(Circulation. 2000;102:1427.)
© 2000 American Heart Association, Inc.
Basic Science Reports |
Assessment of Coronary Stenosis Severity and Transmural Perfusion Gradient by Myocardial Contrast Echocardiography
Comparison of Gray-Scale B-Mode With Power Doppler Imaging
From the Cardiovascular Division (H.M., B.C., B.P., A.N.D.), University of California at San Diego, and the Second Department of Internal Medicine (K.O., K.M.), Kagawa Medical University, Kagawa, Japan.
Correspondence to Anthony N. DeMaria, MD, Cardiovascular Division, UCSD Medical Center, 200 West Arbor St, San Diego, CA 92103-8411. E-mail ademaria{at}ucsd.edu
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Abstract |
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Background—The present study (1) compared the ability of power Doppler imaging with that of gray-scale B-mode tissue imaging to opacify the myocardium and detect coronary stenosis by myocardial contrast echocardiography and (2) compared the response of video intensity (VI) to variable pulsing intervals for each modality.
Methods and Results—Four grades of left anterior descending coronary artery (LAD) stenoses were created in 9 open-chest dogs. Stenoses reduced resting LAD flow by 25%, 50%, 75%, and 100% of baseline by flow probe. Myocardial contrast echocardiography was performed during varying ECG gated pulsing intervals (PIs) from 1:1 to 1:10. By gray-scale imaging, background-subtracted LAD bed VI was less than baseline VI at all PIs for the 100% reduced-flow state but not for any other flow state or interval. By power Doppler imaging, LAD bed VI was less than baseline VI at all intervals for 75% and 100% reduced-flow states but only 1:1 and 1:2 for 25% and 50% reduced-flow states, respectively. Correlation of VI and myocardial blood flow (determined by use of fluorescent microspheres) ratios from stenosed versus normal beds was stronger by power Doppler imaging. A transmural opacification gradient with stenosis was visualized and measured by power Doppler imaging, but it was insignificant by gray-scale imaging. The ratio of endocardial/epicardial flow determined by use of fluorescent microspheres was correlated with VI by power Doppler imaging at all PIs.
Conclusions—Power Doppler imaging has advantages compared with gray-scale imaging in opacifying the myocardium and in detecting coronary stenosis and altered transmural distribution of myocardial perfusion from peak VI. Because VI differences from baseline at long PI vary for mild versus severe (75% and 100%, respectively) reduced-flow states, power Doppler imaging may provide a method to quantify coronary stenoses.
Key Words: echocardiography • perfusion • blood flow
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Introduction |
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Although myocardial contrast echocardiography (MCE) can be achieved after intravenous injection of microbubble agents,1 2 several technical issues remain uncertain. Controversy exists as to whether gray-scale B-mode tissue imaging or power Doppler recording is the optimal technique to perform MCE.3 4 Neither has the relationship between contrast intensity and the pulsing interval of gated images been defined for nonischemic and ischemic segments by either modality. Therefore, the present study was conducted to compare the MCE intensity levels produced by gray-scale B-mode tissue imaging with those observed by power Doppler imaging and to assess the response of each modality to variable image pulsing intervals.
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Methods |
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Animal Preparation
The study was approved by the Animal Research Committee. In 9 open-chest dogs, the heart was suspended in a pericardial cradle, and femoral artery catheters (7F) measured hemodynamics and provided blood samples. The heart was exposed through a left lateral thoracotomy and suspended in a pericardial cradle. The proximal portion of the left anterior descending coronary artery (LAD) was dissected free from the surrounding tissue, and a transit-time flow probe (series 2RB, Transonics System) connected to a digital flowmeter (model T 201, Transonics System) was placed snugly around the vessel. A custom-designed screw occluder distal to the flow probe produced graded stenoses.
Myocardial Contrast Echocardiography
Contrast was produced by the continuous infusion of 0.2 mL/min
FS-069 (Optison, Molecular Biosystems) with a gently
agitated volumetric pump. The dose was selected on the basis of pilot
experiments and was the lowest dose that provided definite visible
myocardial opacification in gray scale. Gray-scale tissue and power
Doppler images were obtained 3 minutes after initiating infusion to
ensure that myocardial opacification had reached a plateau intensity. A
latex bag filled with degassed saline functioned as an acoustic
interface between the heart and the transducer, which was positioned to
image the LAD perfusion territory.
