From the Départment de Cardiologie, Hôpital Charles Nicolle,
Centre Hospitalier Universitaire de Rouen, and Laboratoire de Physiologie
Lyon-Nord et Service de Cardiologie D, Université Claude Bernard (M.O.,
J.L., X.A.-F., Y.M.), Lyon, France.
Correspondence to Geneviève Derumeaux, MD, Service de Cardiologie, Hôpital Charles Nicolle, 1, Rue de Germont, 76000 Rouen, France. E-mail brice.letac{at}chu-rouen.fr
Methods and ResultsIn nine open-chest anesthetized pigs,
various degrees of regional wall motion abnormalities were induced by
graded reduction of left anterior descending coronary artery
(LAD) blood flow. Pulsed Doppler tissue imaging was performed from
an epicardial apical four-chamber view with the sample placed within
the middle part of the septal wall. Peak septal velocities were
calculated during systole, isovolumic relaxation, and early and late
diastole. Regional myocardial blood flow and
systolic and diastolic dysfunctions were assessed
by radioactive microspheres and ultrasonic crystals,
respectively. Ischemia resulted in a significant rapid
reduction of systolic velocities and an early decrease in the
ratio of early to late diastolic velocities. Both changes
were detected by pulsed DTI within 5 seconds of coronary artery
occlusion. The decrease in systolic velocity significantly
correlated with both systolic shortening (r=.90,
P<.0001) and regional myocardial blood flow
(r=.96, P<.0001) during reduction of LAD
blood flow.
ConclusionsThese results suggest that DTI may be a promising new
tool for the quantification of ischemia-induced regional
myocardial dysfunction.
DTI is a new ultrasound technique that is based on color Doppler
imaging principles and allows quantification of intramural myocardial
velocities by detection of consecutive phase shifts of the ultrasound
signal reflected from the contracting
myocardium.17 18 19 To display regional
myocardial velocities, thresholding and filtering algorithms are
changed to reject the low-amplitude echoes from the blood pool. DTI
allows the high-intensitylow-amplitude information from the
myocardium to pass to subsequent determination of the mean
Doppler shift and hence mean velocity determination by use of
standard autocorrelation methodology. Whereas conventional ultrasound
techniques derive their information on myocardial function either from
parameters measured from the blood-myocardial boundaries or
from blood-pool Doppler indexes, DTI directly measures indexes of
myocardial function from within the myocardial wall.
Little is known about the ability of pulsed DTI to identify and
quantify wall motion alterations during regional
ischemia.20 In the present study, we
used a classic pig model of ischemia/reperfusion to investigate
whether pulsed DTI might be a useful tool to analyze regional
myocardial dysfunction. Specifically, we sought (1) to define the
pattern of myocardial velocities during regional sequences of
ischemia and reperfusion and (2) to compare DTI measurements to
modifications in segment length measured by the conventional
sonomicrometry technique.21
Surgical Preparation
Echographic Measurements
Experimental Protocol
Echographic and segment length recordings were performed
sequentially at the following time points: at baseline, during partial
stenosis, during total occlusion, and after reperfusion of the
LAD.
At the end of each experiment, the LAD was briefly reoccluded and 0.5
mg/kg IV Unisperse Blue Pigment (Ciba-Geigy) was injected to delineate
the in vivo area at risk as previously
described.22 Under deep anesthesia,
the heart was stopped by intravenous injection of potassium
chloride (20 mEq), excised, and cut into 5- to 7-mm-thick transverse
slices parallel to the AV groove. We verified that the
interventricular septum in the five apical transverse
slices was unstained, ie, that the Doppler sampling gate was well
in the ischemic area. The correct position of the two
ultrasonic crystals within the risk region was checked, and two
transmural myocardial samples were excised (one from the
ischemic and one from the nonischemic zone) for further
measurement of regional MBF.
Data Analysis
Echographic Measurements
The variation of myocardial velocity during or after coronary
occlusion (Voccl) was expressed as a percentage
of baseline velocity (Vbasal) as
V%=Voccl/Vbasalx100%.
Intraobserver variability was tested in eight pigs by repeating the
measurements on two occasions under the same basal conditions. To test
the interobserver variability, the measurements were repeated from the
videotape recordings by a second observer who was unaware of
the results of the first observer. For measurement of systolic
velocity, and early and late diastolic velocities,
intraobserver and interobserver variability ranged from 3.9% to
4.5%.
