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The sawtooth EKG pattern of typical atrial flutter is not related to slow conduction velocity at the cavotricuspid isthmus
Arunashis Sau, MBBS 1,2 *Markus B Sikkel, PhD 1,2 *Vishal Luther, MBBS 1,2
Ian Wright, BSc2
Fernando Guerrero, BSc 3
Michael Koa-Wing, PhD 2
David Lefroy, MBBS 2
Nicholas Linton, PhD 1,2
Norman Qureshi, PhD 2
Zachary Whinnett, PhD 1,2
Phang Boon Lim, PhD 1,2
Prapa Kanagaratnam, PhD 1,2
Nicholas S Peters, MD 1,2
D Wyn Davies, MD 1,2
* These authors contributed equally to this work
1Imperial College London, London, United Kingdom2Imperial College Healthcare NHS Trust, Department of Cardiology, London, United Kingdom3Boston Scientific, Breakspear Park, Hemel Hempstead, Herts, United Kingdom
CORRESPONDING AUTHOR:Dr Markus B Sikkel, Myocardial Function Section, Fourth Floor, Imperial Centre for Translational and Experimental Medicine, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK Tel: +44 207 594 2734; fax: +44 207 351 8145, Email: [email protected]
Word Count: 4452
Key words: Atrial flutter, rhythmia, cavotricuspid isthmus, conduction velocity,
sawtooth
Disclosures
PBL declares receipt of a research grant and speaker’s fees from Boston Scientific. FG is an employee of Boston Scientific. The other authors have no conflicts to report.
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Abstract
Introduction
We hypothesised that very high density mapping of typical atrial flutter (AFL) would
facilitate a more complete understanding of its circuit. Such very high density
mapping was performed with the Rhythmia mapping system using its 64 electrode
basket catheter.
Methods and Results
Data were acquired from 13 patients in AFL. Functional anatomy of the right atrium
(RA) was readily identified during mapping including the Crista Terminalis and
Eustachian ridge. The leading edge of the activation wavefront was identified without
interruption and its conduction velocity (CV) calculated. CV was not different at the
cavotricuspid isthmus (CTI) compared to the remainder of the RA (1.02 vs. 1.03 m/s,
p = 0.93). The sawtooth pattern of the surface EKG flutter waves were compared to
the position of the dominant wavefront. The downslope of the surface EKG flutter
waves represented on average, 73% ± 9% of the total flutter cycle length. During the
downslope the activation wavefront travelled significantly further than during the
upslope (182 ± 21ms vs. 68 ± 29ms, p<0.0001) with no change in conduction
velocity between the two phases (0.88 vs. 0.91 m/s, p=0.79).
Conclusion
CV at the CTI is not slower than other RA regions during typical AFL. The gradual
downslope of the sawtooth EKG is not due to slow conduction at the CTI suggesting
that success of ablation at this site relates to anatomical properties rather than
presence of a “slow isthmus”.
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Introduction
Typical, counter clockwise (CCW) atrial flutter (AFL) has been classically described
as cavotricuspid isthmus (CTI) dependent, with the CTI region described as the floor
of the right atrium (RA) between the inferior tricuspid annulus and the inferior vena
cava1. An area of slow conduction in the low right atrium has previously been
described, later determined to be the CTI region 2-6 . The P waves during typical AFL
have a classic saw tooth pattern on the EKG, with predominantly negative
deflections in the inferior leads. One of several possible explanations for this pattern
is slow conduction through the CTI region giving a gradual downslope, followed by
fast conduction in a caudo-cranial direction along the septal wall, seen as the sharp
upslope component of the sawtooth.1 Other possible mechanisms include left atrial
and inter-atrial septum activation7.
The RhythmiaTM mapping system (Boston Scientific) offers very high mapping
density8,9. Current 3D electroanatomical mapping systems can achieve high density
mapping, however this is often more time consuming and of a lower point density.