Imaging was performed with a broad-band 4- to 2-MHz transducer (HDI5000, ATL). Second-harmonic (2-MHz transmission, 4-MHz reception), pulse-inversion, 2D gray-scale imaging and color-coded power Doppler recording were performed in the papillary muscle short-axis view during end-systolic ECG triggering. A mechanical index ranging from 1.0 to 1.3 was chosen to obtain optimal myocardial opacification. Pulse repetition frequency was fixed at 1000 Hz for power Doppler imaging. The dynamic range (50 dB), transmitting power, focus, overall gain, image depth, wall filter, and color scale were held constant for each experiment. The interval between the ECG triggers (pulsing interval) was increased from every heart beat (1:1) to every 2 (1:2), 4 (1:4), 6 (1:6), 8 (1:8), and 10 (1:10) cardiac cycles to allow incremental microbubble replenishment. Five end-systolic images were acquired at each pulsing interval, first by gray-scale imaging and then by harmonic power Doppler imaging. In power Doppler imaging, end-systolic ECG gating was adjusted before contrast injection to minimize the clutter (flash) artifact due to cardiac motion, and the same triggering phase was used in gray-scale imaging. The mechanical index and focus were same as those in gray-scale imaging, but the images were displayed in color scale.
Images acquired on S-VHS videotape before and after microbubble injection at each pulsing interval were transferred to an offline computer (Macintosh, Apple Computer Inc) and aligned for background subtraction. Images by power Doppler were converted to gray scale by using NIH Image 1.62 on the offline computer. Color was ignored, and only myocardial luminance was assessed.3 4 Myocardial video intensity (VI) was measured in gray-scale units ranging from 0 to 255 for both modalities. In this software implementation, linear gray-scale intensities are derived, and the brightest intensities in the power Doppler video image (left ventricular cavity) were assigned the highest gray-scale value. The LAD perfusion territory was identified as the transmural area of absent opacification after contrast injection during coronary occlusion. Transmural regions of interest that encompassed the LAD perfusion territory and adjacent nonattenuated area of the left circumflex (LCx) coronary artery but that excluded high-intensity signals from the endocardium-blood border were selected. Background-subtracted VI was calculated for the LAD and LCx beds to derive the ratio of LAD/LCx VI for each image. In addition, the LAD bed was bisected, and the ratio was calculated for the endocardial and epicardial halves.
MBF Measurement
Myocardial blood flow (MBF) was measured by left atrial
injection of 5x106 10-µm fluorescent
microspheres (Molecular Probes) while reference femoral artery
samples were withdrawn. After the animal was euthanized, the heart was
sliced, and the cross-sectional segment corresponding to the short-axis
image was cut into 12 wedge-shaped transmural tissue pieces, each of
which was divided into endocardial and epicardial segments. A flow
cytometer served to count microspheres. Endocardial and
epicardial MBF was calculated from the following equation:
Qm=(CmxQr)/Cr, where Qm is myocardial segment flow (mL/min), Cm is
tissue count, Qr is arterial withdrawal rate (mL/min), and
Cr is arterial reference sample count.5
Transmural MBF (mL · min-1 ·
g-1) to 12 wedge-shaped pieces was calculated as
the quotient of the summed flows to the individual segments within that
piece and their combined weight. MBF to the LAD and LCx beds, defined
by Monastral Blue dye (Sigma Chemical Co) injection, was calculated by
averaging the transmural MBF in the pieces from each bed, respectively.
The ratio of transmural MBF as well as the ratio of
endocardial/epicardial MBF was calculated in both LAD and LCx beds.
Experimental Protocol
Baseline MCE and MBF were obtained when
hemodynamic stability was achieved. Thereafter, by flow
probe guidance, the LAD diameter was progressively reduced to produce 4
levels of stenosis, which reduced LAD flow by 25%, 50%, 75%,
and 100% of the baseline value. MCE was followed by MBF measurement at
each stenosis grade. At the end of the experiment, the LAD was
occluded at the occluder site, and Monastral Blue dye was injected into
the left atrium to delineate the LAD and LCx beds. The dog was then
euthanized, and fluorescent microsphere
analysis was completed.
