(Circulation. 2001;103:2724.)
© 2001 American Heart Association, Inc.
Basic Science Reports |
Comparative Value of Dobutamine and Adenosine Stress in the Detection of Coronary Stenosis With Myocardial Contrast Echocardiography
From the Cardiovascular Division, University of California at San Diego.
Correspondence to Anthony N. DeMaria, MD, Cardiovascular Division, UCSD Medical Center, 200 W Arbor St, San Diego, CA 92103-8411. E-mail ademaria{at}ucsd.edu
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Abstract |
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Background—Controversy continues as to whether adenosine or dobutamine is the superior pharmacological stress agent for myocardial contrast echocardiography (MCE).
Methods and Results—We compared real-time MCE refilling curves and wall thickening during adenosine and dobutamine stress in 14 open-chest dogs with left anterior descending and left circumflex coronary artery stenoses that reduced hyperemia by 40% to 60% and 70% to 90% (mild and severe non–flow-limiting stenosis, NFLS) and resting flow by 10% to 30% and 35% to 50% (mild and severe flow-limiting stenosis, FLS). MCE was performed with low-energy imaging during Optison infusion. After high-energy bubble destruction, time-intensity data from risk beds were fitted for an exponential function as y=A(1-e-bt), from which the rate of intensity increase (b) and maximal plateau intensity (A) were derived. Although severe NFLS and greater stenoses decreased b with both dobutamine and adenosine, with mild NFLS it was reduced in 58% of animals with dobutamine versus 8% with adenosine. The absolute decrease in b, however, was greater for adenosine than dobutamine with FLS. The A parameter was decreased with both adenosine and dobutamine only with the most severe FLS. Wall thickening was decreased with dobutamine in 33% of animals with severe NFLS and in all animals with any FLS; with adenosine, in all with severe FLS.
Conclusions—Both dobutamine and adenosine significantly reduce MCE refilling rates in the setting of severe stenosis and in the absence of contractile abnormalities. Dobutamine decreases refilling rate and wall thickening at a less reduced flow grade than adenosine, but adenosine produces a greater magnitude of change than dobutamine.
Key Words: contrast media • stress • echocardiography • dobutamine • adenosine
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Myocardial opacification can now be achieved with real-time imaging after intravenous contrast agents.1 Moreover, measurement of the time course of reappearance of contrast intensity after high-energy bubble destruction provides a method to quantify coronary blood flow2 3 and thereby identify and quantify coronary stenoses. As is true of radionuclide methods, however, it is likely that the imposition of stress will be necessary to identify stenotic lesions by myocardial contrast echocardiography (MCE).
Pharmacological stress is well suited for echocardiography because it reduces movement artifacts and provides ample time to acquire contrast data. Two approaches have been used: inotropic stress with dobutamine and vasodilator stress with adenosine or dipyridamole. No data exist, however, comparing these 2 approaches in identifying perfusion abnormalities in conjunction with MCE. Therefore, this study systematically compared dobutamine versus adenosine in the detection of graded coronary stenoses by MCE.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Fourteen open-chest mongrel dogs were subjected to variable grades of coronary stenosis in accordance with the "Position of the American Heart Association on Research Animal Use" (Circulation. April 1985). A lateral thoracotomy was performed, and the heart was suspended in a pericardial cradle. An occluder was placed around the proximal left anterior descending coronary artery (LAD) in 12 dogs and around the left circumflex coronary artery (LCx) in 2, and an ultrasonic transit-time flow probe (2.0 to 2.5 mm) was placed proximal to the occluder and connected to a flowmeter (model T201, Transonic System Inc).
MCE was performed with a real-time ultrasound system (HDI5000, ATL) capable of low-energy (0.1 to 0.2 mechanical index) MCE. Short-axis mid–papillary muscle images were obtained with the transducer fixed on a saline-filled latex bag positioned on the left ventricular anterior wall. The tomographic plane encompassing LAD and LCx perfusion territory distal to the occluder was identified by the lack of myocardial contrast during temporary coronary occlusion. Instrument settings were optimized and were subsequently held constant for each dog. Three high-energy fast, low-angle shot (FLASH) images were triggered every 15 cardiac cycles to produce bubble destruction. Optison (Mallinckrodt Medical) was continuously infused at a rate of 12 mL/h by a gently agitated infusion pump.
