(Circulation. 2000;101:1390.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Assessment of Nonuniformity of Transmural Myocardial Velocities by Color-Coded Tissue Doppler Imaging
Characterization of Normal, Ischemic, and Stunned Myocardium
From CHU de Rouen, Rouen (G.D., G.P., A.C.), and Laboratoire de Physiologie Lyon-Nord, Lyon-Nord (M.O., J.L., X.A.-F.), France.
Correspondence to Geneviève Derumeaux, MD, PhD, Hôpital Charles Nicolle 1, Rue de Germont, 76000 Rouen, France. E-mail Genevieve.Derumeaux{at}chu-rouen.fr
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Abstract |
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Background—Transmural myocardial contractile performance is nonuniform across the different layers of the left ventricular wall. We evaluated the accuracy of color M-mode tissue Doppler imaging (TDI) to assess the transmural distribution of myocardial velocities and to quantify the severity of dysfunction induced by acute ischemia and reperfusion in the inner and outer myocardial layers.
Methods and Results—Thirteen open-chest dogs underwent 15 minutes of left anterior descending coronary artery occlusion followed by 120 minutes of reperfusion. M-mode TDI was obtained from an epicardial short-axis view. Systolic velocities were calculated within endocardium and epicardium of the anterior and posterior walls. Regional myocardial blood flow was assessed by radioactive microspheres. Segment shortening was measured by sonomicrometry in endocardium and epicardium of both the anterior and posterior walls. At baseline, endocardial velocities were higher than epicardial velocities, resulting in an inner/outer myocardial velocity gradient. Ischemia caused a significant and comparable reduction in endocardial and epicardial systolic velocities in the anterior wall with the disappearance of the velocity gradient. Systolic velocities significantly correlated with segment shortening in both endocardium and epicardium during ischemia and reperfusion. In the first minutes after reflow, endocardial velocities showed a greater improvement than epicardial velocities, and the velocity gradient resumed although to a limited extent, indicative of stunning.
Conclusions—TDI is an accurate method to assess the nonuniformity of transmural velocities and may be a promising new tool for quantifying ischemia-induced regional myocardial dysfunction.
Key Words: echocardiography • ischemia • reperfusion • stunning, myocardial
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Introduction |
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Experimental studies have demonstrated that circumferential fiber thickening varies across the different layers of myocardial walls and is more pronounced in endocardium than in epicardium.1 2 3 4 This transmural inhomogeneity is important to take into account in the setting of ischemic cardiomyopathy to differentiate the various patterns of contractile abnormalities that may occur during acute ischemia, hibernation, or stunning. Conventional assessment of contractile function is based on the measurement of transmural thickening. Previous ultrasonic studies of myocardial contractility based on M-mode or 2-dimensional images have assessed the differences between end-systolic and end-diastolic myocardial wall thicknesses or have involved digitization of endocardial and epicardial echoes.5 6 However, neither of these approaches provides information regarding the transmural distribution of contractile performance.
Tissue Doppler imaging (TDI) is a recent ultrasound technique that enables quantification of intramural myocardial velocities by detection of consecutive phase shifts of the ultrasound signal reflected from the contracting myocardium.7 8 9 TDI may display velocities with B-mode, M-mode, or pulsed Doppler. M-mode TDI overcomes the temporal resolution problems inherent in the B-mode approach, analyzes in real time endocardial and epicardial velocities, and provides new indexes of myocardial function such as the myocardial velocity gradient (MVG).10 11 Recent experimental studies using 2-dimensional and pulsed TDI have demonstrated that TDI can quantify ischemia-induced regional myocardial dysfunction, but there has been no report that M-mode TDI can characterize transmural distribution of velocities during ischemia and reperfusion.12 13
Therefore, the objectives of this study, performed in the open-chest canine model of ischemia-reperfusion, were (1) to assess the ability of M-mode TDI to quantify endocardial and epicardial velocities with sonomicrometry as a reference method, (2) to analyze the variations of the transmural distribution of systolic myocardial velocities induced by ischemia and reperfusion, and (3) to investigate whether M-mode TDI may help to differentiate ischemia- as opposed to reperfusion-induced contractile dysfunction.
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Results |
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Thirteen dogs were entered into the present study. In 2 dogs, contractile function could not be analyzed during reperfusion because of sustained ventricular arrhythmia. Overall data are presented for 81 matched systolic measurements of TDI velocities and segment shortening (SS).