Statistical Analysis
Data from all animals were expressed as mean±SD. Comparisons of
hemodynamics, MBF, and VI data among the 5 flow states
were performed by ANOVA. The difference in VI produced by prolongation
of the pulsing interval between gray-scale and power Doppler
imaging was tested by paired t test. Correlations between
MBF and VI data were performed by linear regression analysis.
For differences, a value of P<0.05 was considered
significant.
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Results |
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Severity of Coronary Stenosis
Figure 1
shows measurements of LAD
blood flow by flow probe and LAD/LCx ratio of MBF by
microsphere analysis for baseline and the 4 levels of
stenosis. LAD blood flow and LAD/LCx ratio decreased
significantly and progressively from baseline with greater levels of
stenosis.
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Visual Differentiation of Severity of Stenosis by
MCE
Visual assessment of gray-scale images (Figure 2) was difficult at the 1:1 pulsing
interval because myocardial opacification was weak. The intensity of
opacification with the gray scale increased progressively with longer
pulsing intervals. Nevertheless, a clear-cut perfusion defect could not
be identified qualitatively with a 25% flow reduction. Visual
examination did reveal the presence of diminished perfusion for 75%
and 100% reduced-flow states with gating at 1:2 cardiac cycles.
However, the area and magnitude of the opacification deficit became
progressively smaller with increasing pulsing intervals. Thus, even in
the presence of total occlusion, collateral flow was sufficient to
opacify some of the at-risk myocardium if sufficient time
was provided for microbubbles to enter the area between signal
transmissions.
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Figure 3 shows images obtained by the
power Doppler method. Opacification by power Doppler imaging
was greater than that by gray-scale imaging at all pulsing intervals,
and all reduced flow states were visualized, even with gating to every
cardiac cycle. Because opacification at baseline was nearly complete
and intensity was nearly maximal (see below) at a pulsing interval of
1:2 or 1:4, identification of 75% and 100% flow-reduced states was
easier with this pulsing interval than with a pulsing interval of 1:1.
However, visual recognition of 25% reduced-flow stenosis was
more difficult at 1:4 or longer gating than at 1:1 because the VI of
the mildly obstructed LAD bed increased markedly in response to
prolongation of the pulsing interval. As with gray-scale imaging, the
perfusion defect with more marked (75% and 100%) reduced-flow states
observed by power Doppler imaging decreased in area and magnitude
with incremental prolongation of the pulsing interval. Importantly,
because collateral flow filled the at-risk myocardium at
longer pulsing intervals, the spatial distribution of the opacification
deficit was located in the subendocardial region (Figure 3).
Thus, power Doppler imaging provided clear evidence of the
predominant subendocardial distribution of perfusion deficits in the
presence of coronary stenoses.
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Myocardial VI in the Presence of Graded Coronary
Stenosis During Varying Pulsing Intervals
VI measurements of the LAD bed with gray-scale imaging
progressively increased in proportion to prolongation of the pulsing
interval (Figure 4). Although the
increase in VI was continuous to a pulsing interval of 1:10, the
magnitude of increase tended to be greater from 1:1 to 1:6 and was less
marked thereafter. The VIs of the LAD bed at 25%, 50%, and 75%
reduced-flow states were not significantly different from baseline or
from each other at any pulsing interval in gray-scale imaging. However,
total occlusion produced a significant reduction in VI from baseline at
all pulsing intervals.
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P<0.05 vs 25%. GL indicates gray levels.VI measurements with power Doppler imaging also tended to increase progressively with prolongation of the pulsing interval for all flow states, but the increase plateaued at an interval of 1:4 at baseline as well as at the 25% and 50% reduced-flow states. Therefore, although the VI of the LAD bed by power Doppler imaging was significantly decreased compared with baseline for all grades of flow reduction at pulsing intervals of 1:1 and 1:2, these differences became insignificant at pulsing intervals of 1:4 or higher for the 25% and 50% reduced-flow states. Significant differences between baseline and severe (75% and 100%) reduced-flow states continued to be observed at longer pulsing intervals: to 1:8 at 75% and 1:10 at 100%, differentiating these more severe from milder flow-reduced states.
