(Chest. 2001;120:567-572.)
© 2001
American College of Chest Physicians
Detection of Viable Myocardium by Transvenous Myocardial Contrast Echocardiography Using Harmonic Power Doppler*
Canine Model of Acute Coronary Occlusion and Reperfusion
Claudius Teupe, MD;
Masaaki Takeuchi, MD;
Jiefen Yao, MD;
Erick Avelar, MD and
Natesa Pandian, MD
*
From the Cardiovascular Imaging and Hemodynamic Laboratory, Division of Cardiology, New England Medical Center, Tufts University School of Medicine, Boston, MA. Dr. Teupe was supported by a grant from Deutsche Forschungsgemeinschaft, Bonn, Germany.
Correspondence to: Claudius Teupe, MD, University Hospital, Division of Cardiology, Theodor-Stern-Kai 7, D-60598 Frankfurt, Germany; e-mail: Teupe{at}em.uni-frankfurt.de
 |
Abstract
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Study objective: To assess whether
myocardial contrast echocardiography (MCE) using harmonic power Doppler
(HPD) in conjunction with the transvenous contrast agent SHU 563A would
be useful in detecting stunned but viable myocardium.
Design: Acute coronary occlusion (2 to 3 h) followed
by 1 h of reperfusion was created in 10 dogs in an open-chest
model.
Measurements and results: Continuous harmonic
B-mode for wall motion analysis and ECG triggered HPD for assessment of
myocardial perfusion was employed during coronary occlusion and after
reperfusion. Postmortem 2,3,5-triphenyltetrazolium chloride (TTC)
staining was performed to verify infarction. Extent of wall motion
abnormality (WMA), perfusion defect size, and anatomic infarct size
(myocardial infarction [MI]) were analyzed in a 5-segment model. All
10 dogs showed WMA in 23 of 50 segments during coronary occlusion. In
eight dogs, HPD detected perfusion defects in 18 of 50 segments. The
concordance rate between WMA and perfusion defect was 86%. Mean
linearized power (MLP) in segments with WMA was significantly lower
compared to normal segments (60.7 ± 38.9 vs 110.5 ± 108.8,
p < 0.05). After reperfusion, the extent of WMA was larger than the
area of perfusion defect (percentage of left ventricular slice area):
30 ± 13% vs 9 ± 8%, p < 0.01. Eventual infarct size was
6 ± 7%. WMAs were seen in 18 of 50 segments. TTC confirmed MI in 7
of 18 segments. MLP in segments with WMA but no MI was significantly
higher compared to segments with WMA and MI (84.5 ± 67.3 vs
13.2 ± 9.6, p < 0.01). Thus, the extent of WMA after reperfusion
was greater than the size of perfusion defect and eventual MI,
indicating the presence of stunned but viable myocardium.
Conclusion: MCE using HPD and the contrast agent SHU 563A
can demonstrate the efficacy of reperfusion, identify necrotic regions,
and aid in the recognition of stunned but viable myocardium. This
approach could be useful clinically in patients with acute MI
undergoing reperfusion therapy.