Regional Myocardial Function
SS was defined as SS=[(EDL-ESL)/EDL]x100%. LDL was defined as
LDL=[(mSL-EDL)/EDL]x100%, with mSL (minimal segment length) being
the lowest point of the wall motion tracing at any time of the cardiac
cycle (Fig 2
Measurement of Regional MBF
Statistical Analysis
Hemodynamics and Regional MBF
Normal Pattern of Midseptal Wall Velocities
In the five pigs that underwent pulsed DTI analysis before
thoracotomy, similar sequential events were observed, but in all cases,
the IR wave was negative instead of positive (Fig 1
Time Sequence and Pattern of Myocardial Velocity Changes
During Ischemia/Reperfusion
Diastolic abnormalities also occurred very quickly after
the onset of ischemia. Immediately after LAD occlusion,
VE significantly decreased, and
VA increased (Fig 4
In five pigs, we also measured velocities in the remote
nonischemic lateral wall during ischemic episodes
induced by partial stenosis of LAD. Ischemia in the LAD
territory did not significantly alter systolic or
diastolic velocities in the lateral wall:
VS averaged 8.9±0.7 versus 9.1±0.6 cm/s at
baseline (P=NS) and
VE/VA averaged 1.3±0.5
versus 1.3±0.4 at baseline (P=NS).
Comparison Between DTI Velocities and Wall Motion
Abnormalities
Comparison Between DTI Velocities and Regional MBF
The relationship between the decrease in MBF (MBF%) and in
systolic velocity (VS%) was best fitted
by a polynomial expression according to the following equation:
Vs%=-0.004 MBF%2+1.73 MBF%-49.14
(r=.96; Fig 7A
A similar correlation existed between SS and MBF%, but this
relationship was best fitted by a linear regression equation (Fig 7B
Myocardial function became severely depressed when MBF decreased <40%
of baseline values.
DTI is a new echocardiographic method based on the
Doppler principle, which provides a velocity map of the myocardial
wall.17 18 19 DTI velocity maps are available by
use of two-dimensional imaging and M-mode and pulsed-wave Doppler.
Low frame rates available from two-dimensional acquisition associated
with the Doppler angle of insonation of the myocardium
preclude two-dimensional DTI for measurement of rapid myocardial
velocity changes. M-mode DTI interrogation of intramural velocities
overcomes the temporal resolution problems inherent with the
two-dimensional approach and allows the assessment of endocardial to
epicardial velocity gradient.24 25
But it needs the development of special programs for off-line
analysis because M-mode quantification of velocities is not yet
available on our ultrasound system. Pulsed-wave DTI provides
quantitative information available on-line and was therefore used in
this study to analyze septal wall velocity resulting from
long-axis shortening of the heart and its variations after LAD
occlusion.
Normal Patterns of Regional LV Wall Motion and Velocities
In the present experimental preparation, five waves of wall
velocity, including two systolic and three
diastolic events of the cardiac cycle, can be described for
the first time from recordings of midseptal velocities. The
same pattern of velocities was described by Rodriguez et
al26 27 within the mitral annular and Isaaz et
al28 within the LV posterior wall. Both sets of
authors reported a good correlation between myocardial velocities
derived from M-mode tracings and DTI measurements. However, the
determination of myocardial velocities by M-mode appeared difficult,
time-consuming, and poorly reproducible, which might explain why M-mode
echocardiography has been considered an unreliable
tool for assessment of regional wall
function.29
It is worth noting that velocity of isometric relaxation shifted from
negative to positive values when the chest was opened. Although we did
not specifically investigate this issue, we speculate that it may be
related to modifications of the transeptal interaction between the two
ventricles, secondary to reduction of loading conditions and
pericardectomy in the open-chest
preparation.30
Detection and Quantification of Ischemia-Related Wall
Motion Abnormalities by DTI Velocities
Our DTI data are in close agreement with these observations. Pulsed DTI
was able to detect significant systolic and
diastolic velocity changes as soon as 5 seconds after LAD
occlusion, a time frame comparable to those reported when
sonomicrometry was used.31 32 33 Systolic
velocity during the ejection phase was well correlated with segment
shortening, whatever the severity of ischemia. During isometric
relaxation, velocity became positive and markedly increased. This
paralleled postSS observed on segment length recordings
and suggests an asynchrony in myocardial contractility
as previously reported by Gibson et al35 in
patients with coronary artery disease. Early
diastolic velocity decreased and late diastolic
velocity increased, resulting in an inversion of the
VE/VA ratio. Its
correlation with LDL, as described with sonomicrometry, was
statistically significant but obviously much weaker than
analysis of the systolic pattern. The reason for the
poor correlation between diastolic indexes is unclear but
might be related to the complex translation/rotation of the heart
during the cardiac cycle. It might also be related to the fact that DTI
analyzed septal wall motion, which is affected by right
ventricular pressures whose influence is likely more
important in diastole.