Table 1 shows the correlation between VI
and the fluorescent microsphere–derived MBF ratios
from the stenosed versus normal bed at varying pulsing intervals. The
correlation progressively improved in proportion to prolongation of
pulsing interval from 1:1 to 1:10 in gray-scale imaging. The
correlation obtained by power Doppler imaging was stronger than
that by gray-scale imaging for all pulsing intervals except 1:10.
However, the correlation was closest at a pulsing interval of 1:2,
decreased gradually, and disappeared at 1:10.
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Increase in VI Produced by Prolongation of Pulsing
Interval
Figure 5 depicts the change in VI in
the LAD bed due to alteration of pulsing intervals from 1:1 to 1:10 at
all flow states by both modalities. The increases in the
background-subtracted VI during prolongation of pulsing intervals from
1:1 to 1:10 were greater with power Doppler than gray-scale imaging
at all flow states. In addition, by gray-scale imaging, the degree of
increase in VI in response to a gating change from 1:1 to 1:10 was
similar to that of baseline for all flow states, except for total
occlusion, which exhibited a lesser magnitude of amplification.
Conversely, a significantly greater increase in VI than at baseline was
observed by power Doppler imaging for all reduced flow states, with
the greatest augmentation seen with the most severe
stenoses.
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Transmural Differences of VI and MBF
A difference in the transmural distribution of opacification with
stenosis was easily visualized by power Doppler imaging but
was rarely observed by gray-scale imaging (Figures 2
and 3). As expected, with severe flow reductions, there was a
decrease in endocardial opacification, with greater preservation of
epicardial perfusion and a diminution of the ratio of endocardial to
epicardial intensity. By power Doppler imaging, the epicardial side
of the LAD bed appeared slightly opacified with severe stenosis
(75% and 100% reduced-flow states) during 1:1 ECG gating, and this
epicardial opacification became greater at longer pulsing intervals
(Figure 3). Figure 6 shows the
ratios of endocardial/epicardial VI by power Doppler imaging and
microsphere-derived MBF analysis in the LAD bed at all
pulsing intervals at all flow states. The alterations in
endocardial/epicardial ratio by power Doppler imaging coincided
with that obtained by microsphere-derived MBF analysis
and was most easily visualized for more severe flow reductions and at
longer pulsing intervals. Table 2 shows
the correlation between VI– and the microsphere-derived
MBF–endocardial/epicardial ratios in the LAD bed at all the flow
states during varying pulsing intervals. Although no correlation was
observed by gray-scale imaging at any pulsing interval, a significant
correlation was observed by power Doppler imaging at all pulsing
intervals.
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Discussion |
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Considerable controversy exists regarding the preferred imaging modality and gating protocol and the optimal criteria by which to identify abnormalities by MCE. Ever since the initial recognition that microbubbles can be destroyed by the transmitted imaging pulse itself, triggered ECG-gated imaging has been applied to enable the reperfusion of bubbles into the imaging field. However, the influence of pulsing intervals on the contrast intensity produced by graded flow reductions has not been defined with relation to either gray-scale or power Doppler imaging. Traditional gray-scale B-mode recording provides the highest resolution images. However, gray-scale imaging depends primarily on the increased backscatter and resonance phenomenon of microbubbles to produce contrast signals and does not readily differentiate reflections produced by tissue from those of contrast agents. Doppler imaging uses an autocorrelation technique that displays changes in the backscattered signals from multiple packets of ultrasound. Because bubble destruction or movement can produce such changes, power Doppler imaging has a greater sensitivity for detecting microbubbles and can readily distinguish bubble signals from those generated by tissue. However, Doppler imaging offers lesser resolution than does gray-scale imaging and is susceptible to motion artifacts. At present, no data exist comparing the ability of gray-scale imaging with power Doppler imaging to produce MCE and identify coronary blood flow. The present study presents the first data comparing gray-scale and power Doppler imaging and the initial systematic assessment of the response of intensity to variable pulsing intervals.