Key Words: contrast media • harmonic power Doppler • myocardial contrast echocardiography • perfusion • viability
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Introduction
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The
identification of viable myocardium in the setting of
acute myocardial infarction (MI) or chronic coronary artery disease
with impaired left ventricular function has important prognostic and
therapeutic implications. Myocardial contrast echocardiography (MCE) is
a new technique for the evaluation of myocardial perfusion. Previous
studies1
2
3
4
5
have shown that MCE is capable of defining
both risk area and infarct size during coronary occlusion and
reperfusion. Imaging of myocardial perfusion in gray-scale B-mode
echocardiography requires time-consuming postprocessing techniques,
such as image averaging, subtraction, and color encoding for better
appreciation of perfusion abnormalities. MCE using harmonic power
Doppler (HPD) offers the advantage of displaying perfusion defects
on-line in color. Power Doppler echocardiography is a very sensitive
tool for mapping the spatial distribution and the relative amount of an
ultrasound contrast agent in the microvasculature.6
7
8
9
At
low transmit amplitude, the microbubbles act as passive scatterers of
the transmitted ultrasound signal. At higher amplitude ultrasound, the
microspheres are driven into oscillation and resonance. With further
increase of power, the shells of the microspheres become leaky and
liberate free microbubbles.7
During a sequence of color
Doppler echocardiographic pulses, the signal intensity varies as
these free microbubbles are released, undergo acoustic stimulation, and
subsequently collapse. The color Doppler echocardiographic system
interprets this pulse to pulse variation as random Doppler shifts,
which is displayed as a color Doppler echocardiographic signal
depicting the localization of the contrast agent in the capillaries
(loss of correlation imaging).10
Power Doppler
echocardiographic imaging is based on the same principle as the
conventional Doppler echocardiographic technique, but displays the
intensity (number of scatterers) rather than the frequency (velocity
and direction of scatterers) of the Doppler signal, resulting in less
angle dependency.11
Contrast microbubbles exposed to
high-energy ultrasound are driven into nonlinear oscillation. As the
microbubbles oscillate, they emit ultrasound frequencies that are
multiples (harmonics) of the incident ultrasound frequency, while
tissue acts mainly as a linear scatterer. Imaging of harmonic
frequencies results in an increased signal-to-noise ratio of the
contrast agent within the myocardium. The addition of harmonic imaging
to power Doppler echocardiography reduces tissue clutter and improves
the ability to detect myocardial perfusion with contrast agents.
We investigated whether the assessment of myocardial
perfusion by MCE using HPD after IV injection of the new contrast
agent SHU 563A would be useful in detecting stunned but viable
myocardium.
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Materials and Methods
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Animal Preparation
The study protocol was approved by the
institutional animal research committee. Ten adult mongrel dogs
(mean ± SD weight, 29 ± 5 kg) were sedated with IM acepromazine
(20 to 30 mg) and anesthetized with IV sodium pentobarbital (25 mg/kg
body weight). Normal saline solution was administered during the
experiment. After intubation, the dogs received ventilation with a
volume cycle respirator. Additional anesthesia was administered during
the experiment as needed. An arterial line (7F catheter) was placed in
the femoral artery for pressure monitoring. A second 7F catheter was
introduced into the femoral vein exclusively for IV administration of
SHU 563A (Schering AG; Berlin, Germany). Continuous ECG (lead II) was
traced throughout the experiment. A median thoracotomy was performed to
open the chest, a pericardial cradle was created, and the heart was
exposed. After obtaining baseline images, the left anterior descending
coronary artery (seven dogs) or left circumflex coronary artery (three
dogs) was isolated and occluded with a silk snare, which allowed later
release and reperfusion. Lidocaine (1 mg/kg bolus followed by 0.5 mg/kg
infusion IV) was infused before coronary occlusion and reperfusion to
prevent ventricular fibrillation. After 2 to 3 h of coronary
occlusion, the snare was released. Following 60 min of reperfusion,
dipyridamole (0.56 mg/kg over 4 min) was infused to produce maximum
coronary hyperemia and images were acquired. The dogs were killed with
IV potassium chloride, and the heart was explanted. The heart was cut
into slices corresponding to the echocardiographic short-axis views and
stained in a solution of 1.3% 2,3,5-triphenyltetrazolium chloride
(TTC) [Sigma Chemical; St. Louis, MO] for measurement of anatomic
infarct size.
Contrast Echocardiography
A new, second-generation contrast agent, SHU
563A, was used for this study. SHU 563A consists of air-filled
microspheres (mean diameter of 1 to 2 µm) with shells formed by a
thin layer of a biodegradable cyanacrylate polymer. The SHU 563A
microspheres circulate in the blood pool intact for up to 10 min after
IV injection.12
Good myocardial opacification without
long-standing attenuation was achieved by administering a dose of 5 to
10 µL/kg. MCE was performed by using a phased-array system with a
transducer capable of harmonic imaging (HDI 5000 CV, probe P3–2;
Advanced Technology Laboratories, Bothell, WA). Images were acquired at
baseline, during coronary occlusion, and 60 min after reperfusion and
dipyridamole infusion. Dipyridamole increases the blood flow within the
intact microvasculature and unmasks a reduced microvascular flow
reserve in regions with myocardial necrosis, and thereby defines the
area where myocardial salvage is unlikely.4
A water bath
served as the acoustic interface between the transducer and the heart.
