From Washington Hospital Center, Washington, DC, and The Bruce Rappaport
Faculty of Medicine, Technion Institute, Haifa, Israel (L.G., S.A.B.).
Correspondence to Martin B. Leon, MD, Washington Cardiology Center, 110 Irving St NW, 4B-1, Washington, DC 20010. E-mail MBL1{at}mhg.edu
Methods and Results—Measurements of LV endocardial unipolar (UP)
and bipolar (BP) voltages and local endocardial shortening were derived
from dogs at baseline (n=12), at 24 hours (n=6), and at 3 weeks (n=6)
after occlusion of the left anterior descending coronary
artery. Also, 12 patients with prior myocardial infarction (MI) and 12
control patients underwent the LV endocardial mapping study for
assessment of electromechanical function in infarcted versus healthy
myocardial regions. In the canine model, a significant decrease in
voltage potentials was noted in the MI zone at 24 hours (UP, 42.8±9.6
to 29.1±12.2 mV, P=0.007; BP, 11.6±2.3 to 4.9±1.2 mV,
P<0.0001) and at 3 weeks (UP, 41.0±8.9 to 13.9±3.9
mV, P<0.0001; BP, 11.2±2.8 to 2.4±0.4 mV,
P<0.0001). No change in voltage was noted in zones
remote from MI. In patients with prior MI, the average voltage was
7.2±2.7 mV (UP)/1.4±0.7 mV (BP) in MI regions, 17.8±4.6 mV
(UP)/4.5±1.1 mV (BP) in healthy zones remote from MI, and 19.7±4.4 mV
(UP)/5.8±1.0 mV (BP) in control patients without prior MI
(P<0.001 for MI values versus remote zones or control
patients). In the canine model and patients, local endocardial
shortening was significantly impaired in MI zones compared with
controls.
Conclusions—These preliminary data suggest that infarcted
myocardium could be accurately diagnosed and distinguished
from healthy myocardium by a reduction in both electrical
voltage and mechanical activity. Such a diagnostic
electromechanical mapping study might be clinically useful for accurate
assessment of myocardial function and viability.
A new 3-dimensional cardiac mapping procedure (Biosense) offers
a unique mode of assessing myocardial function by obtaining and
integrating electrical and mechanical signals from the left
ventricular (LV) endocardial surface using a catheter-based
navigational system.3 4 5 The information derived
by this LV mapping system regarding cardiac mechanics and electrical
properties has recently been validated in animal
models.3 4 5 Quantitative in vivo assessment of
these electromechanical signals might reflect the status of myocardial
viability, because myocardial necrosis is expected to cause a decrease
in both electrical and mechanical functions.
The purpose of this study is to provide preliminary animal and clinical
data to support the use of such integrated electromechanical signals in
distinguishing infarcted from healthy myocardial regions. The
distinction between normal and infarcted myocardial regions was studied
in animals and patients with prior myocardial infarction (MI) and in
control subjects.
Electromechanical Mapping Study
By setting a "triangle fill threshold" value, the operator chooses
the minimum triangle size for which the program will close a face on
the reconstructed chamber. This feature allows the operator to
determine the degree to which the system will interpolate between
actual data points and will ensure that a minimal level of point
density will be met at each mapped region. All maps were acquired with
an interpolation threshold of 40 mm between adjacent points. The
3-dimensional LV endocardial reconstruction is updated in real time
with the acquisition of each new site and displayed continuously on a
Silicon Graphics workstation.
Postprocessing Analysis
1. The first LS function is based on calculation of differences in
surface areas of adjacent triangles around an index point during end
systole. This function is called triangular local shortening (TLS), and
its equation is
TLS(p)=
2. Additional LS function was used to assess regional
contractility. This function quantifies regional wall
motion by calculating the fraction of linear distances of each
endocardial point from its neighboring points at end systole, relative
to end-diastolic distances. This function is called linear
local shortening (LLS) and uses the following equation:
LLS(p)=
Myocardial areas that manifested both high electrical signals (UP
endocardial voltage
Animal Study
Clinical Study
Comparison of Mapping Findings With Echocardiography
Statistical Methods
Clinical Study
Comparison With Echocardiography Findings
Regression Analysis for the LS Function
Rational for Use of Voltage Potential to Assess Myocardial
Function
Findings of the Study
The clinical findings showed a distinct difference in measured
endocardial voltage between the infarcted and noninfarcted myocardial
regions. Myocardial regions with previous MI were characterized by low
electrical voltage amplitude and by impairment of regional
contractility. The magnitude of electrical impairment
in the infarct zones was even more apparent among patients than in the
canine model. This might reflect enhanced collateral supply to the
infarct zone in the canine compared with the human heart. Also, most of
the human MIs were old infarcts, and the difference between the
measured electrical potentials (human versus canine study) could be
related to time since the infarct. Electromechanical uncoupling
(preserved electrical activity and impaired mechanical activity) was
observed in other regions. The significance of such findings in
noninfarcted regions with impaired mechanical activity and preserved
electrical function remains to be investigated. In particular, it
should be determined whether such areas reflect ischemic or
hibernating myocardial zones. Because this is a preliminary clinical
experience, our study lacked comparative nuclear imaging data to
validate those findings.