Although VS slightly overestimated the degree of
regional wall motion abnormalities, it appears to be a useful index for
assessment of regional wall motion impairment related to severe,
moderate, or even mild ischemia. This was also confirmed by the
correlation of ejection systolic velocity and regional MBF.
Even slight reductions in regional MBF were associated with a decrease
in both myocardial velocities and segment shortening. We observed that
ejection systolic velocity became negative for a reduction in
MBF reaching 40% of baseline values, which is also associated with the
onset of regional bulging as previously
described.22
Interestingly, pulsed DTI was able to identify the hyperemic
response after reperfusion of the ischemic
myocardium. Although this transient increase in regional
contractile function is usually short-lived, its identification may be
useful as an indicator of reperfusion in the setting of acute
myocardial infarction. When postischemic contractile
dysfunction ("myocardial stunning") developed despite restoration
of a normal (or nearly normal) MBF, pulsed DTI clearly identified wall
motion abnormalities similar to those observed during
ischemia.36 37 38 In other words, as
expected, pulsed DTI (as any other technique) failed to distinguish
ischemia from reperfusion-induced contractile dysfunction. With
respect to this, estimation of myocardial perfusion through measurement
of myocardial wall velocities must be done cautiously and is valid only
in situations of ischemia but not reperfusion.
Potential Clinical Implications
Study Limitations
DTI measurements, as any other method assessing myocardial excursion,
are affected by cardiac translation and/or rotation. Nonetheless, the
correlation with segment length measurements (that are poorly
influenced by cardiac translation) is good (r=.90),
suggesting that movements of the heart did not dramatically alter DTI
measurements.
Conclusions
Received September 17, 1997;
revision received October 28, 1997;
accepted December 1, 1997.
© 1998 American Heart Association, Inc.
Basic Science Reports
Doppler Tissue Imaging Quantitates Regional Wall Motion During Myocardial Ischemia and Reperfusion
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Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
BackgroundQuantification of
regional myocardial function is a major unresolved issue in
cardiology. We evaluated the accuracy of pulsed
Doppler tissue imaging (DTI), a new
echocardiographic technique, to quantify regional
myocardial dysfunction induced by acute ischemia and
reperfusion.
Key Words: imaging ischemia echocardiography ultrasonics
![]()
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
Because segmental
wall motion abnormalities are the hallmark of coronary artery
disease, ultrasound technique is widely used for the evaluation of
regional left ventricular function because of its ability
to depict endocardial excursion, myocardial thickening, and wall motion
in real time.1 2 3 4 5 6 7 However, conventional
assessment of wall motion, based on visual interpretation of
endocardial excursion and myocardial thickening, suffers from the
limitations of a qualitative method and is subjective and experience
dependent.8 Quantitative techniques, based on the
manual9 10 11 12 13 14 or
automatic15 16 myocardial edge detection, have
demonstrated acceptable correlations with other available techniques.
However, quantitative analysis is complicated by endocardial
"dropout" and trabeculae, which can impair the tracing
of endocardial border. There is therefore a need for ongoing
development for quantification of global and regional left
ventricular function.9 10 11 12 13 14 15 16
![]()
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
All experiments performed in this study conformed to the
Guiding Principles in the Care and Use of Animals approved
by the American Physiological Society.