HPD mode with intermittent ultrasound transmission and increasing
trigger intervals (every cardiac cycle, every four cardiac cycles, and
every eight cardiac cycles) was employed for image acquisition. The
end-diastolic trigger point was individually adjusted in each dog
before contrast injection in order to diminish motion-derived color
artifacts in the myocardium, and usually selected at immediately before
the P wave. Wall motion artifacts were also reduced by selecting a
maximum wall filter. High-amplitude ultrasound (mechanical index, 1.1
to 1.3), a high frame rate, and a high pulse repetition frequency
(3,000 to 6,000 Hz) were applied in Doppler echocardiographic mode. The
focus point was positioned at the level of the posterior left
ventricular wall. The gains were optimized and kept constant throughout
the experiment. Imaging was performed in short-axis views (midpapillary
muscle level). The triggered images were recorded on videotape for
off-line analysis of perfusion defect size. Digitized triggered images
were stored on a 3.5-inch magneto-optical disk and transferred to a
stand-alone workstation for linearized power measurements.
Wall Motion Analysis
Continuous gray-scale B-mode imaging for analysis of wall
motion abnormalities (WMAs) was performed at baseline, during coronary
occlusion, and after reperfusion preceding the contrast study. The cine
loops were recorded on videotape. Hypokinetic, akinetic, or dyskinetic
segments were classified as WMAs.
Data Analysis
Wall motion, HPD, and TTC data were evaluated by
independent observers. Area of WMA, perfusion defect size, and anatomic
infarct size in corresponding short-axis slices were measured
(planimetry) and calculated as a percentage of the total left
ventricular slice area. Linear regression analysis was performed to
compare results.
A 5-segment model (1 = anterior ventricular septum,
2 = anterior lateral, 3 = posterior lateral, 4 = inferior,
5 = posterior ventricular septum) was used for segmental analysis of
WMA, perfusion defects, and anatomic infarct size in the different
myocardial segments. The concordance rate in 50 segments between WMA,
perfusion defect, and infarct by TTC staining was determined.
The mean of linearized power (MLP) per segment was also
measured in digitized HPD contrast images by tracing the area of the
segments. The MLP of a segment was automatically calculated by a
specially designed software (HDI lab 1.4; Advanced Technology
Laboratories; Bothell, WA) [Fig 1
].
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Figure 1.. Quantification of HPD signals as mean of
linearized power in five short-axis segments (R0, R1, R2, R3, R4).
Segments with reduced perfusion (example: occlusion of circumflex
coronary artery) appear dark (low MLP), while normally perfused
segments show bright power Doppler echocardiographic signals (high
MLP).
|
|
Continuous variables are presented as mean ± SD and were
compared by means of Student’s t test. A value of p < 0.05 was
considered to be significant.
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Results
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Wall motion at baseline was normal in all segments. Also MCE
showed homogenous coloration of the myocardium in all dogs reflecting a
normal myocardial perfusion in all segments.
During coronary occlusion, all 10 dogs exhibited WMAs in 23 of 50
segments. The area of WMA in the short-axis view at papillary muscle
level was 29 ± 10% of the total left ventricular slice area. MCE
demonstrated perfusion defects of varying size and location in 18 of 50
segments in eight dogs during coronary occlusion (Fig 2
). The defect size by HPD in the corresponding short-axis view ranged
from 0 to 36% (16 ± 12%) and was significantly smaller than the
area of WMA. The concordance rate between WMA and HPD by segmental
analysis was 86%. MLP in segments with WMAs was significantly lower
compared to normal segments: 60.7 ± 38.9 (range 7.8 to 159.5) vs
110.5 ± 108.8 (range 3.3 to 370.8), p < 0.05.