In our study, both UP and BP ECG recordings were used for
analysis. Previous studies have shown that the BP
recording might be more accurate in reflecting local changes in
electrical activity because it is less likely to be influenced by
contact stability, electrode size, and "far-field" electrical
potentials.14 On the contrary, the magnitude of
the BP signal might vary according to the orientation of the tip
electrode toward the endocardial surface. In our canine study, the
extent of reduction in voltage tended to be more pronounced with BP
than with UP recordings.14 Although both
UP and BP recordings could clearly identify the presence of MI
in this study, it is unclear at that stage which of the 2 methods would
be more accurate to detect subtle changes in local electrical activity
to differentiate between normal, ischemic, and infarcted
myocardium.
Limitations and Future Directions
Because LV electromechanical mapping is an invasive procedure, safety
must be carefully examined from larger clinical experiences. At
present, catheter design is in a rapid stage of evolution to
improve torque response, tip deflection, endocardial contact stability,
and tip configuration to reduce surface trauma. Ultimately, with
optimized catheter design and proper physician training, this procedure
should permit the routine safe acquisition of LV endocardial mapping,
which may enhance our understanding of intramyocardial detection of
viability among patients.
Conclusions
Received February 16, 1998;
revision received March 24, 1998;
accepted April 21, 1998.
© 1998 American Heart Association, Inc.
Basic Science Reports
Preliminary Animal and Clinical Experiences Using an Electromechanical Endocardial Mapping Procedure to Distinguish Infarcted From Healthy Myocardium
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—A catheter-based left
ventricular (LV) endocardial mapping procedure using
electromagnetic field energy for positioning of the catheter tip was
designed to acquire simultaneous measurements of
endocardial voltage potentials and myocardial
contractility. We investigated such a mapping system to
distinguish between infarcted and normal myocardium in an
animal infarction model and in patients with coronary
artery disease.
Key Words: endocardium • myocardial infarction • electrophysiology
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
In treating patients
with coronary artery disease, it is essential to determine the
extent of myocardial damage and viability to determine which patients
would benefit most from revascularization
procedures.1 2 Currently used noninvasive
diagnostic tests to assess the extent of myocardial
necrosis (eg, nuclear imaging studies or stress
echocardiography) are based on assessment of
myocardial blood flow and function and/or metabolism and
are performed separately from the revascularization
procedure.1 2
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Electromechanical Mapping System
The mapping and navigation system comprises a miniature passive
magnetic field sensor, an external ultralow magnetic field emitter
(location pad), and a processing unit
(Biosense).3 4 5 The catheter tip incorporates
standard electrodes that allow recording of unipolar (UP) or
bipolar (BP) signals and the location sensor. Signals received by the
sensor are transmitted along the catheter shaft to the main processing
unit. The location pad is fixed beneath the operating table and
generates ultralow magnetic fields (5x10-6 to
5x10-5 T) that code the mapping space around
the chest with both temporal and spatial distinguishing
characteristics. The temporal relationship is derived from the
intracardiac recording. These fields contain the information
necessary to resolve the location and orientation of the sensor in 6
degrees of freedom. The locator pad includes 3 coils, each of which
generates a magnetic field that decays as a function of the distance
from the coil. The sensor measures the strength of the magnetic field,
thus enabling determination of the distance from each of its sources.
These distances determine the radii of theoretical spheres around each
coil. The intersection of these spheres determines the location of the
sensor in space.
The mapping catheter was introduced through an 8F or 9F femoral
sheath and placed in the left ventricle. Another reference catheter,
also with a tip sensor, was taped securely to the patient's or
animal's back. The 95% upper confidence limits of location resolution
using an external location reference is <1.1 mm. The location of
the mapping catheter was gated to end diastole and
recorded relative to the location of the fixed reference catheter
at that time, thus compensating for subject or cardiac motion. As the
catheter tip is moved over the LV endocardial surface, the system
continuously analyzes its location in 3-dimensional space
without the use of fluoroscopy. Results were collected from both UP and
BP simultaneous recordings filtered at 0.5 to 400
Hz. The stability of the catheter-to-wall contact was evaluated at
every site in real time, and points were deleted from the map if 1 of
the following criteria was met: (1) a premature beat or a beat after a
premature beat; (2) location stability, defined as a difference of
>5 mm in end-diastolic location of the catheter at 2
sequential heartbeats; (3) loop stability, defined as an average
distance of >5 mm between the location of the catheter at 2
consecutive beats at corresponding time intervals in the cardiac cycle;
(4) cycle length that deviated >10% from the median cycle length; (5)
different morphologies of the local ECG at 2 consecutive beats; (6)
local activation time differences of >5 ms between 2 consecutive
beats; and (7) different QRS morphologies of the body surface ECG.
