Download Effect of Altered Activation Sequence on Epicardial QRST Area and

1346
Effect of Altered Activation Sequence on
Epicardial QRST Area and Refractory
Period in Dogs
Kanji Hanashima, MD; Isao Kubota, MD; Taketoshi Ozawa, MD; Takehiko Shibata, MD;
Michiyasu Yamaki, MD; Kozue Ikeda, MD; and Shoji Yasui, MD
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Background. We investigated the effects of activation sequence on cardiac surface QRST areas
and refractory periods in experiments on dogs.
Meth.ods and Results. Right and left ventricular pacings were performed, and the pacing site
was altered every 6 minutes. After 4 minutes of a given pacing, 54 unipolar electrograms
distributed over the entire cardiac surface were recorded. Next, refractory periods at electrode
sites near pacing electrodes were measured. Paired right ventricular/left ventricular (RV/LV)
pacing data were obtained six or seven times in each sample. Although the QRST isoarea maps
during the two activation orders were qualitatively similar, it was recognized consistently from
the right ventricle-left ventricle difference map that leads around the RV free wall had positive
values and that leads around the LV free wall and apex had negative values. Compared with the
same leads at RV and LV pacing, QRST areas were larger when pacing sites were near the
leads. The local QRST areas of individual leads at which we measured local refractory period
were consistently larger during drive from proximal pacing sites than during drive from distant
pacing sites. Refractory periods were consistently longer during proximal pacing than during
distal pacing, and there was a positive correlation between change in local QRST area and
change in refractory period (r=0.64) during altered activation sequence, whereas there was an
inverse correlation between change in QRST area and change in refractory period (r= -0.91)
during localized myocardial warming.
Conclusions. Both local QRST areas and local refractory periods were dependent on the
activation sequence, and there was a positive correlation between QRST areas and refractory
periods during various activation sequences compared with localized myocardial warming.
(Circulation 1991;84:1346-1353)
R) ecently, the body surface distribution of
OQRST area has been reported to be a
useful parameter in evaluating cardiac
states at high risk of ventricular arrhythmiasl-4 and in
diagnosing myocardial infarction in the presence of
intraventricular conduction disturbances.5-7 The basis for these findings is that QRST area reflects local
recovery properties and is largely independent of
ventricular activation sequence.
QRST areas have been postulated to depend on
differences in the durations of intrinsic ventricular
From the First Department of Internal Medicine, Yamagata
University School Of Medicine, Yamagata, Japan.
Supported in part by grants from the Mochida Memorial
Foundation for Medical and Pharmaceutical Research and the
Uehara Memorial Foundation.
Address for correspondence: Kanji Hanashima, MD, Nora
Eccles Harrison Cardiovascular Research and Training Institute
(CVRTI), Building 500, University of Utah, Salt Lake City, UT
84112.
Received August 29, 1989; revision accepted May 7, 1991.
recovery properties.8
Direct evidence for this relation
was shown by Abildskov et al.9 By measuring QRST
areas in cardiac surface electrograms of dogs and
determining their relation to changes of refractory
period induced by localized warming, Abildskov et al
showed that changes in QRST areas were inversely
correlated with changes in refractory periods.
In their study, Abildskov et a110"11 also found that
the QRST area was largely but not entirely independent of ventricular activation sequence. In addition,
small but definite changes in QRST area with differing activation sequences have been reported in some
studies.12-'4 Previous studies15-17 have also shown
that there are small but significant alterations of
recovery properties resulting from different electrotonic interactions during various activations.
The purpose of the present study was to investigate
the effects of activation sequence on cardiac surface
QRST distributions and to define the relation between local QRST area and local refractory period
Hanashima et al Effect of Activation Sequence
with alterations of activation sequence. These data are
essential for understanding the effects of body surface
QRST area distributions in the evaluation of heart
diseases with intraventricular conduction disturbance.