The present study demonstrates that MCE with harmonic power Doppler imaging has advantages over MCE with gray-scale imaging in opacifying the myocardium and in assessing graded coronary stenoses that are flow limiting at rest. The high VI obtained by power Doppler compared with gray-scale imaging enables detection of small differences in myocardial perfusion in a stenosed bed and yields a closer correlation with fluorescent microsphere–derived MBF measures. In addition, the response of VI to prolongation of pulsing interval is different for power Doppler imaging than for gray-scale imaging. Compared with gray-scale imaging, power Doppler imaging produces a greater increase in VI with prolongation of the pulsing interval, particularly in the presence of the most severe flow reductions and at the longest pulsing intervals. Thereby, the optimal pulsing interval for assessing graded coronary stenoses differs between the 2 imaging modalities, and the variable response of graded stenoses to gating intervals provides an approach to quantifying stenosis severity by power Doppler imaging. Moreover, our data document that power Doppler imaging is superior to gray-scale imaging in depicting transmural differences (endocardium versus epicardium) in myocardial perfusion in the presence of severe flow-limiting stenosis or total coronary artery occlusion.
Assessment of Coronary Stenosis by MCE
In this dog model, the intensity of myocardial opacification was
consistently greater for power Doppler than gray-scale
imaging. MCE with power Doppler imaging correctly depicted the
progressive reduction of regional MBF produced by graded flow-limiting
coronary stenoses. Although the reduction of LAD bed VI
at 100% by gray-scale imaging was significant, the reduction of VI
observed at other reduced flow states was not, and differentiation
between 25%, 50%, and 75% reduced-flow states was impossible.
However, a significant reduction of VI was observed at all reduced-flow
states by power Doppler imaging, and the difference of VI between
25% and 75% reduced-flow states was significant at 1:2 and 1:4
pulsing intervals (Figure 4). In addition, the correlation
between VI and the MBF ratios from the stenosed versus normal bed in
the presence of graded coronary stenoses was stronger
for power Doppler than gray-scale imaging during 1:1 to 1:8 pulsing
intervals. Thus, power Doppler imaging is superior to gray-scale
imaging in assessing graded coronary stenoses because
of both the denser myocardial opacification produced and the greater VI
differences produced by reduced coronary flow.
Different Response of VI to Varying Pulsing Intervals Between
Gray-Scale and Power Doppler Imaging
In gray-scale imaging, LAD bed VI tended to increase slightly with
each prolongation of the pulsing interval from 1:1 to 1:10 at all flow
states (Figure 4). In contrast, VI assessed by power Doppler
imaging plateaued at a pulsing interval of 1:4 at baseline and at 25%
and 50% reduced-flow states but continued to increase to an interval
of 1:10 at 75% and 100% reduced flow. This difference was likely due
to the fact that the number of microbubbles in the imaging field with
normal or mildly decreased coronary flow was sufficient to
saturate the power Doppler signal even at a relatively short
pulsing interval but was insufficient to saturate in the presence of
severe stenosis even at long pulsing intervals. Thus, the use
of varying pulsing intervals may provide useful information regarding
the severity of stenosis: both mild and severe stenoses
can produce abnormalities with a short pulsing interval, whereas only
severe stenoses can produce perfusion defects with a long
pulsing interval. Such analysis may provide a potential
criteria by which to identify stenoses by clinical MCE.
As opposed to previous gray-scale B-mode studies, which reported that
the increase in VI with prolonged pulsing interval was blunted in the
presence of coronary artery disease,2 we observed
a greater augmentation in VI with stenosis by using power
Doppler imaging. This finding was demonstrated by comparing the
change of LAD bed VI to incremental pulsing intervals from 1:1 to 1:10
for the 2 imaging methods (Figure 5). The increase in VI for the
2 techniques during prolongation of the pulsing interval from 1:1 to
1:10 was similar at baseline. However, in the presence of
coronary stenoses, the VI increase was less than that
at baseline when gray-scale imaging was used but greater than that at
baseline when power Doppler imaging was used. Thereby, prolongation
of the pulsing interval to 1:10 was effective in identifying
coronary stenoses by the gray-scale method because a
greater increase in VI occurred at baseline than at any reduced flow
state. Conversely, the prolongation of pulsing interval produced a
greater increase in VI at reduced flow states than at baseline as
assessed by power Doppler imaging, which diminished the VI
difference between stenosed and normal beds. This difference between
the 2 imaging methods is in agreement with the finding that the
correlation between VI- and MBF-derived ratios from the stenosed versus
normal bed progressively improved in proportion to prolongation of the
pulsing interval from 1:1 to 1:10 by gray-scale imaging but was closest
at 1:2 and disappeared at 1:10 by power Doppler imaging (Table 1).
