(Circulation. 1995;92:1452-1457.)
© 1995 American Heart Association, Inc.
Articles |
Alterations in Ultrasonic Backscatter During Exercise-Induced Myocardial Ischemia in Humans
From the University of Naples, Federico II Faculty of Medicine, Cattedra di Geriatria, Naples, Italy, and Northwestern University Medical School, Division of Cardiology, Chicago, Ill (R.O.B.).
Correspondence to Dino F. Vitale, MD, Cattedra di Geriatria, No 2 Faculty of Medicine, Via S Pansini 5, 80131 Napoli, Italia.
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Abstract |
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Background Experimentally induced myocardial ischemia in animals causes tissue modifications that alter characteristics of the ultrasonic beam backscattered from the myocardial muscle. Alterations of backscatter parameters have been evidenced in human subjects with acute or remote myocardial infarction and during ischemia induced by angioplasty balloon occlusion or pharmacological stimuli. The effects of transient effort ischemia in humans have not been reported. The purpose of this study is to assess ultrasonic backscatter parameter changes induced by transient effort myocardial ischemia in human subjects.
Methods and Results Nineteen patients with single left anterior descending coronary stenosis and 15 healthy subjects underwent ultrasonic backscatter analysis (parasternal long-axis view) at rest, immediately after a supine stress test, and 30 minutes later. Two windows were selected in each ultrasonic study: one encompassing the septum; the other, the posterior wall. Integrated backscatter was computed throughout the cardiac cycle, yielding a power curve relative to the midmyocardial region of the myocardial wall (excluding pericardial and endocardial borders). Five parameters were computed from the backscatter power curve: the maximum-minimum difference, amplitude and phase of the first harmonic Fourier fitting, phase-weighted amplitude, and time-averaged integrated backscatter difference from rest (an index of overall myocardial reflectivity). This protocol allowed comparison of the backscatter data from a region at risk of ischemia (the septum) with that from a region normally perfused (posterior wall) and a comparison with the same regions of the control group during the three ultrasonic studies. All backscatter indexes in the septum were altered significantly by exercise compared with rest values, whereas no changes were found in the normally perfused posterior wall or in the septum of the control group. All modified parameters returned to baseline values at the time of the recovery study.
Conclusions These data indicate that transient, exercise-induced ischemia is associated with reduction of the cardiac cycle–dependent variation of the integrated backscatter power curve, a temporal shift in the nadir of the power curve with respect to the R wave (phase increase), and a small but detectable increase of myocardial reflectivity. These changes may be detected noninvasively in humans with ultrasonic backscatter analysis.
Key Words: ischemia • echocardiography
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Ultrasonic tissue characterization is emerging as a new technique capable of detecting and measuring myocardial structural differences related to a number of heart diseases. In the past decade, the most commonly used method to study the interaction between the ultrasound beam and the tissue has used the "raw" radiofrequency (RF) ultrasound signal backscattered from the tissue. Among the various diseases that induce changes in myocardial backscatter detectable by this noninvasive technique, such as hypertrophic1 2 and dilated3 cardiomyopathy, amyloidosis,4 and myocardial ischemia,5 the latter has been the object of the most intensive investigation.
The cyclic variation in backscatter power levels observed in healthy hearts6 is altered during ischemia,7 and the time-averaged integrated backscatter is increased.8 9 The magnitude of such variations has been shown to be related to the severity of ischemia in animal models.10 In addition, recovery of backscatter indexes after reperfusion occurs more quickly than does recovery of regional systolic wall thickening not only in dogs11 but also in patients undergoing thrombolytic therapy for acute myocardial infarction.12 The present study was undertaken to define the changes occurring in the backscatter power signal during transient reversible myocardial ischemia in humans.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Patient Selection
Twenty consecutive subjects (mean age, 49±7 years; 18 male, 2 female) with angiographically documented single-vessel coronary artery disease, involving
80% reduction in luminal
diameter of the left anterior descending coronary artery,
underwent an echocardiographic study with
backscatter analysis and standard M-mode recordings at
rest, immediately after a supine exercise stress test, and 30 minutes
later. One patient, who had pulmonary emphysema, had very
poor-quality cardiographic images and was excluded from
the study. Therefore, 19 patients make up the test population of the
present study. Of the 19 patients, 9 had 80%, 8 had 85%, and 2
had 90% reduction in luminal diameter at the site of most severe
stenosis. Fifteen healthy age-matched volunteers (age,
47±8 years; 14 male, 1 female) underwent the same study protocol and
were used as the control population. None of the healthy subjects had
evidence of cardiovascular disease by history or
physical examination; all had normal ECG at rest; and all had normal
ECG response to exercise. All patients were informed about the study
purpose and protocol, and all gave consent to participate in the
study. Symptom-limited supine bicycle exercise test was performed according to a triangular workload protocol starting at a 30-W workload with a 20-W increment every 3 minutes. Blood pressure and three precordial ECG leads (V1, V3, and V5) were monitored during the study, and conventional end points for exercise testing were applied. Medications such as ß-blockers and calcium antagonists were discontinued at least 72 hours before the study; nitrates were allowed up to 12 hours before testing. The echocardiographic images obtained immediately after the stress test were completed within 2 minutes after the end of exercise.