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Methods
Experiments were performed on 15 dogs initially
anesthetized with 30 mg/kg i.v. sodium pentobarbital. An intravenous infusion of 500 ml 0.9% NaCl in
H20 containing 200 mg pentobarbital was also given
slowly over the 3- or 4-hour duration of each experiment. The large anesthetic dose has been shown to
reduce spontaneous variation of ventricular repolarization properties, probably by reducing fluctuations
of autonomic nerve tone.9
Under artificial ventilation, the thorax was opened
in the fifth intercostal space, and the pericardium was
incised to form a cradle supporting the heart. The
sinus node was crushed. Bipolar stainless-steel hook
electrodes with 1.5-mm separation of poles were used
to deliver basic driving stimuli. They were attached to
the right atrium and the free walls of the right and left
ventricles. The heart was paced at a cycle of 400 msec
with a 2-msec square-wave stimuli at twice diastolic
threshold intensity. An array of 54 fine silver wire
(0.005-in.-diameter) unipolar electrodes, insulated except at their point of attachment and mounted on a
nylon sock, was stretched over the heart and anchored
near the pericardial reflection. The electrode array
had six rows (1-6) and nine columns (A through I).
Rows 1-6 were located around the heart from the
apex to the base (Figure 1).
All recording electrodes were referenced to a Wilson
central terminal and sampled every 2 msec using a
multiplexed data recording system (CD-0055, Chunichi
Denshi, Nagoya, Japan). To minimize beat-to-beat
variations in the electrograms, all recordings were
obtained with the respirator held in full expiration. The
thoracic incision was covered with a clear polyethylene
sheet, which was attached to the edges of the wound. A
surgical lamp was directed over the thorax to maintain
the cardiac surface temperature at 35 ±0.5°C. The left
ventricular pressure was monitored so that suitable
hemodynamic conditions could be maintained.
Altered Activation Protocol
Right ventricular (RV) and left ventricular (LV)
pacings were performed during each experiment.
The ventricular pacing site was changed every 6
minutes, and pairs of RV/LV pacing data were
obtained six or seven times. The right atrium was
paced simultaneously with the right or left ventricle
to avoid retrograde atrial activation. After 4 minutes
of a given ventricular pacing, all unipolar electrograms were recorded simultaneously in all dogs.
Then, in 11 dogs (dogs 5-15), refractory periods at
two sites (two epicardial sites, dogs 5 and 6) or at
three sites (two epicardial sites and one endocardial
site, dogs 7-15) were measured before changing to
the other ventricular pacing.
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QRST Area and RP
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FIGURE 1. Cardiac surface QRST isoarea maps from dog 7
during right ventricular pacing (panel A) and left ventricular
pacing (panel B) and difference map (panel C) constructed
from subtracting panel B from panel A. *Site of pacing.
Although QRST isoarea maps during two activation orders are
qualitatively similar, in the difference map positive and negative areas are located over right and left ventricles (RV and
LV), respectively. Electrode array had six rows (1-6) and nine
columns (A through I), and rows 1-6 were located around
heart from apex to base. Intervals of contour line are 200
mV. msec. LAD, left anterior descending coronary artery; 0,
zero line.
QRSTArea Calculating
The root-mean-square voltages of all 54 epicardial
leads plotted against time were used to assist in
manually selecting the onset of QRS and the end of
the T wave. QRST areas were calculated by integrating each electrogram over the QRST interval. In this
calculation, areas below the baseline were treated as
negative. The right atrium was paced simultaneously
1348
Circulation Vol 84, No 3 September 1991
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with either ventricle, and the P waves were a small
constant value included in QRST areas during both
RV and LV pacing. The activation time at each
electrode site was computed from the minimum
derivative of the QRS, which was time-referenced to
the pacing stimulus.
procedure was repeated. A period of 5 minutes of
warming at each light intensity was allowed, after
which the electrocardiogram was recorded during
simultaneous pacing of the atrium and either the
right or left ventricle. The refractory period was
determined after each electrogram was recorded.