UP and BP endocardial potentials from each sampled point were
recorded from the tip electrode, and electrical maps were obtained
by displaying the voltage potentials on a graded color scale. An
additional endocardial map was then reconstructed to represent
local shortening (LS). This function calculates the fractional
shortening of regional endocardial surfaces at end systole and uses
color scales to highlight areas with different myocardial
contractility. Two different formulas were used to
compile the LS function. 
Ai(ES)/Ai(ED)x100.
In this equation, TLS(p) is the displayed LS of a point p that defines
the area around that mapped point at end systole, normalized to the
area around that point at end diastole (which has been
arbitrarily normalized to 100%). The end-diastolic timing
was determined at the peak of the R wave in the surface ECG. Ai is the
surface area of the neighboring areas derived by triangular connections
between neighboring points. TLS is defined as 100% for every point at
end diastole. On the basis of our preliminary animal
experiments in 12 normal dog hearts, the mean and upper 95% confidence
limits of TLS were 67% and 79%, respectively. Therefore, the TLS was
estimated as (1) <80%, the surface area around the point is normally
decreasing in size during systole; (2) 80% to 100%, the surface area
around the examined point is abnormally decreasing in size during
systole (hypokinesis); and (3) 
100%, no change or paradoxical
increase in the surface area around the examined point during systole
(akinesis or dyskinesis). [Li(ED)-Li(ES)/Li(ED)]xW(i)x100.
LLS(p) denotes the average LS of a point (p) relative to all its
endocardial neighboring points; Li(ED) and
Li(ES) are the distances of an index point from
its neighbors at the end of diastole and systole,
respectively. The LLS(p) value is a ratio that becomes larger as the
distance between the neighboring sites decreases during end systole.
Conversely, the LLS becomes smaller (or even negative) if the
contractility is reduced or has become
paradoxical at the examined point. Also, to minimize potential
"noise" generated by points that are too close (ie, their relative
motion is smaller than the location accuracy of the system) or too
distant (ie, their relative motion might be affected by more than a
single region of interest), the algorithm uses a "weight function"
[W(i) in the LLS equation] to filter the impact
of these points (<5 or >12 mm) from the average LS calculation.
The weight function thus depends on the density of sampled points and
the volume of the heart in addition to its dependency on the distances
between points at end diastole. During end systole, the LLS
is estimated as (1) >12%, the average distances around an examined
point are normally decreasing in size; (2) 8% to <12%, mild
impairment in the relative motion (ie, contractility)
of neighboring points relative to the index point; (3) 4% to <8%,
moderate impairment in the relative motion of neighboring points
relative to the index point; (4) 0 to <4%, severe impairment in the
relative motion of neighboring points relative to the index point (ie,
signifying severe regional hypokinesis or akinesis); and (5) <0%,
paradoxical increase in the distances between neighboring points during
systole (ie, dyskinesis). 10 mV and BP endocardial voltage 2 mV in
humans; UP endocardial voltage 25 mV and BP endocardial voltage 5
mV in dogs) and normal LS (TLS <80% and LLS 12% in humans and
dogs) were interpreted to represent normal myocardial function.
Areas with impaired electrical activity (UP voltage 
10 mV and BP
voltage <2 mV in patients; UP voltage <25 mV and BP voltage <5 mV in
dogs) and impaired mechanical function (TLS 80% and LLS <8%) were
interpreted to represent abnormal electromechanical properties
in MI areas. If the mechanical behavior was impaired and different from
what was expected from the normal electrical activity
(electromechanical uncoupling), the area of interest was suspected to
represent a hibernating myocardial region.