Rhythmia circumvents these issues using a small 64-electrode basket array catheter
(“OrionTM”). The low-impedance electrodes have a small surface area (0.4mm2)
making them highly sensitive in the detection of even the smallest bipolar potentials
(e.g. in the pulmonary veins)10,11. Mapping allows localization of anatomy and
electrograms to 1mm resolution.
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We hypothesised that high-density mapping of typical AFL would allow us to study in
more detail the relationship between the flutter circuit and conduction in the CTI
region.
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Methods
This single centre study recruited patients undergoing AFL ablation who were
mapped with the RhythmiaTM mapping system. The Institutional Committee on
Human Research at our centre approved the study.
Procedure
Femoral venous access was attained using two 7F venous sheaths and one 9F
sheath. The patients were then fully heparinized to maintain an ACT of >300 secs
throughout the procedures. A decapolar catheter was positioned in the coronary
sinus (CS) and the Orion catheter then inserted through the 9F sheath into the right
atrium.
Full details of the RhythmiaTM system, Orion catheter and the system’s electrogram
annotation have been previously described10,12. Briefly, the Orion catheter is a
minibasket catheter with 64 small (0.4mm2) low impedance electrodes arranged in 8
splines. Mapping with the Orion catheter is performed sequentially relative to timing
of a reference catheter positioned in CS. Roving the catheter allows progressive
construction of the anatomic and activation maps. While the Orion catheter is not
specifically designed for right atrial mapping, the smooth contours of the right atrium,
in our experienced, allowed excellent geometry and activation maps to be created.
The original study validating the high density mapping of the Rhythmia system in
vivo was carried out in canine right atria. 10
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A right atrial map was created prior to ablation. The geometry of the cardiac
chambers was acquired based on the location of the outer-most electrodes of the
basket using in-built magnetic and impedance sensing. Following mapping, CTI
ablation was performed with the operator’s preferred ablation catheter with the
assistance of impedance based catheter localization using RhythmiaTM. Points were
automatically and continuously annotated based on pre-assigned beat acceptance
criteria (cycle length within 10 ms, propagation reference within 5 ms, motion within
1mm, EGM stability of 75% and respiration within 5µV) with no further adjustment
made while mapping.
Mapping
The system calculated the median tachycardia cycle length over 10sec and set the
duration of the window of interest (WOI) to 100% of the observed cycle length,
centered on the timing reference electrode. The WOI was represented as a color
wheel running from red to purple, and spanning the colors of the rainbow. These
limits defaulted to red being the earliest in the window and purple being the latest.
These limits could be rotated around the color wheel, and this had the equivalent
effect of sliding the WOI without causing a full map re-compute. The annotation of
local activation time was assigned automatically by the system, based on the
maximum absolute peak of the bipolar electrogram. For electrograms with more than
1 potential, annotation was guided by the relative timings of surrounding
electrograms. Individual electrograms and their annotation of activation timing could
be studied by roving a virtual probe incorporated within system at the desired
location.
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Analysis
Analysis of the maps was performed “offline”. Each map was examined with
particular attention paid to conduction velocities and areas of apparent conduction
delay and/or block. These areas underwent detailed manual inspection of
electrograms. Procedural data was collected from RhythmiaTM and LabSystem
PROTM (Boston Scientific). Analysis of conduction velocity was performed using 2
methods. For both methods, the activation time of the wavefront was recorded using
the RhythmiaTM “wheel” (a circular interface within the software allowing the user to
move the wavefront to a specific point in the tachycardia cycle). Firstly, gross
conduction velocity was calculated. To do this the tricuspid annulus was split into
hours of the clock face, which were then combined into 4 groups of 3, defining the 4
to 7 o’clock region as the CTI. The other 3 regions were the superior RA, inter-atrial
septum and lateral wall. Wavefront activation was followed by rotating the color
wheel and tracking the leading edge of the wavefront around the cardiac chamber.