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Figure 2.. Short-axis views of the left ventricle during
acute occlusion of the circumflex coronary artery. Continuous harmonic
B-mode imaging (left) shows a large area of WMA in the
inferior and posterior left ventricular wall (arrows). HPD
imaging (right) after transvenous injection of SHU 563A
displays bright Doppler echocardiographic signals within the cavity and
normally perfused anterior wall and septal regions, while a large
perfusion defect is noticed in the inferior and posterior wall
corresponding to the area of WMA.
|
|
After reperfusion and dipyridamole infusion, HPD imaging showed
perfusion defects in seven dogs, while no defects were seen in three
dogs. The defect size (9 ± 8%, range 0 to 20%) was smaller
compared to the occlusion state. TTC staining verified MI in
corresponding slices in five of seven dogs with perfusion defects and
no infarction in all three dogs without defects by HPD (sensitivity
100%, specificity 60%; Fig 3
). The segmental concordance rate between perfusion defect by HPD and
TTC-determined infarction was 82% (sensitivity 86%, specificity
81%). HPD images were interpreted by two independent, equally skilled
observers. The concordance rate between the two observers in the
segmental analysis of presence and absence of perfusion defects was
86%.
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|
Figure 3.. Perfusion defect size after reperfusion of the
circumflex coronary artery by HPD imaging (left) in
comparison to anatomic infarct size by postmortem TTC staining
(right). Missing power Doppler echocardiographic signals
in the inferior wall indicate perfusion defects. Viable myocardium is
stained red by TTC, while necrotic areas appear unstained. Differences
in cavity size and left ventricular wall thickness are cause by
postmortem shrinking of the tissue.
|
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The extent of WMA (30 ± 13%, p < 0.01) was significantly larger
than the area of perfusion defect. WMAs were seen in 18 of 50 segments.
TTC proved MI in 7 of 18 segments with WMA. In 8 of 11 segments (73%)
with WMAs but without infarction, HPD showed no perfusion defects. In
segments with WMAs but no infarction, MLP was significantly higher
compared to segments with WMA and confirmed infarction: 84.5 ± 67.3
(range 6.3 to 229.1) vs 13.2 ± 9.6 (range 1.4 to 29.9), p < 0.01.
The anatomic infarct area by TTC staining ranged from 0 to 18%
(6 ± 8%) in slices corresponding to the echocardiographic
short-axis images. The correlation between perfusion defect size by HPD
imaging and the anatomic infarct size confirmed by TTC staining was
good (y = 0.9x + 3.8, r = 0.8, p < 0.005; Fig 4
).
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Discussion
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Our study demonstrates that MCE using HPD imaging and the new
transvenous contrast agent SHU 563A accurately depicts myocardial
perfusion defects during coronary occlusion and reperfusion on-line in
color. In combination with wall motion analysis, this technique can aid
in the detection of stunned but viable myocardium.
In the clinical setting, myocardial viability has been assessed with
various techniques such as single-photon emission CT imaging, positron
emission tomography, and stress echocardiography.13
14
15
Recently, MCE has been shown to provide accurate information about the
spatial distribution of myocardial perfusion during coronary occlusion
and reperfusion.3
16
17
18
19
MCE offers the advantage that it
is widely available and inexpensive, has an excellent spatial and
temporal resolution, and lacks the need for radiation.
We found that the area of WMA was larger compared to the size of
perfusion defect determined by HPD during coronary occlusion. Similar
findings have been reported previously from studies in animals and
humans.20
21
Collateral circulation is known to play a
important role in reducing the size of the infarction. Especially in
dogs, collaterals are well developed. These collaterals can provide a
reduced blood supply to the border zone of the area at risk, where an
intact microvasculature is still present. This blood flow carrying a
certain amount of contrast microbubbles, even when markedly reduced,
might be sufficient to be detected by the sensitive HPD
technique. On the other hand, it has been demonstrated, that a
reduction in blood flow of 80% results in akinesis, while a 95%
reduction causes systolic bulging (dyskinesis).22
Also,
color blooming from adjacent normally perfused myocardium in the border
zone may cause an underestimation of the true risk area.
After reperfusion and dipyridamole infusion, the total area of WMA did
not significantly change. While some segments in the border zone showed
little improvement in wall motion, there was considerable myocardial
stunning and intramyocardial hemorrhage with swelling of the
ventricular wall in the center of the infarction. The duration of
impaired ventricular function after ischemia can be quite prolonged.