Backscatter Data Acquisition and Analysis
The procedure used
in this study was described
previously.13 Briefly, ultrasound studies were performed
with a Hewlett Packard (HP) system (77020A) equipped with a 3.5-MHz
transducer and connected to an HP A900 minicomputer to digitize
(16.7-MHz sampling rate) and store the RF signal (42-dB dynamic range)
of two-dimensional scans (30-Hz frame rate) for off-line
processing. All studies were performed in the parasternal long-axis
view with time gain control adjusted to have equal gain at each depth.
Probe location on the chest wall was marked as a reference for
subsequent positioning. After the initial adjustment, an acquisition
test was made to pilot the adjustments of the transmit and gain
controls to ensure that the greater amplitude of the RF signal relative
to the midmyocardial region (occurring during diastole) was
just below the saturation level and, consequently, the minimum
amplitude value (occurring during systole) was still above the low
signal level. Once adjusted, all controls were held constant during the
three ultrasonic studies per patient. In each study, a window
encompassing only a portion of the myocardial wall was selected, as Fig
1
shows. Two windows were selected in each of the three
studies for each patient: one encompassing the septum; the other, the
posterior wall. Window dimensions ranged from 8 to 10 lines (0.5 to 1.5
cm.), and each line was 2.0 to 3.0 cm long with a resolution of 
200
points per centimeter (given the tissue sound speed equal to 1540 m/s
and a sampling rate of 16.7 MHz).
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The recorded occurrence of the ECG R
wave was used as a reference
to average the corresponding RF data of the 20 to 30 cardiac cycles
acquired for each study set. All cardiac cycles that were 33
milliseconds longer or shorter than the mean cardiac cycle length were
rejected from averaging. Developed software allowed the reconstruction
of image frames from the RF data to draw in each frame of the mean
cardiac cycle areas of interest delimiting the midmyocardial zone of
the wall. Using only the RF data corresponding to each midmyocardial
region of interest, we generated a backscatter power curve spanning a
single cardiac cycle, with a duration equal to the mean RR interval and
with points representing the backscatter power value
integrated over a midmyocardial area and averaged over several RR
intervals. To obtain power values, the original RF amplitude was
rectified and then squared. The averaging described above was performed
after rectification and before squaring. Backscatter power curve values
were normalized by the average power of the cardiac cycle, and this
ratio was expressed in decibels (Fig 2).
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Five parameters
were computed from the backscatter power
curve: the maximum-minimum difference, amplitude and phase of the
curve (obtained by first harmonic Fourier fitting), phase-weighted
amplitude, and time-averaged integrated backscatter.10
The first and the second parameters are two different ways
of measuring the magnitude of cyclic variation, whereas phase measures
the temporal shift of this variation with respect to the ECG R wave.
Fig 2
shows a typical backscatter power curve and its first
harmonic
Fourier fitting overlay, along with the first three computed
parameters.
The fourth parameter, phase-weighted amplitude, is a
composite index from the amplitude and the phase, as conceptualized by
Wickline et al,10 using the ECG R wave as the trigger
reference. To derive the phase-weighted-amplitude, amplitude
values were multiplied by a factor derived from the phase angle using
the following criteria: Factor=-1 if
(0°
phase45°) -cos[2(phase-45°)] if
(45°phase135°) 1 if
(135°phase225°) cos[2(phase-45°)] if
(225°phase315°) -1 if
(315°phase360°)
Therefore, the criteria used to weight the amplitude are such that amplitudes with a phase value of approximately 180° (135° to 225°), considered to be normal, have a weighing factor of 1, while amplitudes with phase values progressively smaller than 135° or >225° are reduced by a factor progressively approaching -1.