Hemodynamic Data and Regional Myocardial Blood
Flow
All dogs had comparable heart rates and blood pressures at
baseline and throughout the experiment (Table 1
). Baseline regional myocardial
blood flow (RMBF) was comparable in endocardium and epicardium in both
the ischemic and nonischemic zones. As expected, left
anterior descending coronary artery (LAD) occlusion
resulted in a dramatic decrease in both endocardial and epicardial RMBF
from 0.88±0.05 to 0.12±0.04 and 0.94±0.04 to 0.27±0.07 mL ·
min-1 · g-1,
respectively (P<0.01 versus baseline for both). At 30
minutes after reflow, endocardial and epicardial RMBF in the anterior
wall averaged 3.81±0.93 and 3.18±0.84 mL ·
min-1 · g-1,
respectively, indicative of hyperemia (P<0.01
versus baseline) (Table 1). In nonischemic
myocardium, RMBF increase during occlusion was not
statistically significant. At 30 minutes after reflow, RMBF increased
significantly in the nonischemic zone although to a lower
extent than in the ischemic zone (P<0.01 versus
baseline, P<0.05 versus ischemic zone).
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Normal Pattern of Myocardial Velocities
Pericardial opening induced a significant decrease in
diastolic velocities but did not significantly alter
systolic velocities (Table 2).
Myocardial velocities recorded after pericardial opening were used
as baseline values for further comparison during
ischemia/reperfusion. Velocity profiles derived from M-mode TDI
traces indicated that distribution of transmural velocities was
inhomogeneous across the myocardial wall. Velocities
significantly and progressively increased from epicardium to
endocardium (Figure 1A). In the
anterior wall, baseline endocardial and epicardial systolic
velocities (Vs) averaged -4.9±0.7 and
-1.7±0.4 cm/s, respectively (Figure 1B). In the posterior
wall, endocardial and epicardial Vs averaged
6.8±0.6 and 3.2±0.2 cm/s, respectively. Thus, a MVG could be measured
(Figure 1C). This MVG profile displayed 2 distinct negative
peaks during systole and 2 positive peaks during diastole.
During systole, the first peak was brief and occurred during isovolumic
contraction, whereas the second peak was more prolonged, of smaller
amplitude, and occurred during the ejection phase. The first
diastolic peak occurred during isovolumic relaxation; the
second, during the early ventricular filling phase. MVG was
abolished during atrial contraction, indicating that during this time
period, inner and outer myocardial layers were contracting at a similar
speed.
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Myocardial Velocity Changes During Ischemia-Reperfusion
Ischemic Wall
Anterior wall thickening decreased from 55±9% at baseline
to 3±1% during ischemia (P<0.0001). As depicted
in Figure 2, Vs
dramatically decreased to a similar extent in the inner and outer
layers. Vs averaged 0.4±0.1 cm/s in endocardium
(P<0.0001 versus baseline) and 0.2±0.2 cm/s in epicardium
(P<0.0001 versus baseline) (P=NS between
endocardium and epicardium). Consequently, the MVG during the ejection
phase was significantly reduced from 3.2±0.5 at baseline to 0.3±0.1
s-1 during ischemia
(P<0.0001). The whole MVG profile was dramatically altered,
with only 1 brief and small negative peak persisting during isovolumic
contraction and mean MVG back to nearly zero during the ejection phase.
As opposed to systolic velocities, diastolic
velocities failed to change significantly (Table 2
).
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Thirty minutes after reflow, anterior wall thickening remained
severely depressed, averaging 11±5% (P<0.0001 versus
baseline) (Figure 3). Similarly,
epicardial Vs remained dramatically low and not
significantly different from the preceding ischemic values. In
contrast, endocardial Vs tended to increase yet
failed to fully recover. At 30 minutes of reperfusion,
Vs recovered to 42±21% of baseline in
endocardium (P<0.05 versus occlusion) but only to 9.5±12%
of baseline in epicardium (P=NS versus occlusion). At that
same time, MVG averaged 2.1±0.3 s-1, a value
lower than baseline but significantly higher than the ischemic
values (P<0.01).
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P<0.05 vs occlusion; 
P<0.01 vs
occlusion.