The animal study was designed to detect electromechanical
changes occurring after coronary occlusion in dogs. Dogs were
used for this study because they have extensive coronary
collateral circulation and can tolerate myocardial ischemia and
infarction. The animal model was an open-chest left anterior descending
coronary artery (LAD) occlusion model. After
anesthesia, a left thoracotomy and exposure of the heart
obtained access to the LAD, and the infarction was produced by suture
ligation of the mid-LAD, between the first and second diagonal
branches. The 2 experimental groups underwent LAD ligation, and
electromechanical mapping was obtained at baseline, after 24 hours
(group 1; n=6), and after 3 weeks (group 2; n=6). In each map, UP and
BP electrical voltage and TLS and LLS values were obtained by the
mapping system at the occluded LAD zone (anterior and/or apical zones)
and compared with the most normal functioning remote from the MI zone
(usually inferior or posterior zones).
In 24 patients (12 with documented clinical history of prior MI
and 12 control patients without prior MI), electromechanical mapping
was obtained after the patients had given informed consent and after
routine diagnostic left heart
catheterization. The mapping catheter was advanced
under fluoroscopic guidance to the descending thoracic aorta. The
catheter tip was deflected to form a J tip, and the catheter was
advanced across the aortic valve into the left ventricle. Once inside
the ventricle, the catheter tip deflection was released, and the
initial 3 points outlining the boundaries of the left ventricle (apex,
aortic outflow, and mitral valve) were acquired with fluoroscopic
guidance. After these boundary points, no fluoroscopy was needed to
acquire points throughout the left ventricle. The chamber 3-dimensional
geometry was reconstructed in real time with 
50 to 80 endocardial
points until all endocardial regions (ie, anteroseptal, anterior free
wall, anterolateral, apex, inferobasal, inferoapical, and posterior
walls) were represented by neighboring points on the map.
After completion of the map, a thorough review of individual points was
performed to obtain only stable points and eliminate "internal"
points that might represent luminal or papillary muscle
locations.
Twelve consecutive patients had
echocardiography before the mapping procedure to
assess regional contractility by echo compared with
electromechanical mapping findings. Each LV map was divided into 6
regions (anteroseptal, anterior free wall, anterolateral, inferobasal,
inferoapical, and posterior walls). Each region was separately
analyzed for mechanical function according to the following
criteria: (1) normal, with TLS <80%; (2) hypokinetic, with TLS
between 80% and 100%; (3) akinetic, with TLS between 100 and 110%;
and (4) dyskinetic, with TLS >110%. These regional wall motion
analyses were compared with echocardiographic
assessment of the corresponding regions. The
echocardiographic data were obtained by 2 experienced
cardiologists who were unaware of the mapping findings and who read the
echo studies independently. When there was a disagreement between the 2
readings, the tapes were reviewed by both
echocardiographers, and consensus was obtained.
All data are presented as mean±SD. Means of
nominal values were compared among groups by ANOVA. Student's
t test was used for paired comparisons (post-LAD occlusion
versus baseline values in the canine study). A regression
analysis was applied to correlate between the 2 LS functions
that were used to calculate regional contractility in
the study. P<0.05 was considered statistically
significant.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
Animal Study
After LAD ligation, a significant decrease in electrical activity
over time was found in the LAD territory compared with baseline values
(UP voltage, 32% reduction in 24 hours, 42.8±9.6 to 29.1±12.2 mV,
P=0.007; 66% reduction at 3 weeks, 41.0±8.9 to 13.9±3.9
mV, P<0.0001; BP voltage, 58% reduction in 24 hours,
11.6±2.3 to 4.9±1.2 mV, P<0.0001; 78% reduction at 3
weeks, 11.2±2.8 to 2.4±0.4 mV, P<0.0001) (Figures 1
and 2,
top). This was associated with impaired mechanical activity, manifested
by abnormal LS values in the infarct zones at 24 hours compared with
baseline (99±23% versus 64±11% at baseline for TLS,
P=0.001; 1.8±1.2% versus 15.3±2.3% at baseline for LLS,
P<0.0001) and after 3 weeks (100±16% versus 65±10% at
baseline for TLS, P<0.001; 1.9±0.9% versus 14.9±2.1% at
baseline for LLS, P<0.0001) (Figures 3 and 4,
top). These values signify severe mechanical impairment (ie, regional
akinesis) in the infarct territory after LAD occlusion. Both electrical
voltage and mechanical LS functions were normal in the
nonischemic (remote) myocardial territory at 24 hours (Figures 1 through 4, bottom). By contrast, a significant but lesser impairment
in TLS and LLS was found in the zone remote from MI (inferoposterior
wall) at 3 weeks after LAD ligation (76±10% versus 66±8% for TLS,
P<0.01; 8.1±0.8% versus 12.7±2.3% for LLS,
P<0.05) with preserved electrical activity (Figures 1 through 4, bottom). These findings together suggest that
electromechanical mapping can differentiate between infarcted and
healthy myocardial regions from a reduction in both electrical and
mechanical activities. A representative canine voltage
map before and 3 weeks after LAD occlusion is given in Figure 5. The decrease in voltage potentials
compared with baseline in the occluded LAD zone (anterior wall) is
evident from this example.