Quantitative Image Analysis
The raw data were analyzed with HDI
Laboratory (ATL) software. Two equal-sized regions of interest were
manually traced in the midwall myocardium: 1 in the LAD
perfusion bed (risk area, RA) and 1 in a control area (CA) equidistant
from the transducer. MCE intensity throughout the imaging sequence was
plotted against time and fitted to the exponential function
y=A(1-e-bt)+c,
where A was the plateau signal intensity, b the rate of rise to the
plateau, and c the intercept at the
origin.3
RA size was measured as the largest area with visually diminished opacification during refilling (nearly always at the beginning of the sequence) and was expressed as the percent total myocardial area from the same frames. Wall motion was measured as wall thickening (WT=end-systolic thickness-end-diastolic thickness/end-systolic thickness).
Qualitative Image Analysis
Myocardial perfusion was abnormal if either
patchy/incomplete or absent and was scaled as 0 if persistent
throughout the sequence, 1 if present in 30% to 60% of the
sequence, 2 if <30%, and 3 for no visualized defect. Qualitative
analysis of both myocardial thickening and endocardial motion
was scaled 0 for akinesia, 1 for severe hypokinesia or very low
response, 2 for moderate hypokinesia or weak response, and 3 for normal
response.
Myocardial Blood Flow Measurement and Dye
Analysis
Myocardial blood flow was measured by standard
techniques.2 Briefly,
fluorescent microspheres were injected into the left
atrium while reference blood samples were withdrawn from the femoral
artery. At the end of the experiment, monastral blue dye was injected
into the left atrium. The left ventricular cross-sectional
slice corresponding to the echocardiographic short-axis
image was photographed for RA size measurement. Then, the slice RA and
CA were cut into 10 wedge-shaped transmural samples for blood flow
analysis with a flow cytometer to count the
microspheres.
Experimental Protocol
For each animal, hemodynamics,
regional blood flow, flowmeter measurements, and real-time MCE were
acquired at baseline. Subsequently, adenosine was infused at
140 (µmol/L)/kg, and measurements were repeated. Fifteen
minutes after adenosine parameters had returned to
baseline, incremental 2.5 µmol/L ·
kg-1 ·
min-1 doses of dobutamine were
infused at 3-minute intervals to reach a 
50% increase from baseline
heart rate (mean dose 12.5 µmol/L ·
kg-1 ·
min-1), and recordings were
repeated. Subsequently, 4 grades of coronary stenosis
were imposed by progressive constriction of a screw occluder: 2 grades
that were non–flow-limiting stenosis (NFLS) at rest but
decreased adenosine-induced hyperemic flow by 30% to
60% and 70% to 90% (mild NFLS and severe NFLS, respectively); and 2
grades that decreased resting coronary flow by 10% to 30% and
35% to 50% (mild flow-limiting stenosis [FLS] and severe
FLS, respectively). At each stenosis, recordings were
obtained before (rest) and after adenosine and
dobutamine infusions.
Statistical Methods
Interobserver and intraobserver variabilities were
assessed by 2 blinded observers by repeating quantitative and
qualitative measurements during rest and adenosine and
dobutamine infusions. Data were expressed as
mean±SD. Comparisons of hemodynamics, myocardial blood
flow, and MCE data were performed with repeated-measures ANOVA and
Student’s t test. RA size by
MCE was correlated with that by blue dye performed by linear regression
analysis. A value of
P<0.05 (2-sided) was
considered significant. Reproducibility was assessed by ANOVA and Cohen
test (
-measurement).