The distances travelled by the dominant wavefront path were measured. The path of
the wavefront was determined by advancing the RhythmiaTM wheel in steps. The
path was then measured using the software ruler tool (a tool allowing measurement
of length in mm along the contour of the RA), and the CV calculated. We then
obtained higher resolution measures of the CV at 8 different points around the
tricuspid valve annulus (TVA) corresponding to compass points (or 12:00, 1:30, 3:00,
4:30, 6:00, 7:30, 9:00, 10:30 on the clock-face). At the centre of each compass point,
when looking at the TVA in a left anterior oblique (LAO) view, the distance travelled
by the dominant wavefront over 5ms was measured, and subsequently the CV
determined (Figure 1 in the Data Supplement).
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The location of the wavefront was compared to the start and end of both the
downslope and upslope of the sawtooth flutter wave in EKG lead III. The time spent
in the downslope vs. upslope of the sawtooth wave was measured and the
percentage time spent in each phase calculated. The start of the downslope was
taken as the point where the upslope ended. The downslope is depicted as the red
and orange lines in Figure 1, with the green line indicating upstroke. Distance
travelled by the wavefront in each downslope and upslope was also measured using
the software ruler tool, in order to calculate CV in each phase. This was achieved by
measuring the path of the leading edge of the dominant wavefront, regardless of
where this was in relation to the TVA.
Statistical analysis was performed using paired two-tailed Student’s t-tests for
normally distributed data. One-way repeated measures ANOVA was used for
comparison of multiple parameters.
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Results
19 patients underwent mapping of the RA and ablation of AFL (89% male, mean age
68 ± 7).
13 patients were in AFL at the start of the procedure. 10 patients were in
counterclockwise (CCW) flutter, with the remainder in clockwise (CW) flutter. Patient
demographics and basic procedural data are shown in Table. 1.
An area of conduction block at the posterior aspect of the CTI between the IVC
running towards the CS os was identified by mapping wavefronts and confirmed by
the presence of electrograms with double potentials in this region in 6 (5 with CCW,
1 with CW flutter) patients. Anatomically this area was consistent with the Eustachian
ridge (ER), as shown in Figure 2A. The average distance between TVA and IVC was
37.3 ± 7.7mm, although in patients with a distinct ER the propagating wavefront
within the CTI was significantly narrower (24.92mm v 37.45mm, p=0.003) than in
those without a distinct ER.
Areas of conduction block with double potentials were found in 12 patients,
consistent with the Crista Terminalis (CT) as shown in Figure 2B. The leading edge
of the dominant conduction wavefront was defined accurately by high density
mapping and took a complex course around the right atrium, which was not
necessarily circumferential around the tricuspid annulus (Figure 3). In all patients the
conduction wavefront travelled both anteriorly and posteriorly to the SVC superior to
the line of conduction block produced by the crista. In 30% of patients with CCW
flutter, the posterior conduction wavefront reached the TA ahead of the anterior
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wavefront and was thus deemed the dominant wavefront in the flutter circuit (Figure
3).
In contrast to the widely accepted belief that the CTI is the slowly conducting isthmus
of the circuit of typical AFL, our activation and propagation maps (Figure 4 and
Movie 1 in the Data Supplement) of the flutter circuit showed consistent CV around
the circuit with no particular slowing seen at the CTI. We analyzed this further by
assessing both gross CV across the lateral, CTI, septal and superior RA and local
CV at different points on the clock face. CV was not significantly different at the CTI
compared to the remainder of the RA (1.02 vs. 1.03 m/s, p = 0.93). When patients in
CW flutter were excluded, CV was still not significantly different at the CTI (1.06 vs.
