TECHNOLOGY
TECHNOLOGY - A
TISSUE DOPPLER IMAGING IN CORONARY
ARTERY DISEASE
Gabriel W. Yip, MD; Steve R. Ommen, MD, FACC
Division of Cardiovascular Diseases and, Internal Medicine,
Mayo Clinic, Rochester, Minnesota, USA
 1.1 Detection and assessment of coronary artery disease
1.2 Evolution of tissue imaging
2.1 Tissue Doppler Imaging
2.2 Strain rate imaging
2.3 Myocardial velocity gradient
3.1 Myocardial Velocity Assessment (Standard
TDI)
3.2 Myocardial strain rate imaging
Tissue Doppler imaging (TDI) has rapidly evolved over the last decade as a sensitive clinical tool of measuring both global and regional myocardial velocities and their relationship to the cardiac cycle with high spatial and temporal resolution.
Measurement of mitral annular velocities reflects global left ventricular LV function at rest or during stress echocardiography.
Regional analysis of peak segmental systolic myocardial velocities during stress improves accuracy of novice readers, of interpreting basal segments, and concordance between observers.
Moreover, it has higher sensitivity and comparable specificity to standard dobutamine stress echocardiography in detecting myocardial viability.
Myocardial velocity gradient, being independent of cardiac translational movement, has also shown promise for detecting resting and induced ischemia and viable myocardium. Strain rate imaging (SRI), based on tissue Doppler technology, has clinical potential of quantitative assessment of regional contractility and function during stress echocardiography.
Abnormal wall motion during isovolumic contraction and relaxation periods and their clinical implications of correlating myocardial viability has been discussed. Improved data acquisition and rapid postprocessing of TDI will facilitate its incorporation into standard regional myocardial assessment.
(Heart Views. 2002;3(1):6-20) © 2002 Gulf Heart Association.
Coronary artery disease (CAD) remains the leading cause of death in the USA,
causing one in every 4.9 deaths and over 12 million people report a history of
angina, previous heart attack or both (1).
Accurate early identification of CAD is critical in reducing morbidity and
mortality. Stress echocardiography is widely used to diagnose flow-limiting CAD.
In general, exercise and pharmacologic stress echocardiography are more
sensitive in detection of myocardial ischemia than electrocardiographic
variables and have evolved as cost-effective alternatives to nuclear methods
(2-4).
Traditional diagnostic criteria of regional dysfunction are based on
detection of: 1) regional delay in myocardial motion, 2) differences in
amplitude and direction of regional wall motion and 3) regional wall thickening
and thinning characteristics. Unfortunately, most stress-echo interpretations
are still based on subjective visual recognition of abnormalities of wall motion
or thickening with segments scored in a semi-quantitative manner.
Furthermore, issues of reproducibility (5) and requirement for adequate
training (6) are also important limitations of the technique.
An objective and quantitative assessment of regional wall motion should
enhance concordance between interpreters and improve accuracy of the novice
readers.
In this regard, tissue Doppler echocardiography (TDI) and strain rate
imaging (SRI) an evolving technology of the former, may herald an
improvement in the noninvasive assessment of regional myocardial function.
Tissue Doppler imaging (TDI) is an extension of conventional Doppler flow echocardiography and has been proven to be a useful and feasible clinical tool for assessing global as well as regional ventricular function since its introduction in the early 90s. Isaaz et al (8) pioneered pulsed-wave Doppler measurements of myocardial wall velocity and mitral annular motion in the late 1980s. In 1994, Sutherland et al (9) and Yamazaki et al (10) introduced color-coded Doppler myocardial imaging which recently became a standard built-in technology in many commercially available equipment packages.
TDI has been validated both in vitro (11-12) and in vivo (13-17). It has been clinically applied in assessing regional and global left ventricular (LV) systolic (18-19) and diastolic function (20-24); estimating the LV filling pressure in various clinical states (25-29) and detecting allograft rejection in cardiac transplant recipients (30-33).
It helps in differentiating constrictive pericarditis from restrictive cardiomyopathy (34-35), differentiating athletic heart from hypertrophic cardiomyopathy (36), and detecting hypertrophic cardiomyopathy (HCM) gene carriers even in the absence of fulminant phenotypic expression (37).
This review will examine the role of tissue Doppler techniques (myocardial velocity assessment and strain rate imaging) in the detection of coronary artery disease.
The pulsed and color Doppler echocardiography can detect motion and velocity
of both moving blood and myocardial tissue.
We have traditionally processed blood flow signals
in the conventional Doppler flow imaging, so that
the high velocity and low amplitude Doppler signals
reflected by the moving blood are measured whereas
the myocardial Doppler signals with high amplitude
but low velocity are suppressed.
To better analyze myocardial signals, the high-pass
filter used to optimize blood flow signals is
minimized. In addition, a signal intensity threshold
filter has to be altered with lower gain amplification
to eliminate the weak intensity of blood flow
signals.
These improve the ability to measure low
velocity myocardial signals that are typically
in the range of 0.6 24 cm/s. TDI analysis, with
generally favorable signal to noise ratio, is
relatively independent of 2-dimensional image
quality. Another important aspect of the TDI is
high frame rate image acquisition, which is crucial
for temporal resolution. With digital parallel
processing techniques, frame rate of >150 frames
per second can be achieved with increased pulse-repetition frequency
(PRF) and narrow sector angle of region of interest
(ROI).