The fifth index used in this study was the time-averaged integrated backscatter. This is a measure of the mean power during the cardiac cycle and represents the overall "reflectivity" of the myocardium. This index is usually computed by normalization to the power of a nearly perfect ultrasonic reflector, a stainless steel plate phantom.14 In the present study, we did not use a stainless steel plate to normalize backscatter power measures; however, we normalized the data of effort and recovery studies to the power of the rest study to obtain the rest-effort and rest-recovery variation expressed in decibels.
Data Reproducibility
Reproducibility of these parameters was
assessed
previously.13 Interstudy variabilities for
maximum-minimum difference, amplitude, and phase of the fundamental
Fourier harmonic were 0.5 dB, 0.25 dB, and 24.4°, respectively,
evaluated by regression analysis residual error and by SD of
interstudy differences.13 Phase-weighted amplitude,
computed from the same data,13 has an interstudy
variability of 0.4 dB. These values are roughly 10 times smaller than
the parameter range and are similar to or smaller than
those previously reported.15 16 It is acknowledged
that
different reproducibility results might arise among various
laboratories because of differences in hardware and
procedures.16 The algorithm used in the present work,
in which data points in the backscatter power curve are averaged over
several cardiac cycles, will reduce fluctuation in the derived
indexes.
Wall Thickness Measurements
For each echocardiographic study,
septal and
posterior wall thicknesses were measured from the M-mode
recordings by use of standard criteria.17 The
difference between systolic and diastolic wall thickness
was expressed as a percent of the diastolic measure.
Statistical Analysis
All data are expressed as
mean±SD. Multiple comparisons among
rest, exercise, and recovery data were performed with ANOVA followed by
Duncan's multiple-range test.18 ANOVA was used to
compare corresponding data between test and control populations. The
correlation between wall thickening and the rest-exercise variation
in phase-weighted amplitude was performed by linear regression
analysis.19
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Test Population
During peak exercise, 13 patients developed flat or downsloping ST depression >1 mm below baseline taken 0.08 second after the J point; 7 of these patients also developed chest pain. Four other patients manifested downsloping ST depression of 0.5 mm with T-wave inversion, which promptly recovered after stress. Mean workload at peak exercise was 82.6±11.9 W, and the exercise duration was 10.8±1.8 minutes. Heart rate increased from 76±5 beats per minute (bpm) at rest to 116±6 bpm at peak exercise.
Fig 3 shows the
septum and posterior wall backscatter
power curves obtained during the rest, effort, and recovery studies in
a single patient with coronary artery stenosis. The
septal power curve is altered markedly by stress; these changes
partially reverse in the recovery study. In contrast, the power curve
of the posterior wall is not altered with stress. Fig 4
gives the individual and mean behaviors of each parameter
for all 19 patients. The maximum-minimum difference of the backscatter
power curve was significantly reduced by stress in the septum (4.6±0.9
versus 2.7±0.8 dB, P<.01) but returned to baseline levels
at the recovery study (4.3±1.0 dB). No significant variation is
observed in the posterior wall among the three ultrasonic studies
(rest, 5.5±0.9; stress, 5.9±1.2; recovery, 5.6±1.0 dB).
Similarly,
the amplitude of the power curve in the septum declined significantly
with exercise (1.9±0.5 versus 0.9±0.4 dB, P<.01) and
returned to baseline values at the recovery study (1.7±0.5 dB).
Posterior wall amplitude values remained constant (rest, 2.2±0.5;
stress, 2.4±0.6; recovery, 2.4±0.5 dB). The phase of the power
curve
increased significantly in the septum from the baseline to the effort
study (195±26 versus 244±42°, P<.01) and then
decreased
to baseline values at the recovery study (210±18°). Again, no
changes were demonstrable in the posterior wall values (rest, 197±20;
stress, 200±16; recovery, 202±18°). Given the concordant
behavior
of amplitude and phase measurement, the composite index, the
phase-weighted amplitude, showed a qualitatively similar trend (Fig
4). Hence, this index decreased significantly in the septum
from rest
to exercise (1.9±0.5 versus 0.5±0.6 dB, P<.01) and
returned toward baseline levels at recovery (1.7±0.5 dB). Posterior
wall values of this index did not show any change with exercise (rest,
2.2±0.5; stress, 2.4±0.6; recovery, 2.4±0.5). Systolic
wall
thickening, expressed as percent of the diastolic
thickness, significantly decreased in the septum from rest to exercise
(55±17% versus 23±15%, P<.01), while posterior wall
values increased significantly (64±23% versus 89±22%,
P<.01). Both septum and posterior wall recovery values
returned to baseline levels (51±13% and 66±22%, respectively).