1.06 m/s, p = 0.999). As shown in Figure 5A, in CCW flutter, no region of the RA had
a significantly different gross CV. Patients in CW also had no significant difference in
CV at the CTI (0.86 vs. 0.91 m/s, p = 0.81). Manual inspection of the activation maps
revealed areas of slow conduction in each CW flutter patient, however these areas
were not common between patients. There was no significant difference in regional
conduction velocity in CW vs. CCW flutter (Figure 2 Data Supplement)
Further analysis was performed excluding CW flutter patients. Local CV was
calculated using the distance travelled in 5ms at the centre of 8 equally spaced
points on the clock face. The average local CV was 1.22 m/s. Each activation map
showed areas of slow conduction, however these were heterogenous between
patients. When all 10 patients were averaged, there was no segment of the RA with
a significantly different local conduction velocity, this is shown in Figure 5B (one-way
ANOVA comparing all segments, p = 0.75).
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The sawtooth pattern of the surface EKG in typical flutter was compared to the
position of the dominant wavefront in the circuit. The typical position of the activation
wavefront at the start of the downslope was at 9.9 ± 0.9 o’clock with 8 (of 10)
subjects starting at between 10 and 9 o’clock. At the end of the downslope, the
wavefront’s position was between 2 and 12 o’clock in all patients, 12.55 ± 0.6 o’clock
on average. Figure 3 in the data supplement shows a representative example of this.
Figure 6 shows the duration, distance travelled and conduction velocity in both
phases of the EKG. The downslope represented on average 73% ± 9% of the total
flutter cycle length (Fig 6A, downslope, 182 ± 21ms vs. upslope, 68 ± 29ms,
p<0.0001). There was no significant difference in conduction velocity during the
downslope compared to upslope (Fig 6B, 0.88 vs. 0.91 m/s, p=0.79). Therefore,
measurement of the distance covered by the wavefront during the downslope
showed a significantly longer distance covered than during the upslope (Fig 6C,
downslope, 157 ± 38 mm vs. upslope, 60 ± 24 mm, p=0.0004). In addition there was
a good correlation between distance covered by the activation wavefront and time of
the upslope/downslope (Fig 6D) confirming that distance covered and not conduction
velocity was the major factor changing between longer and shorter phases of the
sawtooth flutter wave.
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Discussion
The flutter circuit has long been thought to be contingent on slow conduction in the
CTI region1. However, using recently available very high-resolution contact maps of
the flutter circuit we have found that the CV of the dominant activation wavefront, at
the CTI region is the same as in the remaining RA. These high-resolution maps have
allowed accurate identification of the path of the dominant flutter wavefront.
Correlation with the typical EKG pattern has shown slow conduction is not the cause
of the sawtooth appearance of the P wave in the EKG of typical flutter.
Conduction velocity of the flutter circuit
Previous lower resolution mapping studies have shown slower conduction in the
region of the CTI. Olshanky et al described in 10 patients the presence of an area of
slow conduction in the low right atrium2. They used a quadripolar catheter
sequentially placed in approximately 30 sites in the RA. Feld et al, showed that
patients with AFL had significantly slowed CTI conduction velocities compared to
patients free of AFL13, they did this by pacing various sites in sinus rhythm and
calculating gross conduction velocity. Hassankhani et al used a 3D mapping system,
CARTO, to further test this hypothesis and their results agreed with the consensus
demonstrating that conduction was particularly slowed in the medial isthmus and
inferior septal areas3. They divided the TVA into 8 segments, measuring conduction
velocity within 0.5-1cm of the annulus, with a minimum of 8 points mapped around
the TVA. Sawa et al used a similar method with similar findings, using CARTO
mapping and to pick two points on a line parallel to the TA, whilst also within 15mm
of the TA4, the two points used were between 5 and 20mm of each other.
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Kinder et al used pacing and recording sites across the CTI to assess conduction
across the CTI, they did not find evidence of functional slowing or conduction delay
at faster cycle lengths or during AFL 14.