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Two dogs had lethal ventricular fibrillation during dobutamine infusion with a severe FLS. FLASH transmission produced nearly complete microbubble destruction, which was followed by a gradual reappearance of dense generalized myocardial opacification over the 15-cycle sequence. A total of 180 sequences were analyzed, and 360 refilling curves were obtained. No difference was observed between LAD and LCx stenosis qualitatively (perfusion defects and contractile dysfunctions were detected at the same stenosis grades in both beds) or quantitatively (eg, the b parameter increased
4-fold with adenosine and dobutamine in both
beds and was decreased to 2-fold at severe NFLS) at individual flow
states.
Hemodynamics, Myocardial Blood
Flow, RA Size
During adenosine, a trend toward heart rate
reduction was observed, and systolic and diastolic
blood pressures were significantly decreased. At peak
dobutamine infusion, heart rate and systolic and
diastolic blood pressures increased
(Table
).
No significant differences were observed for these
parameters between baseline and coronary
stenoses at rest.
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In the presence of no stenoses or NFLS, coronary flow (flow probe) increased similarly with adenosine and dobutamine (from 23±8 to 74±22 and 62±14 mL/min, respectively, both P<0.05). The response of coronary flow differed with FLS: flow rate increased slightly (less than CA) with dobutamine for both mild FLS and severe FLS, whereas with adenosine, it was unchanged with mild FLS and was reduced (14±4 to 6±5 mL/min) with severe FLS lesions.
Microsphere measurements confirmed the decrease of RA blood flow during FLS, whereas no significant changes were observed with NFLS grades in either CA or RA. RA size with blue dye ranged from 18% to 73% of total myocardial area. Border zones with intermixed red- and blue-stained myocardium were identified in 6 dogs (50%) during coronary occlusion and increased the size of abnormal perfusion from 35% (RA) to 43% (RA+border zone).
Effects of Adenosine and
Dobutamine on Baseline MCE
Qualitatively, contrast intensity appeared to be
greater and more homogeneous during adenosine and
dobutamine than baseline. Because dobutamine
increased heart rate, the number of frames per cardiac cycle decreased
proportionally (from 12±3 to 6±4 frames/cycle at 12 frames/s). Heart
motion thereby yielded increased artifacts, manifested as patchy
myocardial signals in frames immediately after FLASH. No similar change
was observed during adenosine. The mean A parameter
was 3.5±1.4 dB before drug, and it increased to 5.0±1.4 dB with
dobutamine and to 5.4±1.3 dB with adenosine
(P<0.05). Similarly, the b
parameter increased significantly from 0.23±0.07
s-1 without
drug to 0.79±0.32
s-1 with
dobutamine and to 0.83±0.20
s-1 with
adenosine
(Figure 1).
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Qualitative Detection of Reduced
Coronary Flow
Qualitative analysis was performed on
interflash sequences rather than on single static images
(Figure 2). Before drug administration, visual
analysis detected a grade 2 perfusion defect in 10 of 12 dogs
(83%), each of which had an RA >40%, and only for the most severe
stenosis (severe FLS). With dobutamine infusion,
grade 2 MCE defects were observed in 7 dogs with mild NFLS and in 4
additional dogs with severe NFLS. The size of
dobutamine-induced perfusion defects increased
proportionally with higher grades of stenosis. Abnormal
perfusion with adenosine was detected in only 2 dogs with mild
NFLS and in 10 dogs during severe NFLS (grade 2 defect); defect size
and intensity were similar to those with dobutamine.
Conversely, FLS lesions were recognized more easily with
adenosine than dobutamine, because the intensity
difference between CA and RA was greater, and grade 0 defects were
observed only with adenosine.
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Quantitative Detection of Coronary
Flow Reduction
A and b Parameters
Before pharmacological stress, the A
parameter was not altered by stenosis.
Dobutamine produced a significant decrease of the A
parameter only for the severe FLS (5.0±1.4 versus 2.9±1.2
dB, P<0.05), whereas
adenosine significantly decreased A at the mild FLS grade as
well (5.4±1.3 versus 3.2±1.5 dB,
P<0.05). The b
parameter was more sensitive to coronary
stenoses than A. Before pharmacological stress, a significant
decrease of b was observed only with severe FLS (0.23±0.07 versus
0.15±0.05 s-1,
P<0.05).