Refractory Period Measurement
Sites. After recording the electrograms, we measured refractory periods at two epicardial sites (leads
RV and LV) in two dogs (dogs 5 and 6) and at two
epicardial sites and one left ventricular endocardial
site (lead LVE) in nine dogs (dogs 7-15).
The lead RV was located 5-10 mm from the RV
pacing site. The lead LV was located 5-10 mm from
the LV pacing site. When we selected the two
electrodes, we did not consider polarity of the QRST
area. The electrode of lead LVE used for measurement of refractory periods was constructed from
0.005-in.-diameter stainless-steel, Teflon-coated
wire. The insulation was stripped from one end of the
wire, which was formed in a hook. This plunge
electrode was placed approximately opposite the lead
LV by means of a 26-gauge needle.
Procedure. Constant-current, 2-msec, cathodal
stimuli at 1.5-fold diastolic threshold intensity were
delivered to the test site after every 10th basic RV or
LV pacing stimulus. Initially, the interval between
the 10th driving stimulus and the premature stimulus
was shorter than that required for a propagated
response. This interval was increased by steps of 1
msec until the earliest propagated response occurred. The difference between this interval and the
activation time of the test site was taken as the
refractory period.
Localized Myocardial Warning Study
In six of the 15 dogs (dogs 10-15), we examined the
effects of localized myocardial warming on local
QRST areas and local refractory period after completion of the former protocol. This examination was
performed to confirm the finding of previous reports.912 We used the same protocol they used and
examined correlations between actual value of QRST
area and actual value of refractory period and between change in QRST area and change in refractory
period. The electrodes, which had been placed at RV
and LV free walls in the previous part of the experiment, were used to deliver stimuli for ventricular
pacing. The electrode for recording electrograms and
determining refractory periods was one of the 54
electrodes mounted on the sock. It was on the
anterior surface near the septum and was selected
because it was easily warmed by directing a light
beam on it. Warming (up to 42°C) was produced by a
lamp directed through a condenser lens assembly and
a circular aperture so that a 20-mm-diameter light
spot was centered on the electrode.
Electrograms were recorded and refractory periods were measured at seven levels of light intensity.
The ventricular pacing site was changed, and this
Statistical Analysis
Average data of six or seven measurements with
paired RV/LV pacing in each dog were analyzed with
a paired t test. Data were expressed as mean+SD,
and a paired t test was used to assess significance of
difference. Probability values of less than 0.05 were
considered to indicate a significant difference.
The least-squares method of linear regression
analysis was used to determine the correlation coefficient between actual values of local QRST area and
local refractory period and changes in local QRST
area and local refractory period.
Results
Altered Activation Sequence Study
The QRST areas (n=15 dogs) and refractory periods (n = 11 dogs) for different ventricular pacings
are summarized in Table 1. The effects of altered
activation sequence on QRST areas (in 15 dogs) and
refractory periods (in 11 dogs) were similar to each
other dog's data pattern. QRST areas were larger at
leads RV and LV during proximal pacing than during
pacing at a distance. Refractory periods were longer
at leads RV, LV, and LVE during proximal pacing
than during pacing at a distance.
QRSTArea Distribution of Maps
Figure 1, which is a representative example from
dog 7, shows cardiac surface QRST isoarea maps
during RV pacing (Figure 1A) and LV pacing (Figure 1B) and the difference map (Figure 1C) constructed by subtracting the map in Figure 1B from
the map in Figure 1A. A star indicates the site of
pacing. Although the QRST isoarea maps during the
two activation orders were qualitatively similar, in the
difference map there were positive and negative
areas mainly over the right and left ventricles, respectively. This distribution of positive and negative areas
was consistent in all of the difference maps.
