(Circulation. 1998;98:1837-1841.)
© 1998 American Heart Association, Inc.
Brief Rapid Communication |
Comparison Between Left Ventricular Electromechanical Mapping and Radionuclide Perfusion Imaging for Detection of Myocardial Viability
From the Washington Hospital Center, The Cardiology Research Foundation, Washington, DC.
Correspondence to Martin B. Leon, MD, Director, Cardiovascular Research, Washington Cardiology Center, 110 Irving St NW, 4B-1, Washington, DC 20010.
Abstract
Background—A novel 3-dimensional left ventricular (LV) mapping system uses low-intensity magnetic field energy to determine the location of sensor-tipped electrode catheters within the LV. Using this system, we sought to distinguish between infarcted, ischemic, and normal myocardium by comparing LV electromechanical mapping data with myocardial perfusion imaging studies.
Methods and Results—Unipolar voltage potentials and local endocardial shortening (LS) were measured in 18 patients (mean age, 58±12 years) with symptomatic chronic angina having reversible and/or fixed myocardial perfusion defects on single photon emission computed tomography imaging studies using 201Tl at rest and 99mTc-sestamibi after adenosine stress. Overall, a significant difference in voltage potentials and LS values was found between groups (P<0.001 for each comparison by ANOVA). The average voltage potentials (14.0±2.0 mV) and LS values (12.5±2.8%) were highest when measured in myocardial segments (n=56) with normal perfusion and lowest (7.5±3.4 mV and 3.4±3.4%) when measured in myocardial segments with fixed perfusion defects (n=20) (P<0.0001). Myocardial segments with reversible perfusion defects (n=66) had intermediate voltage amplitudes (12.0±2.8 mV, P=0.048 versus normal and P=0.005 versus fixed segments) and LS values (10.3±3.7%, P=0.067 versus normal and P=0.001 versus fixed segments).
Conclusions—In patients with myocardial ischemia, LV mapping, compared with myocardial perfusion imaging, shows (1) mild reduction of endocardial voltage potentials and LS in segments with reversible perfusion defects and (2) profound electromechanical impairment in segments with fixed perfusion defects. Thus, such an LV mapping procedure may allow the detection on-line of myocardial viability in the catheterization laboratory.
Key Words: mapping • ventricles • myocardium • ischemia
A novel left ventricular (LV) mapping system (Biosense Inc) uses low-intensity magnetic field energy to determine the location of sensor-tipped catheter electrodes within the LV.1 2 3 On the basis of previous experimental and human studies correlating the extent of myocardial ischemia with the amplitude of electrical signals,4 5 6 7 we hypothesized that such an integrated LV electromechanical mapping system could be used to distinguish healthy from infarcted or ischemic myocardium on the basis of the extent of electromechanical endocardial signals. If this hypothesis is confirmed, the ability to detect on-line myocardial viability in the catheterization laboratory may be feasible.
The present study attempted to distinguish between infarcted, ischemic, and normal myocardium by comparing LV electromechanical mapping data with myocardial perfusion imaging studies using the dual-isotope technique in symptomatic patients with coronary artery disease.
Methods
Patients
To be included in the study, patients had to have (1) chronic
ischemic coronary syndrome associated with class III or
IV angina, (2) reversible and/or fixed myocardial perfusion defects on
single photon emission computed tomography (SPECT) imaging, (3)
significant coronary artery obstruction documented by
coronary angiography, and (4) LV ejection fraction 
40%.
Exclusion criteria included peripheral vascular disease,
aortic stenosis, unstable ischemic syndrome on
intravenous nitrates or heparin drugs, atrial fibrillation,
LV thrombus, and contraindication to adenosine administration.
Informed consent was obtained from all patients before any
diagnostic procedures.
Mapping System
As described previously,1 2 3 the
electromechanical mapping system uses (1) a triangular location pad
with 3 coils generating ultralow magnetic field energy, (2) a
stationary reference catheter with a miniature magnetic field sensor
located on the body surface, (3) a navigation sensor mapping catheter
(7F) with deflectable tip and electrodes providing endocardial signals,
and (4) a workstation for information processing and 3-dimensional LV
reconstruction.