Nine farm pigs, weighing 28±4 kg, were premedicated with
droperidol (1 mg/kg SC) and anesthetized with pentobarbital (15
mg/kg IV). Additional intravenous administration of
pentobarbital was performed when needed. Pigs were ventilated with room
air through a tracheotomy tube, and tidal volume and rate were adjusted
to provide physiological pH and blood gases. Body
temperature was monitored with a rectal thermometer and kept constant
by means of a heating pad. Cannulas were inserted into the right
jugular vein (for administration of drugs and fluids) and the left
carotid artery (for measurement of blood pressure). A 5F Gaeltec probe
was placed into the LV cavity through the right carotid artery to
measure LV pressure and its first derivative, LV dP/dt. A thoracotomy
was performed in the fourth left intercostal space, and a segment of
the LAD was isolated just before the first diagonal branch. A
micrometric constrictor, designed to gradually reduce coronary
blood flow, was positioned around the LAD. One pair of ultrasonic
crystals, used to assess regional contractile function, was inserted
via a small scalpel incision in the middle myocardial layer of the left
ventricle and oriented parallel to the short axis as previously
described.22 Crystals were placed in the center
of the soon-to-be ischemic LAD territory. A catheter was
inserted in the left atrium through the left atrial appendage to inject
radioactive microspheres for assessment of regional MBF. ECG
limb leads, arterial and LV pressures, LV dP/dt, and
segment shortening were monitored continuously throughout the
experiment on a Gould recorder (Gould Inc). The animals were
allowed 30 minutes after these surgical procedures to stabilize.
The echocardiographic recordings were
performed by means of an ACUSON 128 XP/10 with a 4-MHz transducer
equipped with DTI technology. Before thoracotomy, a first series of
velocity measurements was performed on five pigs that were lying on
their right sides, with the transducer placed over the left
ventricular apex to obtain an apical four-chamber view.
These measurements were performed to determine whether opening the
chest might induce some change in myocardial velocities. In the
open-chest preparation (all pigs), all velocity measurements were
performed with the beam positioned on the anterior wall near the apex
to obtain an epicardial apical four- chamber view. A fixed sampling
gate of 10 mm was placed within the middle part of the
interventricular septum. Care was taken to align the echo
image so that the interventricular septum be parallel to
the DTI cursor. Pulsed-wave DTI was continuously recorded on
super-VHS magnetic tape, with a videotape recorder for off-line
analysis. The spectral Doppler signal
parameters were adjusted to obtain Nyquist limits between
15 and 20 cm/s by use of the lowest filter settings and the optimal
gain to minimize noise and eliminate the signals produced by the
transmitral flow. We therefore analyzed the myocardial
velocities resulting from the long-axis shortening of the
heart.23
After baseline measurements, a graded reduction of the LAD blood
flow was performed by progressively (and, finally, completely)
tightening the micrometric constrictor. In each animal, several degrees
of constriction were adjusted to obtain various values of regional wall
motion abnormalities ranging from hypokinesis to dyskinesis: this was
done in a stepwise manner to reduce function by
40%, 60%, and
finally dyskinesis during total occlusion.
Hemodynamics
Heart rate and arterial and LV blood pressures were
measured and averaged over 5 continuous cardiac cycles in sinus rhythm
at baseline, during coronary artery stenosis or
occlusion, and after reperfusion.
From the DTI tracings, we measured the peak velocity of (1)
isometric contraction (VIC), (2) systolic
excursion (VS), (3) isometric relaxation
(VIR), and (4) early (VE)
and late (VA) diastolic excursion
(Fig 1
). Five beats were averaged for
each of these measurements. By definition, velocities were encoded
positive or negative when the displacement of the
myocardium was directed toward or away from the transducer,
respectively.

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Figure 1. Pulsed-wave DTI velocities obtained in the
longitudinal axis from an apical four-chamber view within midsegment of
the interventricular septum in a closed-chest pig. The
velocity scale is 15 cm/s.
SS and LDL were used as indexes of systolic and
diastolic function, respectively. To define these
parameters, ESL and EDL were obtained from three
well-separated cardiac cycles in each sample period. LV dP/dt was used
to define the timing of the cardiac cycle for segment length
measurements with ultrasonic crystals; EDL was measured at the onset of
the rapid increase in LV dP/dt, whereas ESL was measured at peak
negative LV dP/dt (Fig 2
).