View larger version (40K):
[in a new window]
Figure 1. Average UP endocardial voltage recorded from
infarct zone (top) and from remote zone (bottom) at baseline, 24 hours,
and 3 weeks after LAD occlusion in dogs.
View larger version (38K):
[in a new window]
Figure 2. Average BP endocardial voltage recorded from
infarct zone (top) and from remote zone (bottom) at baseline, 24 hours,
and 3 weeks after LAD occlusion in dogs.
View larger version (37K):
[in a new window]
Figure 3. Average TLS values (normalized to
end-diastolic values=100%) obtained from infarct zone
(top) and from healthy remote zone (bottom) at baseline, 24 hours, and
3 weeks after LAD occlusion in dogs.
View larger version (35K):
[in a new window]
Figure 4. Average LLS values at end systole obtained from
infarct zone (top) and from healthy remote zone (bottom) at baseline,
24 hours, and 3 weeks after LAD occlusion in dogs.
View larger version (66K):
[in a new window]
Figure 5. Representative BP voltage map of
canine LV at baseline (A) and 3 weeks after occlusion of LAD (B). Color
scale is set between 1 mV (red) and 8 mV (blue-purple) for both maps.
Note significant reduction in voltage amplitudes in LAD territory
(anterior wall, arrows) as manifested by red area (BP voltage 1 mV)
compared with high voltage potentials in remote inferior
wall and compared with same area at baseline.
Clinical and electromechanical data in 24 studied patients
are presented in the Table. The voltage
and LS values in the table represent the average ±SD of 7 to
12 endocardial points in each mapped region. The mean procedural time
to acquire a complete electromechanical map was 31±9 minutes.
Electromechanical mapping could clearly define normal
myocardium, as evidenced by normal voltage (10 mV by UP
and 2 mV by BP recordings) and normal LS (TLS <80% and LLS
12%). Conversely, there were areas with low voltage (10 mV by UP
and <2 mV by BP) and abnormal mechanical activity (TLS 80% and LLS
<8%), representing regions previously afflicted by MI.
The average UP voltage in the MI region was 7.2±2.7 mV, compared with
17.8±4.6 mV in normally functioning zones remote from MI and 19.7±4.4
mV in patients without prior infarction (P<0.001 for MI
values versus other zones, P=0.29 for remote versus normal
values) (Table). The average BP voltage in the MI region was 1.4±0.7
mV, compared with 4.5±1.1 mV in the remote (noninfarcted) zone and
5.8±1.0 mV among patients without prior infarction
(P<0.001 for MI values versus other zones,
P=0.17 for remote versus normal values) (Table). Likewise,
mechanical activity was impaired in the MI region compared with remote
zones in all cases when examined by both TLS and LLS functions. In all
cases, the mitral annulus area was defined by low electrical voltage
(<10 mV by UP and <2.0 by BP recording) (Figure 5A
, bottom).
There were other regions with normal voltage and impaired mechanical
activity (eg, remote zone of patients 5 and 8; Table).
Representative voltage maps of patients with and
without prior MI in different myocardial zones are shown in Figures 6 through 8.
View this table:
[in a new window]
Table 1. UP and BP Voltage, TLS, and LLS Values in Patients With Prior
Myocardial Infarction and in Control Subjects
View larger version (113K):
[in a new window]
Figure 6. LV endocardial voltage map (right anterior oblique
projection) from patient without previous MI (patient 16 in Table ).
UP recording of electrical voltage is high (25 mV) throughout
left ventricle (purple-blue-green), except for posterior wall, with a
decrease in voltage (red area, voltage amplitude 10 mV) in mitral
annulus zone (arrow).
View larger version (108K):
[in a new window]
Figure 7. LV endocardial voltage map (right anterior oblique
projection) from patient with prior inferior MI
(patient 1 in Table ); infarct zone is highlighted as area of low
voltage (10 mV), red (arrows). Yellow represents transition
zone between infarct and noninfarct zones. Blue-purple
represents areas with intact (25 mV) voltage in anterior wall
that were unaffected by infarction.
View larger version (95K):
[in a new window]
Figure 8. LV endocardial voltage map (right anterior oblique
projection) from patient with prior anterior MI (patient 2 in
Table ). Infarct zone is highlighted as area of low voltage (10 mV) in
anterior myocardial territory (arrows).