QRST Areas During RV and L V Pacing
Figure 2 (data from dogs 1-15) shows pairs of
average values of QRST areas for RV and LV pacing
at lead RV (Figure 2A) and lead LV (Figure 2B).
The QRST area at lead RV was 665.7±358.9
mV* msec during RV pacing and 69.7±+413.9
mV * msec during LV pacing. When paired data were
analyzed, the QRST area increased 596.0±420.8
mV* msec at the lead RV when the drive was moved
from the left ventricle to the right ventricle. This was
significant for a probability of less than 0.01.
The QRST area at lead LV was 52.5±+439.2
mV * msec during RV pacing and 710.9+389.2
Hanashima et al Effect of Activation Sequence on QRST Area and RP
1349
TABLE 1. Summary of Data
Dog
1
2
3
4
5
6
7
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8
9
10
11
12
13
14
15
n
6
6
6
6
7
7
7
7
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
6
Lead
RV
LV
RV
LV
RV
LV
RV
LV
RV
LV
RV
LV
RV
LV
LVE
RV
LV
LVE
RV
LV
LVE
RV
LV
LVE
RV
LV
LVE
RV
LV
LVE
RV
LV
LVE
RV
LV
LVE
6
6
RV
LV
6
LVE
QRST area (mV* msec)
RV pacing
LV pacing
516
115
-19
535
576
234
-183
287
180
-454
-448
192
1,032
792
13
468
1,324
367
803
1,315
393
1,042
723
1,070
916
667
348
610
.
449
188
38
368
.
.
331
12
-87
382
189
164
-222
366
.
.
.
.
.
.
641
297
404
721
.
.
181
352
92
959
785
-96
-463
1,440
.
.
.
.
978
-707
-263
964
845
-660
-568
986
...
...
Refractory period (msec)
RV pacing
LV pacing
.
.
.
.
.
149.2
133.2
164.3
158.8
182.2
174.7
195.3
175.9
154.8
171.6
158.4
158.3
162.3
160.8
139.4
176.9
158.8
149.1
160.4
168.9
147.1
171.0
170.9
141.3
172.8
151.6
159.3
165.9
135.4
140.0
141.0
162.0
177.0
186.5
200.2
164.5
169.7
176.4
155.0
162.7
166.0
157.6
146.9
179.9
155.4
163.8
164.1
160.0
150.4
173.8
167.7
152.0
178.1
149.2
165.1
168.8
183.4
168.3
191.8
178.3
176.6
199.1
Values are averages from measurements. n, Number of measurements; RV, right ventricle; LV, left ventricle; LVE,
left ventricular endocardium; RV pacing, right ventricular epicardial pacing; LV pacing, left ventricular epicardial
pacing; lead RV, lead near LV pacing site; lead LV, lead near RV pacing; lead LVE, lead on left ventricular
endocardium opposite lead LV.
mV * msec during LV pacing. When paired data were
analyzed, the QRST area increased 658.4+515.0
mV * msec at the lead LV when the drive was moved
from the right ventricle to the left ventricle. This was
significant for a probability of less than 0.01.
Refractory Periods During RV and LV Pacing
Figure 3 (data from dogs 5-15) shows pairs of
average values of refractory periods for RV and LV
pacings at lead RV (Figure 3A) and lead LV (Figure
3B). The refractory period at lead RV was
165.9+11.5 msec during RV pacing and 158±13.4
msec during LV pacing. When paired data were
analyzed, the refractory period increased 7.6±6.4
msec at the lead RV when the drive was moved from
the left ventricle to the right ventricle (p<0.01). The
refractory period at lead LV was 161.4±+13.5 msec
during LV pacing and 153.1±+12.5 msec during RV
Circulation Vol 84, No 3 September 1991
1350
A
B
lead RV
lead LV
msec
301
1500
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pacing site
RV
LV
pacing site
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FIGURE 2. Bar graphs of average values in each experiment
of QRST areas at leads RV (panel A) and LV (panel B)
during right and left ventricular pacings in dogs 1-15. QRST
area at lead RV during right ventricular pacing was significantly larger than that during left ventricular pacing, and
QRST area at lead LV during left ventricular pacing was
significantly larger than that during right ventricular pacing.