The
rest-exercise variation in phase-weighted amplitude, amplitude,
and phase correlated significantly with changes in systolic wall
thickening (r=.77, P<.01; r=.66,
P<.01; and r=-.73, P<.01,
respectively). Time-averaged integrated backscatter differences in
the septum of the stress and recovery studies versus baseline values
were 1.4±1.4 and 0.8±1.3 dB, respectively, while in the
posterior
wall the two measures were -0.9±2.7 and -1.4±2.5 dB.
Only the
stress septum value was significantly (P<.01) different
from zero.
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) and mean (
)
behavior of maximum-minimum difference (A), amplitude (B), phase (C),
and phase-weighted amplitude (D) in the patient population at rest
(B), during effort (E), and during recovery (R).
Control Population
No ST depression developed in the control
population during
exercise. Heart rate increased from 74±6 bpm at rest to 131±7
bpm at
peak exercise. Peak workload and exercise duration were
112.7±12.8 W and 15.4±1.9 minutes, respectively. Compared with
resting values, no significant difference occurred in any of the
measured backscatter parameters during exercise (the
Table). Systolic wall thickening significantly increased
from rest to exercise in both the septum and the posterior wall (the
Table). Backscatter parameters were significantly different
from the corresponding parameters of the test population in
the septum during exercise (maximum-minimum difference, 5.1±1.3
versus 2.7±0.8 dB, P<.01; amplitude, 2.2±0.6 versus
0.9±0.4 dB, P<.01; phase, 202±21° versus
244±42°,
P<.01; phase-weighted amplitude, 2.1±0.6 versus
0.5±0.6 dB, P<.01) but not in the posterior wall. The rest
and recovery backscatter parameters of both the septum and
the posterior wall did not show any significant difference compared
with the corresponding data of the test population. The
rest-exercise variation in phase-weighted amplitude did not
correlate with the changes in systolic wall thickening.
Time-averaged integrated backscatter differences in the septum of
the stress and recovery studies were -0.3±1.6 and -0.1±1.3
dB,
respectively. In the posterior wall, the two measures were 0.2±1.8 and
0.1±1.6 dB. None of these values was significantly different from
zero.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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Modification of the ultrasonic backscattered signal by myocardial ischemia and infarction has received particular attention from several investigators in the past decade. After the first demonstration of the myocardial backscatter power variability throughout the cardiac cycle,6 several investigators demonstrated that such variability is related, at least in part, to the contractile status of the myocardium.20 21 Moreover, induction of ischemia in animals causes an increase in time-averaged integrated backscatter and a reduction in the backscatter cyclic variation, which are restored toward baseline values after reperfusion.13 22 Such changes parallel the modifications induced in myocardial wall kinesis and correlate with the severity of the experimentally induced ischemia.10 Using videodensitometric analysis, Lythall et al23 were able to demonstrate an increase in echo amplitude and blunting of its cyclic variation during coronary occlusion with an angioplasty balloon and reversal of this finding after deflation. Other investigators observed similar behavior of the gray-level intensity using the transesophageal approach during intraoperative ischemia.24 In contrast, using the transthoracic approach, Picano et al25 were able to demonstrate only an increase in echodensity during transient ischemia induced by ergonovine, dipyridamole, or angioplasty balloon occlusion.
To obtain detailed descriptions of backscatter features during effort ischemia in humans, we investigated the response of backscatter indexes to transient myocardial ischemia induced by exercise in human subjects. To accomplish this, we studied patients with single-vessel coronary artery disease involving the left anterior descending coronary artery because the echocardiographic parasternal long-axis view in these patients offers the opportunity to investigate both the myocardium at risk of ischemia (the septum) and the normally perfused posterior wall. Data obtained in these regions at rest, immediately after exercise, and after 30 minutes of recovery delineate the behavior of the region at risk of ischemia (the septum) during the three studies in comparison with the trend observed in the normally perfused posterior wall and with the trend of the septum in control population.
Our results clearly demonstrate that exercise modifies all measured backscatter indexes in the septal region supplied by the stenosed artery but not in the normally perfused posterior wall or in the septum of healthy subjects. The association with ECG markers of ischemia in 13 patients and ECG changes suggestive of ischemia in 4 others, as well as the return to baseline values of all indexes in the recovery study 30 minutes after exercise, strongly implicate transient ischemia as the cause for the changes in backscatter parameters. The lack of ECG alterations during exercise in 2 patients, despite the presence of ultrasound modifications, does not exclude the development of myocardial ischemia because of the low sensitivity of stress ECG in single-vessel coronary artery disease patients26 and because the ECG was limited to three precordial leads to allow adequate ultrasound probe positioning on the chest wall.
