coronary sinus) recording electrodes that had more easily
standardized
positions. 2) Patients were not enrolled into
treatment groups in a random fashion. This may serve to
weaken our conclusions regarding the utility of isthmus conduction block. However, in group 1 the ablation was performed
using isthmus conduction block as an observational technique
only. In these patients. the association of ahlation success with
isthmus conduction block was clear. 3) In the present study the
validity of reversal in the sequence of activation at the coronary
sinus OS and His bundle sites during pacing at site 2, as
representative of isthmus conduction block, was less extensively established than criteria used to define conduction block
during site 1 pacing. In effect, the site 2 pacing criterion was
“tested” in,only five patients in group 1 in whom flutter could
be reinitiated after termination. It is likely thai reversal will
also occur during site 2 pacing with intact but markedly slowed
isthmus conduction.
In a recent report, Sarter et al. (17)
documented this phenomenon
in ‘some patients. Thus, this
criterion requires further evaluation for determination
of its
FLC:lTER
Nowmtw
JACC Vol. 28. No. 6
15. 1w6:1519-31
sensitivity sod specificity. 4) It is critical to emphasize that the.:
present study cannot address thevalue of the isthmus conduc-,
tion block end point independent of the flutter, ablation end,
point in which tachycardia is terminated during radiofrequency
application and cannot be reinitiated afterward. Conceptually.
the optimal technique would be one in which permanent flutter
suppression was achieved with the smallest cardiac lesion.
Recurrence rates of flutter using an end point of tachycardia
termination with the inability to reinitiate flutterplus
isthmus
conduction block. as in the present study, appear low relative
to most reports in which isthmus conduction was not assessed
after ablation (2-8.10.12.13.15.16,18-21).
However, the inability to reinitiate flutter&
isthmus conduction block end point
represent relatively short-term follow-up and has &en performed by investigators previously experienced with radiofrequency application
in the isthmus. It is plausible that a
procedural end point that includes isthrrus conduction block
during atrial pacing in sinus rhythm may unnecessarily require
more extensive lesions, resulting in increased procedural morbidity. 5) The optimal method of radiofrequency
lesion application in the isthmus cannot be discerned from our data.
Although the ability to perform flutter ablation during sinus
rhythm may be advantageous in certain patients, as stated
previously, no general conclusions can be drawn as to the
advantages or disadvantages of this technique relative to lesion
application during flutter. Similarly, the optimal modality of
ablation site selection. whether anatomically or electrophysiologically guided, is unknown. In a recent report by Chen et al.
(20). a randomized comparison of these two modalities showed
no difference in acute or chronic success, although the anatomic approach required shorter procedure and fluuroscopy
times. In addition. our data do nut permit comparison of
anatomic techniques in which the ablation electrode is dragged
during continuous radiofrequency
energy application, versus
those in which energy is applied at discrete sites along a
conceptual line.
Implications.
‘IM additional observations in the present
study were of particular interest. First, during pacing from site
1 after isthmus conduction block we observed. in all but one
case, reversal of the activation sequence o: all Halo electrode
pairs, rather than just those pairs located in the isthmus. In
these patients, the pattern closely resembled the right atrial
activation pattern during counterclockwise
flutter. This linding
is consistent with maintenance of a posterior right atrial barrier
to transverse conduction, described by Olgin et al. (22) during
flutter. However, because the Halo electrodes were at a
,distance from the posterior right atrium, this observation does
not exclude the. presence of slowed conduction across the
barrier. Second, we experienced frequent difficulty in creating
isthmus block, often requiring numerous energy applications
despite adequate electrode contact. This experience, combined
‘with the common occurrence of p&ablation
recovery of
isthmus conduction, has important implications for catheter
ablation in other regions of the atria. Many investigators are
pursuing catheter ablative approaches td atrial fibrillation
in
which long contiguous transmural lesions forming barriers to
conduction are conceptualized. similar to those resulting from
the incisions of CUR et ~1. (2.3) in their dcscriptbn of the Max
procedure. Our esperience in a relatively discrete region of
atrial mycardium
underscores the potential limitations of this
concept usins currently available ablation technology.
isthmu* block as dswscd
h\ law clcrtroph~4qic
qucrx? ablatitm of atnal t&&r lalwractj.
iACE
I I. Sath S. Hsirw
raditlfrcquenr?
elcr Ahlalion
Iwc:y-4k
I!.
radiofrc’
DE. Pathuph!rioh+y
of Ic\ion formation hy transcathetcr
ablaticm. In: Huang SKS (cditw).
Radiofrequrncy
Cathof Cardiac .Arrhythmiar.
.&monk.
Wcw York: Futura.’
Cwio FG. Goicolca A, lupcr-Gil
M, Arrihsr
Huttcr circwtx. PACE ILw?;16:637--42.
contml.after
I’)c)h:lU:hSl.
F. Cathctcr
ablarion of rlrial
.3. Ix\h
1.1. Rirkorian G. Moncada F. (:hc\alicr
P. e: al. RadioircqurnL)ablation of
,ltrial AFL: &cat:
~:f .m anatomically guldcd approach. Circulrtion
IYU!:
‘YI:2H(U-I4
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