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Figure 2. Representative recordings
of segment length tracings (SL) during control (baseline),
coronary stenosis, coronary occlusion, and
reperfusion. ECG, aortic pressure (AP), LV pressure (LVP), and LV dP/dt
are also shown. LV dP/dt was used to define the timing of the cardiac
cycle for segment length measurements with ultrasonic crystals: EDL was
measured at the onset of the rapid increase in the LV dP/dt, whereas
ESL was measured at peak negative LV dP/dt. Segment lengths at end
systole and at end diastole are indicated with the dotted
vertical lines. During coronary stenosis, a decrease in
the extent of SS was observed. After coronary occlusion, a
holosystolic bulging occurred, reflecting the paradoxical
expansion of the ischemic zone. MSL indicates minimal segment
lengthening.
). Both SS and LDL during each sample period were expressed
as percentage of the respective baseline values. Measurements of SS and
LDL were performed at baseline, during partial and total LAD
occlusions, and during reperfusion.
This measurement was performed in each pig to assess the
severity of ischemia during partial or total occlusion of the
LAD. Regional MBF (in milliliters per minute per gram) was measured by
use of radioactive microspheres labeled with either
141Ce or 103Ru (Dupont-New
England Nuclear) as previously described.22
Regional MBF was measured at baseline (n=1), during partial
stenosis (n=6), or during total coronary occlusion
(n=4). Briefly, microspheres were injected into the left atrium
via the left atrial catheter, and a reference blood sample was obtained
from the carotid artery at a fixed rate of 2.0 mL/min. At the end of
the protocol, samples were cut from the center of the ischemic
and nonischemic zones, weighed, and counted with the reference
blood samples in a gamma counter. Blood flow in the ischemic
area (in milliliters per minute per gram) was then computed and
expressed as percentage of MBF in the nonischemic region.
Differences between baseline measurements and subsequent values
were assessed by repeated-measures ANOVA. Standard linear regression
analysis was used to relate changes in myocardial velocities to
SS or segment lengthening. Polynomial regression analysis was
used to study the relationship between systolic velocities and
regional MBF. Myocardial velocities and MBF data (expressed as
fractions of control values) obtained from 11 measurements in eight
pigs were compared by use of the nonparametric Spearman
test because of the small sample size. All values are presented
as mean±SE. A value of P<.05 was considered to indicate a
statistically significant difference.
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Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
Nine pigs were entered into the present study. Each animal
underwent 1 to 5 episodes of either partial stenosis or total
occlusion of the LAD, each separated by an intervening reperfusion
period. The total duration of these ischemic events averaged
6±2 and 6±1 minutes, respectively. This design allowed us to
record 59 matched measurements of DTI velocities and segment
lengths among the nine animals.
All pigs had similar heart rate and blood pressure at baseline
(Table 1
). Neither partial
stenosis nor total coronary artery occlusion
significantly altered heart rate or blood pressure. After partial
stenosis, MBF in the risk area averaged 57±2% of that in the
nonischemic bed (Table 1
). As expected in this
collateral-deficient species, total LAD occlusion resulted in a
dramatic decrease in MBF that averaged 9±2% of MBF in the remote
nonischemic zone (Table 1
).
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Table 1. Hemodynamics and Regional MBF
In the open-chest pig under baseline conditions, pulsed DTI of
midseptal wall velocities displayed five consecutive waves whose
directions varied according to the phase of the cardiac cycle. During
systole, two positive waves occurred, one positive and short wave
corresponding to the isometric contraction (VIC)
(starting at the beginning and ending at the end of the QRS complex)
and one single ogival wave corresponding to LV ejection
(Vs) (starting at the end of the QRS complex and
ending at the end of the T wave). During diastole, one
positive and two negative waves were sequentially observed: a positive
isometric relaxation wave (VIR) followed by a
negative early (VE), rapid-filling wave and a
negative late-filling (VA) wave corresponding to
atrial contraction.
). In addition, peak
systolic velocity values were slightly but significantly higher
than in open-chest preparations (Table 2
). Myocardial velocities obtained in the
open-chest preparations were used as control values for further
comparison during LAD occlusion.