In the present study, the magnitude of cyclic variation was evaluated by the maximum-minimum difference index and the amplitude of the first Fourier harmonic. Both indexes showed a blunting of the cyclic variation during effort in only the septal region. Because the amplitude of the first Fourier harmonic is derived from all power curve points, it should be a more "robust" measure than the maximum-minimum difference (computed from only two points of the curve). However, our data did not show any difference between the SDs of the two parameters. The reduction of data noise obtained by averaging corresponding points of several cardiac cycles could explain this result.
The significant increase in the phase of the first Fourier harmonic in the septum during effort is related to a shift in the nadir of the power curve toward the end of the cardiac cycle and causes a backscatter power curve pattern that is asynchronous to that obtained in the normally perfused regions.10 22 This ischemia-induced asynchrony closely resembles the regional wall motion asynchrony, as detected by radionuclide angiography, of ischemic myocardium in both dogs27 28 and human subjects,29 30 suggesting that a common denominator may underlie the changes in backscatter and wall motion during ischemia.
Amplitude and phase are separate, independent measures of the power
curve that relate to different aspects of myocardial dynamics.
Therefore, as with the detection of wall motion abnormalities by
radionuclide angiography,31 we combined the information
obtained with these two variables into a single variable, the
phase-weighted -amplitude. The change in this index from rest to
exercise directly correlates with the change in myocardial wall
thickening during ischemia (Fig 5).
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) and posterior wall data (
It is noteworthy that, despite the significant correlation between the
two variables, there was considerable individual variability; in 2
patients with no exercise ECG change, the backscatter index showed a
clear reduction in the septum during exercise, while the percent wall
thickening showed a small increase. This observation suggests that
backscatter changes might be more sensitive to ischemia than
mechanical changes in some patients. Moreover, when the septum and
posterior wall data were analyzed separately, the septal
backscatter changes of the phase-weighted amplitude correlated with
changes in wall thickening (r=.60, P<.01),
whereas no such correlation existed for the posterior wall data
(r=.04, P=NS) either for the septum and
posterior
wall data of the control population (r=.27,
P=NS;. Fig 6) or when posterior wall data of
the control and test populations were plotted together
(r=.06, P=NS). Thus, the changes in
backscatter
indexes induced by exercise appear to be determined by factors other
than wall thickening alone. These findings suggest that backscatter
indexes may provide an independent contribution to the evaluation and
detection of ischemic myocardium. Because our study
protocol was not designed to determine sensitivity, specificity, or
predictive accuracy of the backscatter indexes or to elucidate the
mechanisms responsible for changes in these indexes during
ischemia, these particular observations must be considered
tentative until confirmed by larger series.
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The statistically significant increase of 1.4-dB time-averaged
backscatter in only the septum of the test population during exercise
agrees with experimental data8 9 and is in accord
with the
results of other methods that used gray levels for echodensity
evaluation in humans.25 This value is smaller than that
observed in animals (3 dB), and some variability among subjects was
present (1.4 dB). This could indicate that a minor degree of
ischemia developed during effort in our subjects, resulting in
a smaller time-averaged integrated backscatter increase or
alternatively that myocardial reflectivity in humans is less influenced
by ischemia than in animals. This issue warrants further
investigation.
Our data have several implications. First, transient ischemia in humans induces changes in ultrasound backscatter signal, as observed in animals, that are detectable noninvasively. This procedure is feasible in conjunction with standard exercise testing as implemented in the present study or theoretically with other provocative tests (such as dobutamine administration), thus expanding the potential clinical applications of the technique. From a methodological point of view, computation of the backscatter power curve by averaging of several cardiac cycles significantly reduces data noise and therefore improves accuracy of the derived indexes, as suggested by the excellent reproducibility observed in our study. The data of the present study also serve to define the backscatter pattern induced by transient ischemia in humans, a mandatory step in the process of determining both the ability of this technique to distinguish reversible from irreversible myocardial injury, as suggested by some authors,32 and the diagnostic accuracy of the method in unselected populations. Further investigation in a larger number of patients, as well as standardization of the technique to minimize heterogeneity of hardware and algorithms used for ultrasonic tissue characterization, will be necessary to accomplish these goals.
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Acknowledgments |
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We would like to thank Andrea Giordano and Giuseppe Minuco of the Fondazione Clinica del Lavoro, Veruno, Italy, for their support.
Received December 8, 1994; revision received March 15, 1995; accepted April 1, 1995.
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