Dobutamine significantly decreased b even with mild NFLS
(0.79±0.32 versus 0.48±0.12
s-1,
P<0.05)
(Figure 1
). With adenosine, b was not significantly
changed with mild NFLS but was decreased with severe NFLS (0.83±0.20
versus 0.42±0.17
s-1,
P<0.05). The degree of
decrease of b between grades was greater with adenosine than
dobutamine
(Figure 1). Thus, a significant difference in b was observed
between mild NFLS and severe NFLS with adenosine but not
dobutamine. Moreover, the magnitude of decrease in b was
greater for adenosine than dobutamine for FLS, and
a significant reduction between rest and stress was observed at the
severe FLS grade only with adenosine (rest: 0.15±0.05
s-1;
adenosine: 0.04±0.05
s-1,
P<0.05) and not with
dobutamine (rest: 0.15±0.05
s-1;
dobutamine: 0.14±0.08
s-1,
P=NS).
Difference in A and b Parameters
Between CA and RA
In the presence of NFLS, adenosine and
dobutamine produced slight decreases in the RA/CA ratio
only for the b parameter. In the presence of mild and
severe FLS at rest, however, the ratio of b in RA to b in CA was
significantly less with adenosine than dobutamine,
but not for A at the last stage
(Figure 3). These data provide the quantitative basis for the
qualitative observation that identification of the hypoperfused RA was
easier with adenosine than dobutamine during
FLS.
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Determination of RA Size
In the absence of stressor agents, correlation between
MCE and blue-dye measures of RA size could be performed in the 10 dogs
with defects during severe FLS grade and yielded a general correlation
(r=0.71). Correlations were
similar for dobutamine and adenosine for NFLS and
mild FLS grade lesions. For the severe FLS grade, the correlation of
MCE with blue-dye values for RA was close for both
dobutamine and adenosine and was superior to rest
(r=0.82 and
r=0.94, respectively, both
P<0.05).
Wall Motion Analysis
Without any stenosis, WT was 35±8% at rest,
55±6% during dobutamine
(P<0.05), and 43±5% during
adenosine (P=NS)
(Figure 4). A significant WT decrease was observed only
during dobutamine with severe NFLS and mild FLS in RA
versus CA: severe NFLS, 46±12% versus 55±4%; mild FLS, 33±4%
versus 53±7%, both P<0.05.
Finally, a greater WT decrease occurred with severe FLS for both
dobutamine and adenosine in RA versus CA: 21±4%
versus 50±6%, 15±5% versus 40±6%, both
P<0.05, respectively (absolute
values). Qualitative analysis of wall motion yielded similar
findings.
Figure 5 summarizes data both from qualitative wall motion
and perfusion analysis showing high discordance between
perfusion and contraction in 100% and 75% of animals for mild and
severe NFLS, respectively, but not for severe
stenoses.
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Reproducibility
Concordance calculation for perfusion defect yielded a
high of 0.88 at rest and a slightly higher of 0.82 with
adenosine than 0.74 with dobutamine
(P<0.05). Interobserver and
intraobserver variabilities of refilling measurements were 15.4% and
13.0% for A and 12.5% and 10.1% for b, respectively. for the
wall motion analysis was 0.79, and interobserver and
intraobserver variabilities were 7.5% and 8.2%,
respectively.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The present study is the first systematic comparison of the effects of dobutamine and adenosine on qualitative and quantitative parameters of myocardial perfusion and function in the setting of graded coronary stenoses. Our findings indicate that (1) without pharmacological stress, MCE enables detection of only severe reductions of coronary flow (severe FLS at rest) by either qualitative or quantitative analysis, (2) application of either dobutamine or adenosine enables MCE to identify lesions that do not reduce coronary flow at rest but do decrease coronary reserve, (3) both dobutamine and adenosine can produce perfusion abnormalities with grades of coronary stenosis that do not always result in contractile dysfunction, (4) dobutamine yields perfusion defects and wall motion abnormalities at lesser grades of stenosis than adenosine, and (5) adenosine yields images that both qualitatively and quantitatively more readily identify abnormal perfusion than dobutamine.