The difference between the 2 imaging modalities also influenced the definition of the risk area at various pulsing intervals. The mean value of the risk area of an occluded coronary artery expressed as a percentage of the left ventricular short-axis area was 48±8% by Monastral Blue staining. The mean value of the risk area at the 1:1 pulsing interval was 33±3% by gray-scale imaging and 38±13% by power Doppler imaging (P=NS), and at the 1:10 pulsing interval, it was 20±6% by gray-scale imaging and 14±6% by power Doppler imaging (P<0.01). Thus, both imaging modalities underestimated the risk area at all pulsing intervals. However, the underestimation of risk area during long pulsing intervals was slightly greater by power Doppler than by gray-scale imaging, whereas that during short pulsing intervals was greater by gray-scale imaging.
Transmural Distribution of Myocardial Perfusion
Controversy continues regarding the ability of MCE to determine
the ratio of endocardial/epicardial MBF.6 7 In a carefully
performed recent study using mathematical analysis of
microbubble destruction, Linka et al7 demonstrated good
correlation between MCE-derived and microsphere-derived
endocardial/epicardial MBF ratio values. In the present study,
identification of disturbed transmural distribution of myocardial
perfusion by simple visual examination was uncertain with gray-scale
imaging but was possible with power Doppler imaging. Abnormal
endocardial/epicardial ratios were particularly apparent with severe
stenosis (75% and 100% reduced-flow states) and during long
pulsing intervals (1:4 or greater) (Figure 3). In addition, the
ratio of endocardial/epicardial VI derived from power Doppler at
baseline and all reduced flow states correlated with the ratio of
endocardial/epicardial MBF measured by microspheres (Table 2). The correlation between the endocardial/epicardial ratios by
MCE and microsphere-derived MBF in the present study was
not as close as the data that included velocity of microbubble filling
reported by Linka et al.7 This difference suggests that
peak VI combined with the velocity of microbubbles will be superior to
peak VI alone for quantification of flow. However, power Doppler
imaging can identify low levels of flow in the epicardial region in the
presence of stenosis. Our data clearly establish that the
greater sensitivity of the power Doppler than the gray-scale method
to image-contrast microbubbles translates to a superior capability to
delineate endocardial/epicardial blood flow, despite lower spatial
resolution. This ability to depict transmural distribution of
myocardial perfusion may be of value in the detection and quantitative
assessment of coronary stenoses by clinical MCE.
Methodological Considerations
Although the present study was performed in open-chest dogs,
we believe the principles established remain valid. The experiments
used one instrument and one contrast agent, but the properties of each
are relatively generic. The dose of the agent used saturated the
imaging field during some pulsing intervals and flow states with power
Doppler imaging. Although the precise results obtained with other
doses might differ, these data have established the basis for the
interaction of the pulsing interval and lesion severity in power
Doppler recordings. Finally, in the protocol, we examined
only stenoses with resting flow reductions in an anterior
location and did not apply vasodilator stimuli. Because resting MBF is
affected only by stenoses that are >85% in
diameter,8 the differences in cross-sectional LAD area
among the reduced flow states in the present study were likely
smaller than the non–flow-limiting stenoses in previous
studies.9 10 This may explain why the differentiation
among 25%, 50%, and 75% reduced-flow states was limited in
gray-scale images. Nevertheless, we established the feasibility of and
criteria for evaluating graded stenoses by MCE at rest,
principles that should be applicable to lesions that do not impede
resting flow and are best studied with vasodilator stress.