Studies using non-contact mapping have found the CTI region to have a significantly
slower CV 5,15. Schilling et al used non-contact mapping to investigate 13 patients
with AFL. They used short straight-line distances (<5mm) in the direction parallel to
wavefront propagation to calculate CV. They found that the CTI was significantly
slower than the remaining RA, however once patients with previous ablation were
removed, this difference was no longer statistically significant 16. As ablation in the
CTI region that had not fully abolished the atrial flutter circuit would be expected to
slow conduction in that area, the data excluding these patients are likely to be more
representative. Dixit et al also studied the flutter circuit using non contact mapping
and similarly found no differences in regional conduction time17.
In contrast to previous methods, high-resolution mapping has permitted accurate
identification of the dominant wavefront and leading edge at any part of the circuit. It
is possible that previous, lower resolution, studies identified regions of slow
conduction that were not part of the main flutter circuit. Previous studies have
artificially picked points close to the TA, with a wavefront direction parallel to the TA
3,4. With high-resolution mapping we were able to accurately determine the location
of the dominant wavefront, which was not always close to the TVA. Similarly,
conduction was not always parallel to the TVA. Therefore our data represents the CV
of the main flutter wavefront, whereas previous studies may have analyzed passive
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areas that were not participating in the dominant wavefront. Although our previous
studies using non-contact mapping have also shown that wavefront distance from
the TVA varies around the flutter circuit 16, the resolution of this technique was
insufficient to define the leading edge of the conduction wavefront as accurately as in
this study. Looking at the CTI region, we have found that conduction velocity of the
wavefront of atrial flutter is not significantly different from the remainder of the RA.
We have shown that an understanding of the location of the leading edge of the
activation wavefront is vital in obtaining an accurate CV at the CTI because of
conduction slowing seen at the ER in the posterior aspect of the CTI. Sampling in
this region would give the false impression of conduction slowing at the CTI.
Explanation of the classic ‘Sawtooth’ EKG pattern
Although our study accurately defines cardiac activation during the different phases
of the sawtooth flutter wave and excludes slow conduction at the CTI as the cause
for the slow downstroke in the flutter EKG it cannot explain why the sawtooth pattern
occurs in the first place. The typical flutter waveform is composed of a gradual
downslope (also known as plateau or flat phase), sharp negative component, and
upstroke (which often overshoots)1, this is depicted in Figure 1 as the red, orange
and green lines respectively. A comparison of the vector of activation during the
upslope with the surface EKG vector of lead III (Data Supp. Figure 3) shows some
correlation but this is imprecise and certainly does not explain why within a small
segment of the TA circumference (approx. 1 o’clock to 10 o’clock) the EKG vector
reverses. In fact this would be impossible if the RA was activating in isolation. The
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explanation must therefore in part relate to either activation of the LA or passive
activation of portions of the right atrium, in particular the posterior wall.
Indeed experimental studies have suggested the LA may be responsible for the
majority of the surface EKG pattern 7,18,19. Rosen et al demonstrated that rapid pacing
at the CS reproduces a sawtooth EKG similar to the typical atrial flutter 19. The typical
flutter sawtooth surface EKG pattern contains a sharp terminal negative deflection.
Using body surface mapping, Sippens, Groenwegen et al concluded that this steep
component of the downstroke corresponds to caudocranial activation of the
interatrial septum, while the medial portion of the subeustachian isthmus generated a
period of relative electrical silence 20. Bernstein et al showed that during termination
of AFL by ablation there was no sharp terminal negative component to the
downstroke, implying therefore that this component was a result of conduction past
the CTI region, into the interatrial septum and LA21. The authors concluded that the
sharp terminal negative deflection was unlikely to be solely a result of the
depolarization of the interatrial septum, given its relatively small mass in relation to
the rest of the atria. Adding further weight to this is evidence that patients’ with
previous LA ablation may have atypical surface EKG patterns when in typical CTI
dependent atrial flutter22, similarly LA enlargement or disease has been correlated
with terminal positivity of the flutter wave23. Our data showed that the terminal portion
of the downslope correlated with conduction around the interatrial septum thus
providing some support to the theory that either the interatrial septum or LA is
responsible for the sharp negative deflection of the sawtooth. Left atrial activation
therefore likely plays a major role in the genesis of the classic ‘sawtooth’ EKG
pattern.