RV, right ventricle; LV, left ventricle.
pacing. When paired data were analyzed, the refractory period increased 8.3+4.2 msec at the lead LV
when the drive was moved from the right ventricle to
the left ventricle (p<0.01).
Correlation Between QRST and Refractory Period
Figure 4 shows the relation between change in
QRST area (A QRST) and change in refractory
period (A RP) (dogs 5-15). The values are averages
of six measurements during each drive; there was a
positive correlation between them (r=0.64). However, there was no correlation between actual values
lead LV
B
lead RV
A
1801
180
170
0
-v
2_
[l
-2000
-
n=
22
1000
0
1000
2000
mVmsec
delta QRST
FIGURE 4. Scatterplot of relation between change in QRST
area (delta QRST) and change in refractoy period (delta RP)
from average values in each experiment (dogs 5-15). There
was a positive correlation (r = 0.64). Regression line:
y=0.0071x-0.23; y, delta RP; x, delta QRST.
of QRST
ods using
areas and actual values
average values from six
of refractory perimeasurements.
Refractory Period of LV Endocardial Lead
The LV endocardial lead (lead LVE) was placed
approximately opposite the lead LV, which was on the
LV free wall. The refractory period (average values
from six measurements in each experiment, dogs 7-15)
at lead LVE was 178.5-+±13.1 msec during LV pacing
and 174.2±+12.1 msec during RV pacing. When paired
data were analyzed, the refractory period at the lead
LVE increased 4.3+± 1.5 msec when the drive was
moved from the right ventricle to the left ventricle
(p<0.01) (Figure 5A). Although the site at lead LVE
always had a longer refractory period than the site at
lead LV, the difference was always less during LV
pacing than during RV pacing. The difference was
19.5±11.1 msec during RV pacing and 14.7±11.9 msec
during LV pacing. When paired data were analyzed,
the difference decreased 4.7±4.0 msec when the drive
was moved from the right ventricle to the left ventricle
(p<0.01) (Figure 5B).
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>,
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as
140-
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1301
n=l1
RV
LV
pacing site
n=1 1
RV
LV
pacing site
FIGURE 3. Bar graphs of average values in each experiment
ofrefractory periods at leads RV (panel A) and LV (panel B)
during right and left ventricular pacings in dogs 5-15. Refractory period at lead RV during right ventricular pacing was
significantly longer than that during left ventricular pacing,
and refractory period at lead LV during left ventricular pacing
was significantly longer than that during right ventricular
pacing. RV, right ventricle; LV, left ventricle.
Correlation Between QRSTArea and Refractory
Period During Localized Myocardial Warming
We measured refractory period in six dogs (dogs
10-15) during localized myocardial warming. We
calculated the correlation coefficient of actual QRST
with actual refractory period and the correlation
coefficient of A QRST with A RP. Data from both
RV and LV pacings with seven light intensity levels
were analyzed. There were high negative correlation
coefficients between QRST area and refractory period with increasing light intensity during pacing of a
given site. However, the correlation between QRST
area and refractory period with increasing warming
was not as good as if data during pacings of both sites
were considered together. Correlation coefficient between actual QRST and actual refractory period
varied between -0.40 and -0.98 (average, -0.74).
Hanashima et al Effect of Activation Sequence on QRST Area and RP
A
lead LVE
200
_
_ 190
0
E
0
B
_ 50- lead LVE-lead LV
ES
between A QRST and A RP that we found with
altered activation sequence (Figure 4).