Nonischemic Wall
During occlusion, wall thickening slightly but not significantly
increased in the nonischemic territory to 115% of baseline
values. Endocardial Vs and SS increased to 121%
and 119% of control values, respectively (P=NS), whereas
epicardial Vs and SS remained unchanged. After 30
minutes of reperfusion, all parameters returned to baseline
values.
Correlations Between Vs, SS, and Myocardial Blood
Flow
To evaluate whether the severity of regional contractile
dysfunction induced by ischemia could be accurately evaluated
by TDI, Vs was plotted versus SS (both expressed
as percentage of baseline values) within endocardium and epicardium.
VS% was significantly correlated to SS% within
both endocardium (r=0.94, P<0.0001) and
epicardium (r=0.91, P<0.0001) (Figure 4).
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The relationship between Vs and RMBF in the
anterior wall at baseline, during ischemia, and after 30
minutes of reperfusion is summarized in Figure 5. During occlusion, the decrease in
endocardial and epicardial RMBF was accompanied by a dramatic reduction
in endocardial and epicardial Vs Thirty minutes
after reflow, despite hyperemia in both layers of the anterior
wall, Vs remained significantly depressed to
42±21% and 9.5±12% of baseline values in endocardium and
epicardium, respectively.
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Discussion |
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TopAbstractIntroductionResultsDiscussionMethodsReferences |
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The present study demonstrates that M-mode TDI can accurately assess the nonuniformity of the transmural distribution of myocardial contractile performance. Specifically, M-mode TDI was able to differentiate and quantify ischemia- and reperfusion-induced endocardial and epicardial contractile dysfunction and assess the transmural MVG.
Nonuniformity of Left Ventricular Circumferential
Thickening in Normal Myocardium
Conventional quantitative echocardiographic
methods classically address transmural but not inner or outer layer
myocardial function. Their principle is to analyze the
displacement of the endocardial border, which does not take into
account the nonuniformity of wall thickening.14 15 16 In a
previous study, we used pulsed-wave TDI to analyze septal wall
velocity resulting from left ventricular (LV) long-axis
shortening and its variations after LAD occlusion.13 We
demonstrated that pulsed-wave TDI is accurate to quantify online
ischemia-induced dysfunction. But we were unable to
discriminate endocardial and epicardial velocities.
In the present study, M-mode TDI allowed interrogation of
intramural velocities to quantify LV circumferential contraction. This
TDI modality is the first noninvasive method that can quantify in the
in situ heart the velocity of myocardial thickening that has been
recognized as an index of regional contractility in
isolated papillary muscle preparations.17 Theoretical
considerations based on various models of the LV and numerous in vivo
experiments have clearly demonstrated that wall thickening is not
uniform and the ratio of inner to outer half-thickening approximates
2.0:1.0.1 3 4 The present M-mode TDI data are
consistent with these previous studies. As depicted in Figure 7, the ratio of endocardium to epicardium systolic
velocities was close to 2.0:1.0. This progressive increase in
velocities from inner to outer layer created, under baseline
conditions, a velocity gradient that may represent an
interesting new index of regional myocardial
function.10 18
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Detection and Quantification of Ischemia- and
Reperfusion-Induced Wall Motion Abnormalities by M-Mode TDI
During LAD occlusion, endocardial and epicardial SS was replaced
by passive bulging consistent with a severe reduction in
myocardial blood flow. TDI data were closely related to sonomicrometric
measurements, indicating that M-mode TDI allows accurate quantification
of contractile function during ischemia and reperfusion.