In 12 patients undergoing echocardiography,
the correlation of regional wall motion analysis by
electromechanical mapping and echocardiography was
evaluated. There were 84 regions (6 regions per patients), and the
concordance was 78% (56/72) between the 2 modalities. There was
complete concordance in the anteroseptal and anterior free wall
regions. In 10 of 72 segments (14%), the mapping showed TLS
abnormality (>80%), and the echocardiography
interpretation was normal. In another 6 of 72 segments (8%), the
mapping showed normal TLS values and the
echocardiography was read as hypokinesis. The
greatest discordance, occurring in 7 of 16 segments (42%), was in the
posterior wall, where the electromechanical map suggested impaired
mechanical function and the echocardiogram was read as normal.
A regression analysis was applied to assess the
correlation between the TLS and the LLS functions in the studied
patients. Both TLS and LLS functions were evaluated in 288 segments of
24 patient (12 segments in each patient; septal, anterior, lateral,
inferoposterior/apical, mid, and basal segments for each region). The
regression model yielded a significant correlation (r=0.68,
P<0.0001) between TLS and LLS values in the same region
with the following regression equation:
TLS(%)=97.2-1.59xLLS(%).
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
Our study has made the first attempts to use catheter position in
space throughout the entire cardiac cycle to calculate fractional
shortening together with voltage of the intracardiac ECG to make the
distinction between normal and infarcted myocardium. On the
basis of our preliminary clinical and animal experiences using such
electromechanical mapping procedures, we conclude that (1) MI can be
diagnosed and differentiated from non-MI zones by a reduction in both
electrical and mechanical activities and (2) such catheter-based
electromechanical mapping studies might be clinically useful for
real-time assessment of myocardial function in previously infarcted
versus healthy myocardial zones.
Previous animal studies have identified profound
electrophysiological alterations after
experimental coronary occlusion.6 7 8 At
the cellular level, these alterations include a marked diminution of
the resting membrane potential, the action potential amplitude, the
upstroke rate of depolarization, and the action potential
duration.9 10 11 Sustained coronary
occlusion induces a layer of surviving epicardial tissue overlying a
core of necrotic myocardium.12
Intracellular recordings from this surviving epicardial layer
showed cells with variable degrees of partial repolarization,
reduced action potential amplitude, and decreased upstroke velocity.
Monophasic action potentials recorded from ischemic
endocardial surfaces in dogs have demonstrated a progressive and
significant loss of electrical amplitude and upstroke velocity within
minutes after LAD occlusion.13 Thus, electrical
signals derived from ischemic and/or infarcted regions could
differentiate between normal, necrotic, and ischemic
myocardium and might be used as a sensitive quantitative
tool for the assessment of myocardial viability.
Our animal data suggest that the extent of myocardial damage after
infarction can be assessed from measurements of electromechanical
endocardial signals. Myocardial necrosis is reflected by a
simultaneous decrease in the measurable endocardial voltage
and LS. Mechanical dysfunction could indicate irreversible myocardial
necrosis as well as restorable ischemic or hibernating
myocardium. The distinction between the 2 scenarios may be
made by the assessment of local intracardiac voltage potentials. The
existence of electromechanical uncoupling (impaired mechanical activity
while electrical activity is intact) might signify retained myocardial
viability. With myocardial necrosis, a decrease in electrical voltage
follows the impairment in myocardial contractility,
which together signify loss of myocardial viability. In our study,
initial signs of electrical impairment in dogs (as manifested by
reduced endocardial voltage) were noted at 24 hours and more so at 3
weeks after coronary artery occlusion.
The electromechanical paradigm for distinguishing between
infarcted and healthy myocardium, with potential ability to
detect myocardial viability, should undergo further validation, first,
by comparison with established methods of assessing myocardial
viability, such as nuclear imaging tests (eg, PET scan or thallium
imaging with reinjection) or stress
echocardiography. Animal data should be correlated
with histopathology in areas of infarction/ischemia versus
normal zones. The electrical thresholds to distinguish between normal
and abnormal viability zones should be further delineated. For example,
in the posterior wall, physiological
electroanatomic "abnormalities" were commonly seen as the catheter
approached the mitral annulus area. This should be distinct from areas
with pathological alterations due to previous infarction. According to
our findings, at the present stage we cannot distinguish between
normal and small infarct zones in the posterior wall near the mitral
annulus (unless an extension of the MI to the inferobasal or the
posterolateral areas is evident in the map). Also, electrical activity
in transmural infarctions should be distinguished from nontransmural
MIs. The impact of myocardial wall thickness on measurable electrical
activity should also be defined. In addition, the effect of
antiarrhythmic and anti-ischemic drugs on measurable
electromechanical signals should be determined. Importantly, the
potential for electromechanical restoration in
ischemic/hibernating regions with electromechanical
dissociation should be studied as the true "gold standard" for
functional viability. This would necessitate larger studies with
comparative electromechanical mapping before and after
revascularization procedures (angioplasty or
coronary artery bypass graft surgery). Finally, it remains to
be determined which of the LS functions (TLS, LLS, or others) have
better accuracy in detecting subtle change in regional
contractility in response to acute or chronic
ischemic insults.