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Table 2. Comparison of Myocardial Velocities (cm/s) Within
Mid Septal Wall in Pigs Before and After Surgery
The time to onset of regional myocardial velocity
abnormalities in the ischemic myocardium is
presented for the first 60 seconds for 10 episodes of total LAD
occlusion in eight pigs (Fig 3
). Within 5
seconds of occlusion, systolic velocities
(VS) in the ischemic segment decreased to
46% of baseline values (P<.0001). Systolic
velocities became negative at
30 seconds and peaked at 1 minute of
occlusion. These negative velocities corresponded to the paradoxical
expansion of the ischemic segment observed on sonomicrometry
tracings (Figs 2
and 4
). This early
decrease in VS was associated with a
simultaneous increase in velocities during both isometric
systole (VIC) and isometric
(VIR) relaxation (Fig 3
). Velocity during
isometric relaxation progressively increased and peaked at 1 minute
after coronary artery occlusion (Fig 3
). At 1 minute after
reflow, VS and VIR
exhibited a transient positive and negative peak, respectively,
corresponding to the hyperemic phase (Fig 3
). Within 5 minutes
of reperfusion, VS progressively decreased,
whereas VIR increased and appeared as a positive
wave as reperfused myocardium developed
postischemic stunning (Figs 3
and 4
).

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Figure 3. Graph of the sequential changes during a
brief total occlusion of LAD on systolic and isovolumic
relaxation velocities (left) and on diastolic velocities
(right). Ten episodes of brief total occlusion of LAD were performed in
8 pigs. Immediately after LAD occlusion, early and significant decrease
of systolic ejection velocities (VS) was associated
with the increase of velocities during isometric relaxation
(VIR), the decrease of early diastolic
velocities (VE), and the increase of late
diastolic velocities (VA), leading to a
significant decrease in the ratio VE/VA. After
1 minute of occlusion, VS became negative whereas
VIR markedly increased. Immediately after reperfusion,
VS returned positive and recovered to a significant higher
value than at baseline. However, within 3 minutes of reperfusion,
VS decreased again, whereas VIR increased,
identifying myocardial stunning. *P<.05 vs baseline;
**P<.01 vs baseline; ***P<.001 vs
baseline.

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Figure 4. Representative recordings
of DTI tracings at baseline (open-chest pig) and during
coronary stenosis, coronary occlusion, and
reperfusion. During coronary stenosis, a decrease in
systolic velocity (VS) was associated with the
increase in isometric relaxation velocities (VIR), the
decrease in early diastolic velocities (VE),
and the increase in late diastolic velocities
(VA). After coronary occlusion, VS
became negative, reflecting the paradoxical expansion of the
ischemic zone. Immediately after reperfusion, systolic
velocities increased to higher values than at baseline but decreased
again within 3 minutes of reperfusion, identifying myocardial
stunning.
). As a consequence,
VE/VA ratio decreased and
further remained stable until reperfusion (Fig 3
).
VE/VA peaked at 1 minute
after reflow (hyperemic response) and thereafter returned
nearly ischemic values as diastolic alterations of
myocardial stunning appeared on segment length recordings.
To evaluate whether the severity of ischemia could be
accurately predicted by DTI, the individual systolic velocity
and diastolic
VE/VA ratio (both expressed
as a percentage decrease from baseline) were plotted versus
corresponding modifications in segment length. There was a significant
correlation between the variations of systolic velocity
(VS%) and those of SS:
VS%=0.78(SS)+10.6 (r=.90,
P<.0001; Fig 5
). This
strongly supports that the DTI measurement of VS
accurately quantifies the ischemia-related regional wall motion
abnormalities. The diastolic ratio
VE/VA also showed a
significant correlation with late diastolic lengthening,
but the relationship was weak (r=.39, P=.0049)
(Fig 6
).

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Figure 5. Linear relationship between percent decrease in
regional segment length shortening (SS%) (abscissa) and % decrease in
systolic velocities (Vs%) (ordinate). There is a significant
correlation between systolic velocities and segment
shortening.

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Figure 6. Linear relationship between percent decrease in
regional segment lengthening (LDL%) (abscissa) and percent decrease in
the ratio of early to late diastolic velocity
(VE/VA%) (ordinate). Relationship between the
two diastolic indexes was significant but weak.
Eleven measurements of regional MBF were obtained in eight pigs
and plotted versus simultaneous myocardial systolic
velocities (Fig 7
).

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Figure 7. A, Polynomial relationship between percentage of
decrease in regional MBF (MBF%) (abscissa) and percentage of decrease
in systolic septal velocities (VS%) (ordinate).