Importantly, this accuracy of M-mode TDI applied for any severity of
regional dysfunction exhibited by endocardium and epicardium. Both
endocardial and epicardial velocities were markedly and uniformly
decreased during ischemia and resulted in the disappearance of
MVG. This absence of MVG across the anterior wall during severe flow
reduction is congruent with previous investigations that reported the
abolition of the transmural thickening gradient during dramatic flow
deprivation.19 20 It is worth noting that no
significant decrease occurred in diastolic velocities
during ischemia. This may be related to the fact that the
pericardial opening had already significantly reduced
diastolic velocities, thereby possibly blunting further
reduction related to ischemia.13
After reperfusion, wall motion in the distribution of the LAD remained
severely depressed, indicative of stunning. Conventional M-mode imaging
failed to detect any significant improvement in transmural wall
thickening. In contrast, M-mode TDI was able to detect a slight but
significant increase in endocardial (but not epicardial) velocities,
resulting in the resumption of a MVG. This MVG, however, was short
lived because endocardial and epicardial velocities were no longer
different at 90 minutes of reperfusion. The greater improvement in
endocardial velocities early after reflow was likely a consequence of
the hyperemic response to the preceding ischemic
insult, as suggested by Figure 4. Despite hyperemia,
epicardium failed to recover early after reperfusion, suggesting the
development of severe stunning and possible tethering to
endocardium.21 These data are in close agreement with
those from a study by Bolli et al20 that reported
comparable time course of nonuniform transmural functional recovery
after reflow in dogs submitted to 15 minutes of LAD occlusion followed
by 7 days of reperfusion. In that study, dogs exhibited a transmural
systolic thickening gradient at baseline that disappeared
during ischemia. On reperfusion, the inner/outer gradient first
resumed, was maximal during the first hour after reflow, and decreased
thereafter.20
Study Limitations
During reperfusion, RMBF and TDI velocities were
simultaneously measured 30 minutes after reflow. At that
time point, as previously demonstrated,22 there is
considerable variability in the response of both RMBF and myocardial
wall velocity to reperfusion and no relationship between wall velocity
and myocardial perfusion (Figure 5).
Our data demonstrate that M-mode TDI is a sensible technique that can detect and quantify mild changes in regional wall motion that may occur during ischemia or reperfusion. The present study has potential important clinical implications, ie, identification and quantification of the regional endocardial or epicardial contractile dysfunction that may arise during or as a consequence of acute coronary syndromes. However, further studies are needed to determine whether these data can apply to human patients.
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Methods |
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All experiments performed in this study conformed to the Guiding Principles in the Care and Use of Animals approved by the American Physiological Society. Thirteen adult mongrel dogs weighing 20 to 39 kg were instrumented as previously described.13
Echocardiography
Echocardiography was performed by use of a
SEQUOIA system (ACUSON) with a 7-MHz transducer. Measurement of
myocardial velocities resulting from the left ventricular
(LV) circumferential contraction was performed with the beam positioned
on the midanterior wall, from an epicardial short-axis view at the
level of the papillary muscles (Figure 6). A first series of velocity
measurements was performed before the pericardium was opened to
determine whether this might induce some change. Thereafter, all
measurements were performed with the heart suspended in a pericardial
cradle. Gray-scale receive gain was set to optimize the clarity of the
endocardial and epicardial boundaries. Doppler receive gain was
adjusted to maintain optimal coloring of the myocardium.
Doppler velocity range was set as low as possible to avoid aliasing
occurrence. The angle of interrogation of the M-mode beam was carefully
aligned to be perpendicular to the LV walls. Freeze-frame images were
then downloaded to a magneto-optic disk and transferred to an
IBM-compatible computer for offline analysis. Custom-made
software was designed to analyze myocardial velocities from
M-mode TDI traces. This computer program converted the digital
representation of colors into velocity values with the use of
color values obtained from the velocity scale bar. This color bar
displays a linear representation of velocities (64 colors
representing 32 positive and 32 negative velocities) and
was used as a lookup table for the conversion. Thus, a velocity value
was determined for each pixel by finding the best matching color value
stored in the lookup table. By convention, velocities were encoded
"positive" and "negative" when the displacement of the
myocardium was directed toward or away from the
transducer, respectively.
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To provide validation of this computer program, we specifically set up
an in vitro model to measure velocities in a continuous hydraulic,
nonturbulent jet. We used an electrical syringe (Harvard
Apparatus, model 55–1119) generating a forward and
backward flow (from 1.59 to 31.8 mL/min in both directions) through a
4.8-mm-diameter catheter. Fluid was composed of 70% water and 30%
glycerol to obtain a viscosity comparable to that of blood. Fluid
velocity within the catheter was calculated by the following formula:
Velocity=[flow (mL/min)/60]x
D2/4. Four
positive and 4 negative velocity values were obtained: 2.9, 1.18, 0.58,
and 0.3 cm/s.These velocities were then plotted against the mean
velocity measured within the catheter by use of TDI technology with a
5-MHz probe at a 0.27- and 0.34-m/s Nyquist limit. As depicted in
Figure 7, the correlation between fluid
and TDI velocities was excellent (r=0.97). In addition, the
Bland-Altman test confirmed that both methods provided comparable
results.