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In broad agreement with our findings are data from Sasaki et al24. They described
four phases to the flutter wave and found that the upslope indicated conduction on
the RA Free Wall from 12 to 8 o’clock similar to our findings showing this correlated
with the wavefront between1 to 10 o’clock.
Posterior boundaries of the flutter circuit
The Crista Terminalis (CT) is generally accepted as a major component of the
posterior border of the typical flutter circuit. The use of entrainment mapping and
intracardiac echocardiography (ICE) demonstrated that areas anterior to the CT are
within the re-entrant circuit, whereas areas just posterior to it are not 25. In our study,
12 out of 13 patients had clear evidence of a CT, which appeared to be the posterior
boundary of the flutter circuit. The ER has been described as an additional posterior
boundary to the flutter circuit between the coronary sinus ostium and the inferior
vena cava 25. Nakagawa et al described the ER as a region of fixed anatomical block
26. In our study we identified 50% of typical flutter patients with a manifest ER,
potentially reducing the length of isthmus ablation required to block the flutter circuit
at the CTI. However a previous attempt at this had mixed results27, with ablation at
this site having an increased risk of AV nodal damage. in some centers, it is
possible that through more detailed mapping with the Rhythmia mapping system,
these limitations could be overcome.
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Limitations
As all patients were in AFL of obvious RA origin there was no clinical indication to
access the left atrium. We were therefore unable to perform LA maps, which may
have allowed further investigation into the contribution of LA activation to the surface
EKG in typical flutter. The broad definition of the sawtooth wave into upslope and
downslope was made because more nuanced distinction between slow (also
referred to as flat or plateau phase) and fast downslope, and brief overshoot of
upstroke could not be reliably discerned in all patients. While the manual
identification of start and end of upslope and downslope may not always be precise,
the variation due to this is unlikely to exceed a few ms and is therefore unlikely to
significantly impact on the results. Due to the novel nature of the Rhythmia mapping
system, only a small number of patients were studied. The point density of the 3D
maps varied from case to case due to operator and patient anatomy. Even the
lowest point density (52 points/cm2) is substantially more than achieved by previous
studies of the right atrium in atrial flutter.
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Conclusion
Investigation of the circuit of typical CTI dependent atrial flutter with high-density
mapping has shown that the activation wavefront in AFL has a complex path around
the TA contributed to by the functional anatomy of the RA, in particular the presence
of the Crista Terminalis and Eustachian Ridge. Within this complex path, the
conduction velocity is not significantly slower at the CTI than in other regions and
therefore the gradual downslope of the sawtooth EKG is not due to slow conduction
at the CTI. This understanding was enabled by the use of the Rhythmia mapping
system producing accurate very high-density 3D maps which helped us to better
define the direction and velocity of the leading edge of the conduction wavefront in
different parts of the right atrium and in the context of the functional anatomy of the
chamber which was also well defined using this system. The knowledge that the
established ablation target of the CTI is not associated with slower conduction also
reinforces the message that ablation of an anatomical isthmus is often important in
terminating macroreentrant tachycardias.
Acknowledgements
We would like to acknowledge the BRC, BHF and ElectroCardioMaths Programme
of the Imperial Centre for Cardiac Engineering
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Tables
Table 1. Procedural data
Case No.