0o
Discussion
Local QRST Area During Altered
Activation Sequence
The present study demonstrated that cardiac surface QRST was not totally independent of ventricular
activation sequence. The QRST area during drive
from a near site was consistently larger than that
during drive from a distant site. Abildskov et a110
recorded body surface QRST isoarea maps of a dog
during ventricular drive from the left and right ventricles via catheter-mounted stimulating electrodes and
found that peak areas were displaced slightly toward
the stimulating electrodes. Their finding is supported
by our cardiac surface QRST area results.
40-
0. 30
0
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"
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0
160
150n=9
-
LV
pacing site
RV
1351
RV
LV
pacing site
n=9
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FIGURE 5. Panel A: Bar graph of refractory periods (average
values in each experiment for dogs 5-15) at lead LVE during
right and left ventricular pacing. Refractory period was significantly longer during left ventricular pacing than during right
ventricular pacing. Panel B: Bar graph of difference in refractory period at leads LVE and LVduring right or left ventricular
pacing. Average values in each experiment (dogs 5-15) were
plotted. Difference was significantly less during left ventricular
pacing than during right ventricular pacing. QRST area is
realized as difference in refractory period between endocardium
and epicardium. Although difference in refractory period at left
ventricular endocardium and epicardium decreased during left
ventricular pacing compared with during RV pacing, QRST
area on left ventricular epicardium (lead LV) was larger during
left ventricular pacing than during right ventricular pacing
(Figure 2). QRST area change during altered activation sequence was not explained by the relation between endocardial
and epicardial recovery properties. RV, right ventricle; LV, left
ventricle; LVE, left ventricular endocardium.
Correlation coefficient between A QRST and A RP
varied between -0.84 and -0.97 (average, -0.91).
There was a high inverse relation between A QRST
and A RP. Figure 6 shows an example of the relation
between A QRST and A RP (r= -0.96) (dog 15). This
is inverse compared with the positive correlation
localized myocardial warming
Local Refractory Period During Altered
Activation Sequence
We also found that refractory periods were altered
by activation sequence. At any lead (RV, LV, or
LVE), the refractory period during drive from a near
site was consistently longer than that during drive
from a distant site. These changes of refractory
periods between RV and LV pacings can be explained by different electrotonic interactions during
the various activation sequences.15-17 During repolarization, the ventricular site at which the depolarization wave starts can be expected to receive a depolarization effect from surrounding tissue, and the site
at which a depolarization wave terminates can be
expected to receive a repolarization effect from surrounding tissue. Therefore, ventricular pacing would
be expected to prolong the duration of the action
potential in the region near the pacing site and to
shorten it in the region far from the pacing site. Such
an electrotonic interaction can also explain other
observations: the longer refractory periods at both
LV epicardium and LV endocardium during LV
pacing than during RV pacing and the larger change
in refractory periods between RV and LV pacing at
LV epicardium compared with LV endocardium.
101
r
0-
-0.96
0
._
-10-
0
to
E -20-
0.
a_30
D
-40s
-h;u
-%JV l5
-1000
n=14
_
2000
0
1000
delta QRST (mV msec)
3000
FIGURE 6. Representative scatterplot of relation between x
(change in QRST area, delta QRST) and y (change in
refractory period, delta RP). There was an inverse correlation.
Regression line: y= -0.022x-3.3.
Relation Between QRST Area and Refractory Period
Localized myocardial warning. In experiments in
which myocardium was warmed, Abildskov et a19
found an inverse relation between QRST area and
refractory period. They attributed this to the theory
that the QRST area is determined by the difference
between recovery properties at the electrode site and
those in the remainder of the ventricles. A regional
decrease (increase) of refractory period follows the
proportional increase (decrease) of QRST area at
that region. We confirmed this negative correlation
between QRST areas and refractory periods using a
method similar to that of Abildskov.
Altered activation sequence. In contrast to the relation of change in QRST area to change in refractory
period with localized myocardial warming, this neg-
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Circulation Vol 84, No 3 September 1991
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ative relation does not hold true between changes of
QRST area and refractory period during altered
activation sequence. There was a positive correlation
(r=0.64) between A QRST and ARP (Figure 4).