Quantification of Perfusion by
Real-Time MCE
Visual analysis of MCE is limited by ultrasonic
artifacts as well as subjectivity. The recognition that ultrasound
destroys microbubbles has provided the basis for deriving
destruction/refilling curves as a quantitative measure of perfusion.
Because real-time MCE has greatly facilitated the clinical acquisition
of these data, we used this technique to assess the ability of
dobutamine and adenosine to identify graded
coronary stenoses.
In contrast to previous triggered
MCE2 3 4
studies, we observed an increased plateau signal intensity during both
adenosine and dobutamine
(Figure 1). This discrepancy is probably related to the
multiple-pulse real-time MCE in this
study.5 With a single-pulse
technique such as gray-scale B-mode imaging, hyperemia would
increase the rate of reappearance of opacification and not the peak
steady-state intensity. The power-pulse inversion method used here
applies autocorrelation analysis to measure the difference in
the returning signal from consecutively transmitted interrogating
impulses. Microbubbles can produce changes between pulses by moving,
dissolving, or breaking into smaller bubbles. The power-pulse inversion
method is therefore sensitive to both the concentration and the
velocity of microbubbles, and both the refilling rate and peak
intensity plateau reflect a combination of blood flow velocity and
blood volume.
Stress Agents in Perfusion Imaging
Fung et al6
compared dobutamine echocardiography
and dipyridamole scintigraphy in dogs and
demonstrated a greater ratio of CA to RA blood flow induced by
dipyridamole and a higher prevalence of contractile
abnormalities with dobutamine. Consistent with Fung
et al, with FLS at rest we observed a more clearly delineated defect
and a greater decrease of intensity parameters during
adenosine. Conversely, dobutamine induced both
perfusion abnormalities and contractile dysfunction at lower grades of
stenosis. In a large clinical study, Marvick et
al7 did not observe a
significant difference between dobutamine and
adenosine single photon emission CT (SPECT), although
adenosine yielded higher sensitivity. Porter et
al8 demonstrated that
adenosine and dobutamine can produce a perfusion
defect with triggered-MCE imaging. Our study is the first, however, to
systematically compare qualitative and quantitative evidence of
perfusion and contraction at graded levels of stenosis using
microbubble destruction/reperfusion analysis.
Adenosine infusion resulted in a major (4-fold)
increase in the b parameter at baseline and a lesser
(<2-fold) increase in the A parameter. Thus, the major
effect of adenosine was to increase blood flow velocity, with a
smaller increase in microcirculatory volume, probably related to direct
vasodilation. In response to progressive stenoses, the
adenosine-induced increase in the A and b
parameters was reduced and ultimately eliminated at severe
grades, whereas the b parameter actually showed a reduction
below baseline levels at the most severe stenoses, indicative
of a coronary steal. At these severe grades, coronary
steal (that is, a redistribution of blood flow toward normal areas via
collaterals9 ) decreases blood
flow below resting values in the capillaries of the stenosed vessel. As
a consequence, blood velocity in capillaries is then dramatically
reduced, as demonstrated by the decrease of the b
parameter.
In the absence of stenoses, the major effect of
dobutamine was also to increase the b
parameter, although only 2-fold, with a proportionately
smaller increase of the A parameter compared with
adenosine. Similar results were observed in the CA under all
conditions in our study. A comparable difference in the abilities of
adenosine and dobutamine to augment
coronary blood flow was found by Skopicki et
al10 by PET imaging. Thus,
although the major effect of dobutamine was to increase
microcirculatory blood velocity, the agent also produced an increase in
microcirculatory blood volume by vasodilatation due to the increased
oxygen demand as well as perhaps the vasodilating effect of direct
ß-adrenergic receptor stimulation. The response of both the A and b
parameters to dobutamine in the RA during
ischemia was a diminution or elimination of the increase,
although no steal phenomenon was observed.