Sex Age Direction Cycle length (ms)
Points on map
Volume of RA (cm2)
Surface area of RA (cm2)
Point density (points/cm2)
Time to create flutter map (mm:ss)
Points collected (points/sec)
1 M 56 CCW 204 20989 147 86 243 11:16 31.052 F 75 CCW 274 23687 221 171 138 14:17 27.643 M 69 CCW 278 11091 184 138 82 23:14 8.094 M 69 CCW 249 13199 126 105 126 16:05 13.685 M 71 CCW 250 13074 160 131 100 23:08 9.426 M 61 CCW 331 7111 154 119 60 14:35 8.137 M 74 CCW 196 10283 163 129 79 12:41 13.518 M 81 CCW 240 46157 268 120 385 38:21 20.069 M 64 CCW 240 10883 141 124 88 14:01 12.94
10 M 68 CCW 236 18509 102 105 176 16:27 18.7511 M 67 CW 256 16710 209 177 95 16:44 16.6412 M 57 CW 255 19032 182 137 139 24:30 12.9513 M 65 CW 314 7256 209 141 52 21:37 5.59
Mean 67±7
255±38 16767±10233
174±44 129±25 136±91 19:00±07:16 15±8
CW: clockwise, CCW: counter clockwise, RA: right atrium
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Figure 6
Figure 5
The upstroke and downstroke of the sawtooth flutter wave compared to conduction
velocity and distance travelled by the wavefront, in patients in CCW flutter. A, The
downstroke phase of the sawtooth flutter waveform EKG is significantly longer in
duration than the upstroke. B, There is no difference in CV between upstroke and
downstroke of the EKG. C, The flutter wavefront in the downstroke phase of the EKG
covers a significantly longer distance. D, Distance travelled by the wavefront and
duration of each phase of the EKG is correlated
30
A B
C D
Page 31
Figure legends
Figure 1
Surface EKG leads II, III and AVF showing a typical flutter waveform. This is
composed of a gradual downslope, sharp negative component, and upstroke shown
as the red, orange and green lines respectively.
Figure 2
The Eustachian ridge and Crista Terminalis in Atrial flutter. The window of interest
has been manually altered to half of the cycle length. Color wheel shown in top right.
A, Local activation time (LAT) map showing area of block and double potentials (*)
in the inferior segment of the CTI, consistent with the Eustachian ridge. B, LAT map
showing area of block and double potentials (*) at the lateral RA wall consistent with
the Crista Terminalis.
IVC: Inferior vena cava, SVC: Superior vena cava, TVA: Tricuspid valve annulus
Figure 3
Local activation time (LAT) maps showing complex activation of the flutter
wavefront. A, shows the septal wall with activation proceeding both around the TA
(red arrow) but more rapidly in a posterior direction across the free wall and over the
Crista Terminalis. B, The wavefront from the free wall enters the lateral TA region
(white arrow) ahead of the wavefront passing circumferentially around the TA (red
arrow). These images demonstrate the complex course of the flutter wavefront,
which does not necessarily take a circumferential path around the TA.
IVC: Inferior vena cava, SVC: Superior vena cava
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Figure 4
Local activation time (LAT) map showing the inferior portion of the RA, including
the CTI. Each color isochrone represents 34.75ms. There is no evident region of
slow conduction in the region of the CTI.
IVC: Inferior vena cava, SVC: Superior vena cava, TVA: Tricuspid valve annulus
Figure 5
Conduction velocity around the RA in CCW AFL. A, CV at each area of the RA in
patients in CCW AFL, B, CV at each point as defined by placing the TVA in the LAO
position, in patients in CCW AFL
NS: Nonsignificant (p >0.05)
IVC: Inferior vena cava, SVC: Superior vena cava, TVA: Tricuspid valve annulus
Figure 6
The upstroke and downstroke of the sawtooth flutter wave compared to conduction
velocity and distance travelled by the wavefront, in patients in CCW flutter. A, The
downstroke phase of the sawtooth flutter waveform EKG is significantly longer in
duration than the upstroke. B, There is no difference in CV between upstroke and
downstroke of the EKG. C, The flutter wavefront in the downstroke phase of the EKG
covers a significantly longer distance. D, Distance travelled by the wavefront and
duration of each phase of the EKG is correlated
32