Mapping Procedure
The patients were heparinized (70 U/kg). The mapping catheter
was advanced under fluoroscopic guidance to the descending thoracic
aorta, its tip was deflected to form a J shape, and it was introduced
across the aortic valve into the LV. Once inside the LV, the tip
deflection was released, and the initial 3 points outlining the
boundaries of the LV (apex, aortic outflow, and mitral inflow) were
acquired with fluoroscopic guidance. Subsequently, no fluoroscopy was
needed to acquire additional sampled points throughout the LV. The
operator acquired points only when the catheter tip was stable on the
endocardium, as evidenced by local activation time stability, location
stability, loop stability, and cycle-length
stability.1 2 3 The system uses a triangular
algorithm to reconstruct the LV anatomy, which is
presented in real time on a Silicon Graphics workstation. By
setting a "triangle fill threshold" value, the operator chose the
size of triangles, for which the program closes a "surface" on the
reconstructed chamber. This feature allowed the operator to determine
the degree of the system interpolation between actual data points and
ensured that a minimal level of point density was met at each mapped
region. All maps were acquired with an interpolation threshold of
40 mm between adjacent points. Once all endocardial regions were
represented on the map, the operator completed the
reconstruction of the LV map, and the catheter was removed from the
LV.
Electromechanical Data
From the electrical data, a color-coded unipolar voltage map (in
mV) was generated. From the mechanical data, regional
contractility was obtained by use of the local
endocardial shortening (LS) formula:
LS(p)=
[Li(ED)-Li(ES)/Li(ED)]x100;
LS(p) denotes the average LS of a point (p) relative to all its
endocardial neighboring points, and Li(ED) and
Li(ES) are the distances of an index point from
its neighbors at end diastole and end systole,
respectively. The LS(p) value is a ratio that becomes larger as the
distance between the neighboring sites decreases during end systole.
Conversely, the LS becomes smaller (or even negative) if regional
contractility is reduced or becomes paradoxical.
A fixed cylindrical polar reference coordinate map (regional view map)
was defined with anatomic reference points acquired at end
diastole (Figure 1
). The
"center of mass" of the reconstructed LV chamber was automatically
calculated by the system from the set of endocardial points sampled.
The long axis of the LV was defined as the line connecting the apex
(the most distal point from the center of mass) and the center of mass.
The long axis was divided into 3 segments: apex, midventricle, and
base, consisting of 20%, 40%, and 40% of the long-axis length,
respectively. Thus, the longitudinal location of each endocardial site
was determined on the basis of its projection on the long axis. The
midventricular and base segments were further divided into
4 regions: anterior, septal, inferoposterior, and lateral (Figure 1).
Thus, in total, endocardial sites were divided into 9 regions for
comparative analysis with nuclear imaging data.
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Myocardial Perfusion Imaging
All patients underwent myocardial perfusion imaging with the
SPECT technique. Dual-isotope imaging was performed with
201Tl for rest and 99mTc
sestamibi for stress imaging. Under resting conditions, 3 mCi of
201Tl was administered intravenously.
Patients were then positioned in a standard SPECT camera in the supine
position, and rest imaging was performed beginning 15 minutes after
thallium injection. After completion of acquisition of the rest images,
subsequent imaging was performed using pharmacological stress with
adenosine administration. Adenosine 140 µg ·
kg-1 · min-1 was
administered with constant monitoring of heart rate and rhythm and
blood pressure. 99mTc sestamibi was administered
at peak vasodilator effect (at 4 minutes of a 6-minute
adenosine infusion). Heart rate, rhythm, and blood pressure
were monitored for at least 7 minutes after completion of vasodilator
infusion. Stress imaging was performed beginning 60 minutes after
sestamibi injection. In patients with a suspected or objectively
determined irreversible perfusion defect, who might have reduced
perfusion at rest to viable tissue, redistribution images of the rest
thallium data were performed. This was achieved by a second acquisition
of thallium data at 3 to 4 hours to represent redistribution
activity. After the rest-redistribution thallium study, the patient
underwent stress imaging as indicated above.
The cardiac images were oriented in standard orthogonal views. Images were read by an experienced operator who was unaware of LV electromechanical mapping data. A 9-segment model was used for analysis in which the short-axis slices were selected for interpretation, representing basilar, midventricular, and apical levels of the LV. The mid and basilar short-axis slices were subdivided into 4 segments representing the anterior, anteroseptal, inferoposterior, and lateral regions, similar to the subdivision obtained by the LV electromechanical mapping. A qualitative assessment for these 9 segments (normal, reversible defect, fixed defect) was performed for both the rest thallium and stress sestamibi data sets.
A comparative analysis of the myocardial perfusion images in relation to LV electromechanical data was performed using calculated average voltage and LS values in each myocardial segment defined as having normal, reversible, or fixed perfusion defects.