Experimental Protocol
After baseline measurements, the left anterior descending (LAD)
coronary artery was occluded for 15 minutes and reperfused for
120 minutes. Echographic and sonomicrometric recordings and
regional myocardial blood flow (RMBF) measurements were performed
sequentially at the following time points: at baseline, during
occlusion, and 30 minutes after reperfusion. Echographic measurements
were also performed at 5, 15, 30, 60, and 90 minutes after reflow.
At the end of each experiment, the LAD was briefly reoccluded, and 0.5 mg/kg Unisperse Blue Pigment (Ciba-Geigy) was injected intravenously to delineate the in vivo area at risk, as previously described.23 Under deep anesthesia, the heart was stopped by intravenous injection of potassium chloride, excised, and cut into 5 to 7 (10-millimeter-thick) slices parallel to the AV groove. We verified that the anterior wall at the level of the papillary muscles was unstained, ie, that the TDI interrogation was well in the ischemic area. The correct position of the 2 pairs of ultrasonic crystals was checked within both the area at risk and the remote nonischemic zone. Each slice was then incubated for 15 minutes in triphenyltetrazolium chloride at 37°C to exclude any necrosis.
Data Analysis
Hemodynamics
Heart rate and arterial and LV blood pressures were
averaged over 5 continuous cardiac cycles in sinus rhythm at baseline,
during occlusion, and after reperfusion.
Echographic Measurements
Conventional echographic measurements (LV wall thickness, wall
thickening, and LV cavity dimensions) were obtained from gray-scale
M-mode tracings according to the criteria of the American Society of
Echocardiography. The anterior and posterior walls
were arbitrarily divided from the endocardial to epicardial borders
into 2 layers of equal thickness by manual tracing of endocardial and
epicardial boundaries. This allowed calculation of endocardial and
epicardial velocities by M-mode TDI and further comparison with
sonomicrometry. Endocardial and epicardial mean velocities were defined
as the average values of the velocity estimates measured along each
M-mode scan line throughout the thickness of the inner and outer layers
of myocardial walls. Peak mean systolic velocity
(Vs) was defined as the maximum value of the mean
velocity during the ejection phase. MVG was defined as the difference
between endocardial and epicardial velocities divided by wall
thickness. Three beats were averaged for each of these measurements.
During occlusion or after reperfusion, velocity was expressed as a
percentage of baseline values. Myocardial velocities and MVG were
measured by 2 independent observers in 10 animals to determine
interobserver and intraobserver variabilities. Interobserver
variability was low: 0.27±0.2 cm/s for Vs and
0.12±0.15 s-1 for MVG. Intraobserver
variability was low: 0.24±0.2 cm/s for Vs and
0.1±0.12 s-1 for MVG.
Regional Myocardial Function
Segment shortening (SS), used as an index of systolic
function, was defined as follows: SS=[(EDL-ESL)/EDL]x100%, where
ESL and EDL are end-systolic and end-diastolic
lengths, respectively. ESL and EDL were obtained from 3 cardiac cycles
in each sample period. EDL was measured at the onset of the rapid
increase in LV dP/dt, whereas ESL was measured at peak negative LV
dP/dt. SS during each sample period was expressed as percentage of
baseline values (SS%).
Measurement of RMBF
RMBF (mL · min-1 ·
g-1) was assessed by injection of radioactive
microspheres labeled with 141Ce,
95Nb, or 103Ru (Du
Pont–New England Nuclear), as previously described.23
RMBF in the ischemic area was expressed as a percentage of RMBF
in the nonischemic region. RMBF was measured at baseline
(n=12), during occlusion (n=12), and reperfusion (n=10).
Statistical Analysis
Baseline and subsequent echographic and sonomicrometry
measurements were compared by use of repeated-measures ANOVA. Standard
linear regression analysis was used to relate changes in
systolic velocities to either SS or RMBF. All values are
presented as mean±SEM. A value of P<0.05 was
considered statistically significant.
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Footnotes |
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The Methods section of this article can be found at http://www.circulationaha.org
Received June 2, 1999; revision received October 7, 1999; accepted October 20, 1999.
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