Clinical Implications
We believe that our data demonstrate potential advantages of power
Doppler over gray-scale B-mode imaging. Higher myocardial intensity
levels are achieved, perfusion defects are more readily identified both
visually and quantitatively, and disturbed endocardial to epicardial
ratios can be identified by power Doppler imaging. As was evident
in the present study, MCE perfusion defects could be visually
absent under certain imaging conditions, even in the presence of total
arterial occlusion. We believe that our findings support
the need to derive quantitative measures of contrast intensity to
accurately assess myocardial perfusion. Including microbubble
velocity7 in addition to peak VI may provide more accurate
assessment of coronary stenosis and transmural
distribution of MBF in power Doppler and gray-scale imaging. Our
data indicate that peak background-subtracted VI from power Doppler
imaging compared with gray-scale imaging provides new and different
information for the assessment of regional microcirculatory flow.
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Acknowledgments |
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We gratefully thank Biguang Yao, MD, Oi Ling Kwan, RDCS, G. Monet Strachan, RDCS, and Karen McClure, RDCS, for excellent technical assistance.
Received February 2, 2000; revision received April 17, 2000; accepted April 22, 2000.
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 A Hagendorff, A Goeckritz, A Neugebauer, T Rother, T Linke, D Pfeiffer, and H Becher Assessment of Regional Myocardial Hypoperfusion with Myocardial Contrast Echocardiography Using Intravenous Bolus Application in Patients with Acute Chest Pain: A Double Case Report Eur J Echocardiogr, December 1, 2003; 4(4): 320 - 326. [Abstract] [Full Text] [PDF]
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Y. Takagi, K. Ohmori, K. Yukiiri, I. Kondo, Y. Yu, A. Oshita, H. Takeuchi, K. Mizushige, and M. Kohno Quantitative assessment of coronary stenosis by harmonic power Doppler with a simple pulsing sequence and vasodilator stress in patients J. Am. Coll. Cardiol., June 4, 2003; 41(11): 2060 - 2067. [Abstract] [Full Text] [PDF]
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H. Masugata, N. Fujita, I. Kondo, B. Peters, K. Ohmori, K. Mizushige, M. Kohno, and A. N. DeMaria Assessment of right ventricular perfusion after right coronary artery occlusion by myocardial contrast echocardiography J. Am. Coll. Cardiol., May 21, 2003; 41(10): 1823 - 1830. [Abstract] [Full Text] [PDF]
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T Muro, T Hozumi, H Watanabe, H Yamagishi, M Yoshiyama, K Takeuchi, and J Yoshikawa Assessment of myocardial perfusion abnormalities by intravenous myocardial contrast echocardiography with harmonic power Doppler imaging: comparison with positron emission tomography Heart, February 1, 2003; 89(2): 145 - 149. [Abstract] [Full Text] [PDF]
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S Fukuda, T Muro, T Hozumi, H Watanabe, K Shimada, M Yoshiyama, K Takeuchi, and J Yoshikawa Changes in transmural distribution of myocardial perfusion assessed by quantitative intravenous myocardial contrast echocardiography in humans Heart, October 1, 2002; 88(4): 368 - 372. [Abstract] [Full Text] [PDF]
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 L. Agati, S. Funaro, M. Madonna, C. Volponi, G. Veneroso, and G. Tonti Clinical utility of contrast echocardiography in the management of patients with acute myocardial infarction Eur. Heart J. Suppl., March 1, 2002; 4(suppl_C): C27 - C34. [Abstract] [PDF]
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 H. Masugata, S. Lafitte, B. Peters, G. M. Strachan, and A. N. DeMaria Comparison of Real-Time and Intermittent Triggered Myocardial Contrast Echocardiography for Quantification of Coronary Stenosis Severity and Transmural Perfusion Gradient Circulation, September 25, 2001; 104(13): 1550 - 1556. [Abstract] [Full Text] [PDF]
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F. S. Villanueva, E. W. Gertz, M. Csikari, G. Pulido, D. Fisher, and J. Sklenar Detection of Coronary Artery Stenosis With Power Doppler Imaging Circulation, May 29, 2001; 103(21): 2624 - 2630. [Abstract] [Full Text] [PDF]
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