The postischemic depression of the myocardium may persist for several
days following a brief coronary occlusion (< 15 min), which is not
enough to produce myocardial necrosis.22
23
24
In the dog,
when reperfusion is restored after a coronary occlusion time of > 20
min but < 180 min, the subendocardial portion of the region at risk
is generally found to be infarcted, whereas variable quantities of
subepicardial tissue remain viable.25
Recovery of
contractile function in this subepicardial tissue salvaged by
reperfusion may require days or weeks.23
24
26
Thus
reperfusion results in an admixture of infarcted subendocardium and
stunned subepicardium. In particular, the evaluation of a therapeutic
effect is complicated by the complex mixture of necrotic and stunned
myocardium in highly variable proportions.
Our results showed a good correlation between perfusion defect size by
HPD imaging and anatomic infarct size. Other studies using gray-scale
B-mode imaging with or without postprocessing and color encoding also
confirmed good correlation between perfusion defect and infarct
size.5
18
27
In this study, the infarcts were delineated
predominantly in the endocardium, where the greatest cell death is
expected.28
Overall, the infarcts created were relatively
small (6 ± 8%), thereby displaying the ability of this technique to
identify small endocardial perfusion defects. Infarcts in the anterior
and posterior left ventricular wall after occlusion of the left
anterior descending artery and the circumflex artery, respectively,
were depicted by HPD with the same accuracy. In the segmental analysis,
HPD revealed a sensitivity of 86% in detecting MI. When the whole
slice was analyzed, however, 100% of infarcts were detected. This
difference in sensitivity is likely due to the inability to
exactly align echocardiographic images with the anatomic slices.
Furthermore, false-positive Doppler echocardiographic signals can be
caused by motion artifacts. Ultrasound attenuation especially in the
lateral and posterior segments may result in false-negative Doppler
echocardiographic signals.
The power Doppler echocardiographic signal intensity in a certain
region of interest can be quantified by MLP measurement. In this study,
myocardial segments with stunned but viable myocardium exhibited a
significant higher MLP compared to necrotic segments. The higher MLP in
viable segments indicates the presence of contrast microbubbles. Since
microbubbles demonstrate the same rheology than RBCs,29
higher MLP values reflect an intact microvasculature that provides
blood flow to this segments. Therefore, regional analysis of MLP aids
in the discrimination between stunned but viable and infarcted
myocardium.
Study Limitations
Optimal imaging conditions were obtained in an open-chest model
using epicardial echocardiography. Thus, we could not determine whether
these findings can be applied to transthoracic imaging, where
false-positive perfusion defects due to ultrasound attenuation are more
likely. The anatomic area at risk during coronary occlusion was not
verified by other methods (ie, radiolabeled microspheres),
so that the true area of risk might have been underestimated by HPD.
However, previous studies5
18
27
in dogs have shown that
MCE is accurate in determining myocardial area at risk after injection
of a contrast agent into peripheral veins or the right atrium. Power
Doppler echocardiographic mode is known to be very sensitive to motion,
and this may cause motion-derived artifacts. However, we individually
selected the trigger point in each dog in order to minimize color
artifacts in the precontrast images. We also used a high pulse
repetition frequency and maximum wall filter to suppress artifacts due
to tissue movements.
In conclusion, MCE with HPD imaging in conjunction with wall motion
analysis can demonstrate the efficacy of reperfusion, identify necrotic
regions, and aid in the recognition of stunned but viable myocardium.
This approach could be useful clinically in patients with acute MI
undergoing reperfusion therapy.
|
Acknowledgements
|
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We thank Dr. T. Fritzsch (Schering AG; Berlin,
Germany) for his comments and technical support.
|
Footnotes
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Abbreviations: HPD = harmonic power Doppler;
MCE = myocardial contrast echocardiography; MI = myocardial
infarction; MLP = mean linearized power;
TTC = 2,3,5-triphenyltetrazolium chloride; WMA = wall motion
abnormality
Received for publication August 14, 2000.
Accepted for publication January 4, 2001.
|
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Abstract
Introduction