Recent data have supported the concept that an adenosine-induced decrease of myocardial contrast intensity in ischemic beds is due to a reduction in the number of patent capillaries ("capillary derecruitment"4 ). This derecruitment occurs in an attempt to maintain capillary perfusion pressure in the face of diminished pressure in the precapillary arterioles. The mechanism for dobutamine-mediated reductions in myocardial perfusion has been less clear. The data in this study suggest that the impaired perfusion to the ischemic bed during dobutamine stress is related both to the inability to increase microcirculatory blood velocity as well as, to a small extent, a reduction in microcirculatory blood volume. Again, this may be related to capillary derecruitment, although dobutamine yields less reduction of poststenotic pressure than adenosine.10
Ischemic Detection Versus Perfusion
Abnormality
This study demonstrated that real-time perfusion
defects antedated contractile abnormalities, which were observed only
with more severely abnormal NFLS and FLS
(Figure 5). The discrepancy between perfusion and contraction
abnormalities was probably emphasized by the ability of real-time MCE
to detect slight blood velocity decreases in capillaries. During NFLS,
defects were observed at the beginning of bubble refilling, rather than
at the termination, which represents steady-state perfusion and
is the condition evaluated by radionuclide, PET, and conventional MCE.
A discordance between perfusion defects and contractile abnormalities
has previously been reported in
clinical11 12 and
experimental13 studies,
which were generally similar to ours in detecting dyssynergy at more
advanced levels of flow
reduction.11 13
Study Limitations
The use of open-chest dogs has implications for
extrapolating the data to the clinical setting, but we believe that the
findings established in this study remain valid. Drug interactions or
the cumulative effect of the agents during the protocol could have
influenced the response to subsequent doses. We analyzed both
CA perfusion and contraction, however, and observed no significant
variations in response between each grade of stenosis. Our
protocol had the potential to induce stunning, but except for the most
severe grade, no consequence of flow reduction was observed on
myocardial contraction. Finally, we elected to set a 50% increase in
heart rate as the goal for dobutamine infusion. This
represents a smaller percentage increase in resting heart rate
and resulted in a smaller dosage of dobutamine than is
typically used clinically. A mean heart rate of 177 bpm was achieved,
however, and even at this level, 2 of 14 animals experienced fatal
ventricular fibrillation with the severe FLS. The artifacts
seen with dobutamine-induced tachycardia would
also most likely have been amplified at higher rates. Furthermore,
larger doses of dobutamine probably would only have
accentuated its advantages of producing abnormal perfusion and WT with
lesser grades of stenosis and would not have altered the
advantages of adenosine, which were related to reduced blood
flow to the RA. Therefore, although a disparity exists between the
doses used clinically and the doses used in this study for
dobutamine but not adenosine, we believe that our
findings depict the characteristics of these agents that will be
experienced in patients.
Clinical Implications
As is evident from our findings, if MCE is to achieve a
role in the clinical identification of coronary
stenoses, some form of stress will be required. Although
pharmacological stress provides longer imaging and reduces motion
artifacts, it remains uncertain whether inotropes, such as
dobutamine, or vasodilators, such as adenosine,
will be superior for stress MCE. Our data document that both
dobutamine and adenosine are effective agents in
conjunction with MCE. Dobutamine is already widely used in
stress echo and induces perfusion abnormalities and contractile
dysfunction at lower grades of stenosis. Adenosine has
the advantage of creating perfusion abnormalities that are more readily
detectable by visual examination and of greater magnitude by
quantitative analysis. At present, it is impossible to
predict which stress agent will predominate in the clinical
arena.
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Acknowledgments |
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Dr Lafitte was supported by the French Federation of Cardiology.
Received October 11, 2000; revision received February 7, 2001; accepted February 7, 2001.
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H. Leong-Poi, S.-J. Rim, D. E. Le, N. G. Fisher, K. Wei, and S. Kaul Perfusion Versus Function: The Ischemic Cascade in Demand Ischemia: Implications of Single-Vessel Versus Multivessel Stenosis Circulation, February 26, 2002; 105(8): 987 - 992. [Abstract] [Full Text] [PDF]
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