On the basis of our preliminary findings in animals and humans, LV
endocardial mapping using a new electromechanical catheter may provide
unique insights into regional and global myocardial function. Recent MI
zones could be identified by a reduction in both electrical and
mechanical endocardial activity and could be differentiated from normal
endocardial regions. The clinical utility of such
diagnostic intervention in the assessment of myocardial
function and viability will require further evaluation.
Acknowledgments
This study was supported by a grant from the
Cardiology Research Foundation, The Washington
Cardiology Center, Washington, DC.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
This article has been cited by other articles:
 |
|
 |
|
  D. J. Abrams, M. J. Earley, S. C. Sporton, P. M. Kistler, M. A. Gatzoulis, M. J. Mullen, J. A. Till, S. Cullen, F. Walker, M. D. Lowe, et al. Comparison of Noncontact and Electroanatomic Mapping to Identify Scar and Arrhythmia Late After the Fontan Procedure Circulation, April 3, 2007; 115(13): 1738 - 1746. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Takahashi, M. D. O'Neill, M. Hocini, P. Reant, A. Jonsson, P. Jais, P. Sanders, T. Rostock, M. Rotter, F. Sacher, et al. Effects of Stepwise Ablation of Chronic Atrial Fibrillation on Atrial Electrical and Mechanical Properties J. Am. Coll. Cardiol., March 27, 2007; 49(12): 1306 - 1314. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. de Silva, L. F. Gutierrez, A. N. Raval, E. R. McVeigh, C. Ozturk, and R. J. Lederman X-Ray Fused With Magnetic Resonance Imaging (XFM) to Target Endomyocardial Injections: Validation in a Swine Model of Myocardial Infarction Circulation, November 28, 2006; 114(22): 2342 - 2350. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. L. Huang, C.-T. Tai, Y.-J. Lin, B.-H. Huang, K.-T. Lee, S. Higa, Y. Yuniadi, Y.-J. Chen, S.-L. Chang, L.-W. Lo, et al. Substrate Mapping to Detect Abnormal Atrial Endocardium With Slow Conduction in Patients With Atypical Right Atrial Flutter J. Am. Coll. Cardiol., August 1, 2006; 48(3): 492 - 498. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Saeed, A. J. Martin, R. J. Lee, O. Weber, D. Revel, D. Saloner, and C. B. Higgins MR Guidance of Targeted Injections into Border and Core of Scarred Myocardium in Pigs Radiology, August 1, 2006; 240(2): 419 - 426. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Grothues, O. Wolfram, C. Fantoni, H. Boenigk, A. Götte, C. Tempelmann, H.U. Klein, and A. Auricchio Volume measurement by CARTOTM compared with cardiac magnetic resonance. Europace, January 1, 2006; 8(1): 37 - 41. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. B. Leon, R. Kornowski, W. E. Downey, G. Weisz, D. S. Baim, R. O. Bonow, R. C. Hendel, D. J. Cohen, E. Gervino, R. Laham, et al. A Blinded, Randomized, Placebo-Controlled Trial of Percutaneous Laser Myocardial Revascularization to Improve Angina Symptoms in Patients With Severe Coronary Disease J. Am. Coll. Cardiol., November 15, 2005; 46(10): 1812 - 1819. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Gyongyosi, A. Khorsand, S. Zamini, W. Sperker, C. Strehblow, J. Kastrup, E. Jorgensen, B. Hesse, K. Tagil, H. E. Botker, et al. NOGA-Guided Analysis of Regional Myocardial Perfusion Abnormalities Treated With Intramyocardial Injections of Plasmid Encoding Vascular Endothelial Growth Factor A-165 in Patients With Chronic Myocardial Ischemia: Subanalysis of the EUROINJECT-ONE Multicenter Double-Blind Randomized Study Circulation, August 30, 2005; 112(9_suppl): I-157 - I-165. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Corrado, C. Basso, L. Leoni, B. Tokajuk, B. Bauce, G. Frigo, G. Tarantini, M. Napodano, P. Turrini, A. Ramondo, et al. Three-Dimensional Electroanatomic Voltage Mapping Increases Accuracy of Diagnosing Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia Circulation, June 14, 2005; 111(23): 3042 - 3050. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Samady, C. J. Choi, M. Ragosta, E. R. Powers, G. A. Beller, and C. M. Kramer Electromechanical Mapping Identifies Improvement in Function and Retention of Contractile Reserve After Revascularization in Ischemic Cardiomyopathy Circulation, October 19, 2004; 110(16): 2410 - 2416. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Graf, M. Gyongyosi, A. Khorsand, S. G. Nekolla, C. Pirich, K. Kletter, R. Dudczak, D. Glogar, G. Porenta, and H. Sochor Electromechanical Properties of Perfusion/Metabolism Mismatch: Comparison of Nonfluoroscopic Electroanatomic Mapping with 18F-FDG PET J. Nucl. Med., October 1, 2004; 45(10): 1611 - 1618. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. W. Losordo and S. Dimmeler Therapeutic Angiogenesis and Vasculogenesis for Ischemic Disease: Part I: Angiogenic Cytokines Circulation, June 1, 2004; 109(21): 2487 - 2491. [Full Text] [PDF]
|
|
|
|
 |
|
 S.R. Underwood, J. J Bax, J. v. Dahl, M. Y Henein, A. C van Rossum, E. R Schwarz, J.-L. Vanoverschelde, E. E.v. d. Wall, and W. Wijns Imaging techniques for the assessment of myocardial hibernation: Report of a Study Group of the European Society of Cardiology Eur. Heart J., May 2, 2004; 25(10): 815 - 836. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Bolotin, F. H. van der Veen, T. Wolf, R. Shofti, R. Lorusso, S. A. Ben-Haim, and G. Uretzky Use of Novel Nonfluoroscopic Three-Dimensional Electroanatomic Mapping System To Monitor and Analyze Heart Surgery in Animal Models Chest, May 1, 2004; 125(5): 1830 - 1836. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Higa, C.-T. Tai, Y.-J. Lin, T.-Y. Liu, P.-C. Lee, J.-L. Huang, M.-H. Hsieh, Y. Yuniadi, B.-H. Huang, S.-H. Lee, et al. Focal Atrial Tachycardia: New Insight From Noncontact Mapping and Catheter Ablation Circulation, January 6, 2004; 109(1): 84 - 91. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.e. Garot, T. Unterseeh, E. Teiger, S. Champagne, B.e. Chazaud, R. Gherardi, L. Hittinger, P. Gueret, and A. Rahmouni Magnetic resonance imaging of targeted catheter-based implantation of myogenic precursor cells into infarcted left ventricular myocardium J. Am. Coll. Cardiol., May 21, 2003; 41(10): 1841 - 1846. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Chazaud, L. Hittinger, C. Sonnet, S. Champagne, P. Le Corvoisier, N. Benhaiem-Sigaux, T. Unterseeh, J. Su, P. Merlet, A. Rahmouni, et al. Endoventricular porcine autologous myoblast transplantation can be successfully achieved with minor mechanical cell damage Cardiovasc Res, May 1, 2003; 58(2): 444 - 450. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Wiggers, H. E. Botker, P. Sogaard, A. Kaltoft, F. Hermansen, W. Y. Kim, L. Krusell, and L. Thuesen Electromechanical mapping versus positron emission tomography and single photon emission computed tomography for the detection of myocardial viability in patients with ischemic cardiomyopathy J. Am. Coll. Cardiol., March 5, 2003; 41(5): 843 - 848. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Keck, K. Hertting, Y. Schwartz, R. Kitzing, M. Weber, B. Leisner, C. Franke, E. Bahlmann, C. Schneider, T. Twisselmann, et al. Electromechanical mapping for determination of myocardial contractility and viability: A comparison with echocardiography, myocardial single-photon emission computed tomography, and positron emission tomography J. Am. Coll. Cardiol., September 18, 2002; 40(6): 1067 - 1074. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Kornowski Left ventricular electromechanical mapping for determination of myocardial function and viability J. Am. Coll. Cardiol., September 18, 2002; 40(6): 1075 - 1078. [Full Text] [PDF]
|
|
|
|
|
|
E. C. Perin, G. V. Silva, R. Sarmento-Leite, A. L.S. Sousa, M. Howell, R. Muthupillai, B. Lambert, W. K. Vaughn, and S. D. Flamm Assessing Myocardial Viability and Infarct Transmurality With Left Ventricular Electromechanical Mapping in Patients With Stable Coronary Artery Disease: Validation by Delayed-Enhancement Magnetic Resonance Imaging Circulation, August 20, 2002; 106(8): 957 - 961. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Lessick, G. Hayam, A. Zaretsky, S. A. Reisner, Y. Schwartz, and S. A. Ben-Haim Evaluation of inotropic changes in ventricular function by NOGA mapping: comparison with echocardiography J Appl Physiol, August 1, 2002; 93(2): 418 - 426. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|