During localized myocardial warming, recovery
property should change only at local myocardium,
whereas during altered activation sequence, recovery
properties of varied myocardium were expected to
have an influence. We must consider the interaction
between recovery properties at local sites and those
around local sites.
Refractory periods at endocardium and epicardium.
The relation of QRST area and refractory period to
altered activation sequence is not explained by only
local recovery property. A decrease in QRST area
would be expected if the LV epicardial refractory
period was the only factor involved. QRST area
increased during proximal pacing despite the fact
that the refractory period increased during proximal
pacing. Therefore, we examined the relation between
LV epicardial and endocardial refractory periods
(dogs 7-15). We speculated that the refractory period difference between LV endocardium and LV
epicardium would increase during pacing at LV
epicardium; however, the result was the opposite
(Figure 5B). The resulting QRST area during proximal pacing could not be explained by the relation
between LV endocardial and epicardial refractory
periods.
QRST area on cardiac or body surface has been
thought to be the difference between endocardial
and epicardial action potential configuration (polarization). QRST area could be the difference between
endocardial and epicardial action potential durations
when the magnitude of action potential does not
change. If amplitude of action potential above baseline changed, this might explain the fact that QRST
area increases with proximal pacing. Measurement of
action potential at some leads around the pacing site
will be necessary.
Definition of local site affecting electrocardiogram on
an electrode. QRST area on a electrode is theoretically equal to the difference between recovery property at the local site and that in the remainder of the
ventricle. We measured refractory period at a lead
only 0.5-1.0 cm from the pacing site to assess recovery property at the local site. However, we believe
that recovery property at a local site affecting an
electrocardiogram on an electrode is a sum of recovery property around the electrode site. It is unknown
how widely epicardium around the electrode affects
QRST area as local site information. If QRST area
was constructed from the difference between the sum
of the polarization around an electrode and the
remainder of the ventricle, it would be possible for
QRST area to be larger during proximal pacing.
Further investigation measuring many leads of refractory periods around the pacing site is necessary.
Study Limitations
In the present study, global QRST area findings
were not compared with global recovery property
because of the difficulty of measuring refractory
periods from many leads in the few critical minutes
available. However, a proper investigation of global
change in recovery property would use other parameters (e.g., activation recovery time).
In the present study, we could not find a direct
mechanism to explain the different effects of localized
myocardial warming and altered activation sequence
on the relation between QRST area and refractory
period. Further investigation, which should include
observations of the changes of action potential configuration during varied activation sequences, and many
measurements of recovery properties at many sites in
the free wall of the ventricles around the pacing site
are necessary.
Clinical Significance
The present study does not necessarily deny the
clinical usefulness of QRST areas for the assessment
of heart diseases; we found the cardiac surface
QRST isoarea maps during RV and LV pacings to be
qualitatively similar, as reported in previous studies.9,1" However, the relation between QRST areas
and refractory periods following altered activation
sequence must be taken into account. For example, if
there is a local myocardial region with prolonged
refractory period and corresponding decreased
QRST area during normal activation, the ectopic
rhythm occurring within the region may further increase the refractory period yet normalize the QRST
area.
In conclusion, there was a paradoxical relation
between QRST areas and refractory periods during
altered activation sequence. When we use body surface QRST areas in the evaluation of ventricular
recovery properties, transmural and neighboring epicardial as well as local epicardial refractory periods
must be considered.
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KEY WORDS * QRST mapping * ventricular recovery
Downloaded from http://circ.ahajournals.org/ by guest on June 15, 2017
Effect of altered activation sequence on epicardial QRST area and refractory period in
dogs.
K Hanashima, I Kubota, T Ozawa, T Shibata, M Yamaki, K Ikeda and S Yasui
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Circulation. 1991;84:1346-1353
doi: 10.1161/01.CIR.84.3.1346
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