Statistical Methods
All data are presented as mean±SD. Means of nominal
values (voltage and LS) were compared between myocardial segments with
normal, reversible, or irreversibly fixed perfusion by ANOVA.
Intergroup comparison was made by t test with Bonferroni
correction. A value of P<0.05 was considered statistically
significant.
Results
Eighteen patients (14 men, 58±12 years old) were studied. The
majority (n=16) had class III angina. Six patients had previous
myocardial infarction, and the majority had prior
revascularization procedures (10 patients with
prior angioplasty and 12 with prior coronary bypass). No
procedural complications were noted during or after the mapping
procedure. Of 162 myocardial segments, 132 were available for
comparative analysis. In 30 segments, no definite
interpretation could be made because too few (<3) sampled points were
taken during the electromechanical mapping procedure. The
Table summarizes the electromechanical
mapping data obtained in examined segments grouped according to the
results of the perfusion study. As shown in the Table, an overall
significant difference in voltage potentials and LS values was found
between groups (P<0.001 for each comparison by ANOVA). The
average voltage potentials (14.0±2.0 mV) and LS values (12.5±2.8%)
were highest when measured in myocardial segments with normal perfusion
(n=56) and lowest (7.5±3.4 mV and 3.4±3.4%) when measured in
myocardial segments with fixed perfusion defects (n=20). Myocardial
segments with reversible perfusion defects (n=66) had intermediate
voltage amplitudes (12.0±2.8 mV, P=0.048 versus normal and
P=0.005 versus fixed segments) and LS values (10.3±3.7%,
P=0.067 versus normal and P=0.001 versus fixed
segments). A representative LV voltage map is shown in
Figure 2.
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Discussion
In a previous study, we found that electromechanical mapping can
distinguish infarcted myocardium from noninfarcted zones by
simultaneous reduction in electrical and mechanical
activity.8 However, this preliminary experience
lacked a comparison with radionuclide perfusion imaging studies to
validate the assessment of myocardial viability. Thus, in the
present study, we performed a comparative analysis between
LV electromechanical mapping data and radionuclide perfusion imaging to
differentiate between infarcted, ischemic, and normally
perfused myocardium. Our results show (1) a moderate
(
15%) reduction in endocardial potentials and LS in segments with
reversible perfusion defects and (2) a profound electromechanical
impairment in segments with fixed perfusion defects. These results may
indicate that such LV mapping may be useful for detecting myocardial
viability in the catheterization laboratory on the
basis of measurements and localization of electromechanical
signals.
Assessment of Myocardial Viability
In treating patients with coronary artery disease, it is
essential to determine the extent of myocardial damage and
ischemic burden to determine which patients would benefit most
from revascularization.9 At
present, the extent and severity of myocardial ischemia in
coronary artery disease are assessed by use of noninvasive
myocardial imaging modalities such as nuclear scintigraphy,
PET imaging, or stress
echocardiography.9 Previous
studies have identified profound
electrophysiological alterations after
experimental induction of acute or chronic myocardial
ischemia.10 11 Electrical signals derived
from ischemic and/or infarcted endocardial regions can be
measured to differentiate between normal, necrotic, and
ischemic myocardium.4 5 6 7 The
combination of electrical recordings with mechanical data,
using the location sensors, seems to be a novel approach for on-line
quantitative assessment and localization of myocardial
viability.8 Larger clinical studies are necessary
to test whether the use of such electromechanical mapping procedures
may indeed serve as a novel diagnostic tool for on-line
detection and precise localization of myocardial viability.
Limitations
First, in this study, the sampled population was relatively small.
Nevertheless, the segmental analysis method allowed us to
obtain relatively large samples for comparative assessment. Second, the
regional analysis that was performed in the present study
may limit the resolution accuracy of the mapping data due to the
"smearing" (ie, averaging) effect of sampled points with different
characteristics within the same region. An additional limitation is the
use of somewhat "oversimplistic" assessment of voltage amplitudes
as the only measure of myocardial electrical activity. Future
algorithms incorporated within the LV mapping system will allow the
evaluation of other electrical measures, such as the electrical signal
duration and the ratio of voltage to duration. These measures may
enhance the accuracy of the mapping system for detecting
ischemic areas manifested by subtle changes in the electrical
activity.
Acknowledgments
This study was supported by a grant from the Cardiology Research Foundation, The Washington Cardiology Center, Washington, DC.
Received June 3, 1998; revision received August 11, 1998; accepted August 31, 1998.
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