The amplitude of the systolic velocity decrease depends on the
severity of ischemia during coronary artery
stenosis/or occlusion. B, Linear relationship between
percentage of decrease in regional MBF (abscissa) and percentage of
decrease in regional SS (SS%) (ordinate). As expected, SS is
significantly related to the degree of regional MBF reduction.
).
).
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Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
In the present study, we report for the first time that pulsed
DTI can identify and quantify myocardial wall velocities during
regional ischemia and reperfusion. As demonstrated by
concomitant measurement of wall motion by sonomicrometry and assessment
of regional MBF by the radioactive microsphere technique,
pulsed DTI appears to be accurate and reproducible.
Understanding of the normal pattern of myocardial wall movement is
necessary for comprehensive assessment of DTI. The complex overall
motion of the heart can be divided into three different types of
movements: circumferential contraction assessed by short-axis view
interrogation, longitudinal contraction assessed by long-axis view, and
rotation. The translation of the whole heart also affects the
measurement of actual wall velocities, especially in the short-axis
view. In the present study, a long-axis recording of mid
septal velocities was preferred to a short-axis view to avoid the large
incidence angle between the direction of the circumferential septal
wall motion and that of the Doppler beam. Indeed, in the short-axis
view, a part of the myocardium, particularly the septal or
the lateral wall, moves perpendicularly toward the Doppler beam and
does not allow accurate myocardial velocity measurement.
To investigate whether pulsed DTI could accurately identify and
quantify the alterations of myocardial wall motion induced by
ischemia, we compared the changes in velocities to those in
segment lengths as measured by the reference method, ie,
sonomicrometry.21 Within 15 seconds of
coronary occlusion, systolic contraction decreased and
resulted in passive bulging of the myocardium in case of
severe ischemia. As expected, these modifications of
systolic wall motion were also significantly correlated with
the reduction of regional MBF as measured by the radioactive
microsphere technique.31 32 33
Simultaneous diastolic dysfunction developed
with a rapid increase in EDL and LDL.34
There are major potential clinical implications to the use of
pulsed DTI. In particular, we currently lack a reliable technique to
accurately quantify regional contractile function in humans. Contrast
and radionuclide ventriculography and conventional two-dimensional
echocardiography only allow semiquantitative
evaluation of LV function. Today, only cine MRI can quantify wall
motion, but it is not easily accessible for a large number of patients.
Pulsed DTI appears to be a sensitive, reproducible, accurate,
noninvasive echographic technique that may become a very useful
clinical tool for the diagnostic, follow-up, and evaluation
of the prognosis of cardiac diseases. Whereas effective clinical
application of DTI was hampered by low acquisition frame rates and a
lack of postprocessing software, a new third generation of Doppler
myocardial imaging system, with high temporal and spatial resolution,
has been developed that allows real-time acquisition with subsequent
on-line analysis of regional mean velocities. This new system
has recently been shown to provide reproducible and accurate
quantification of LV circumferential and longitudinal contraction in
all myocardial segments and therefore will allow stress
echocardiography to be
quantified.39 40 However, further studies are
needed to determine whether data in this experimental preparation can
be extrapolated to human patients.
Because of the version of the ultrasound machine used in this
study, we could not record simultaneously DTI
velocities and two-dimensional regional wall motion abnormalities. The
DTI velocity measurements were performed in the middle part of the
interventricular wall septum, whereas segment length data
were recorded from the anterior wall. However, these two regions
are supplied by the LAD; moreover, the middle part of the
interventricular wall septum was clearly included in the
area at risk as shown by the Uniperse Blue Pigment injection in the
heart slices. It is therefore likely that wall motion abnormalities in
the septum were comparable to those observed in the anterior wall.
DTI is a new, accurate, sensitive, noninvasive tool to quantify
on-line systolic and diastolic
ischemia-induced myocardial dysfunction. It appears to be a
promising method to quantify regional wall motion abnormalities in the
setting of ischemic heart disease.
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Selected Abbreviations and Acronyms
DTI
=
Doppler tissue imaging
EDL
=
end-diastolic lengthening
ESL
=
end-systolic lengthening
LAD
=
left anterior descending coronary artery
LDL
=
late diastolic lengthening
LV
=
left ventricle/ventricular
MBF
=
myocardial blood flow
SS
=
segment shortening
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References
Top
Abstract
Introduction
Methods
Results
Discussion
References
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