As in the blood flow Doppler,
the myocardial velocity can be assessed using
pulsed-wave or color-encoded for both speed and
direction. Color Doppler allows for visual semiquantitation
of myocardial motion, superimposed on conventional
M-mode and two-dimensional images. However, the
color-encoded TDI signal processing gives mean
velocities whereas real-time pulse-Doppler analysis
represents the highest peak velocity from the
sample volume selected. With narrow sector angle,
the color TDI has now achieved a temporal resolution
comparable to the pulsed-wave Doppler but requires
off-line analysis that can be time-consuming and
the facility may not be widely available. Using
specific software, the color Doppler data can
also be processed to display in-color M-mode,
by drawing a straight or curve line anywhere within
the color available. Such anatomically curved
TDI M-modes display direction, timing and synchronicity
of motion with high frame rates (5-20msec) within
the selected segments.
In order to optimize the TDI
signals, the color gain should be set to level
just below the color-noise artifact. The upper
velocity range for the myocardial velocities should
also be maximized to a level just below the highest
velocity recorded at rest or during stress echocardiography
so as to enhance sensitivity of velocity measurement.
The usual setting of the upper limit of the velocity
scale is around 14 to 20cm/sec for both resting
and stress TDI. The myocardial velocity data can
then be analyzed real-time or off-line by computer
workstation.
Figure 1
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Figure 3. Strain rate acquisition. Two velocity components V1, V2 separated by a distance d. The strain rate (SR) is calculated by the differential velocity (V2-V1) over a distance d.
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As mentioned, pulse-waved TDI as opposed to color-coded
TDI measures peak, rather than mean myocardial
velocities. It does not require off-line analysis
and provides instantaneous temporal display of
Doppler spectral velocity data (Figure 1). The
sampling, however, cannot be localized to the
endocardial or epicardial layers. While requiring
off-line analysis, color Doppler has the advantage
of simultaneously acquiring multiple segments
in one view and this is particularly useful within
a limited acquisition window of stress echocardiography
(Figure 2).
First introduced in 1973 by Mirsky and Parmley (40), strain
(e) and strain rate (SR) are measures of regional myocardial thickening and
thinning of the heart muscle. Myocardial strain is a dimensionless index of
change in myocardial length in response to an applied force. Strain rate is the
time derivative of strain with unit of change per second (sec -1)
and represents the differential velocity of two points adjusted for the distance
between them (Figure 3). Strain rate imaging (SRI) is therefore an extension of
technology derived from the tissue Doppler imaging (TDI).
Previously, intrinsic myocardial deformation or strain was
invasively measured by tracking movement of implanted radio-opaque markers (eg.,
metallic beads) by biplane cineangiography (41-42) or video technique (43),
measuring mutual motion and angulation of three needles pierced into the
myocardial wall, using an electromagnetic inductive technique (44), or by
sonomicrometry in the myocardium (45).
Now both parameters (strain and strain rate) can be derived non-invasively
from either magnetic resonance imaging (MRI) tagging techniques (46-48) or
echocardiography using M-mode (49-50) or more commonly high frame rate (>150
frames/sec) tissue Doppler velocity data after post-processing (51-52) (Figures
4-5). These non-invasive techniques overcome the inherent
limitations of overall cardiac translation and motion
influence by adjacent segments in assessment of local intrinsic LV function
(53).
It is important to note that the MR and echo techniques assess different
strains that are not interchangeable. There are inherent strengths and
weaknesses to each that are beyond the scope of this review.
Figure 4
The MVG is simply a measure of
regional radial strain rate of a small area of
myocardium. Unfortunately, based on processed
color-encoded velocity data, it lacks spatial
resolution and, therefore, may not detect lower
strain rate. Technical development of on-line,
high speed and large quantity image acquisition
and storage system together with an automated
myocardial edge detection technique should facilitate
such application in future. Normally, the endocardium
moves faster than the epicardium except during
isovolumic relaxation when the reverse is seen.
Thus, there is a gradient of increasing velocity
from the epicardium to the endocardium as myocardial
wall thickens in systole, which can be served
as a marker of regional contractility. The myocardial
velocity gradient (MVG) can be obtained from color
M-mode recording of anteroseptal or posterior
wall from parasternal position using either high
frame rate M-mode data (38) or lower frame rate
(up to 59 frames/sec) two-dimensional data (39).
Several other methods, including
centerline methods (54), color kinesis (55), and
automatic boundary detection (56) have been proposed
to aid qualitative interpretation of wall motion
scoring and to give some semi-quantitative measure
of regional contractility. In general, these methods
require reasonable endocardial border definition
and /or lengthy time for post-acquisition data
analysis.
The global LV systolic function can be assessed by peak mitral annular (MA) velocity in apical views.
Although myocardial synchronous contraction and relaxation depends critically on coordination of circumferential and longitudinal fibers, the longitudinal fibers are particularly vulnerable to myocardial ischemia and activation disturbance likely related to their subendocardial position (57).
Because the epicardial apex is relatively fixed (58), the longitudinal fiber shortening draws the atrioventricular ring towards the apex of the ventricle. Not only does this contribute to the fall in the left ventricular cavity volume with ejection, but at the same time increases the volume of the left atrium.
Similarly, during diastole, the backward movement of the atrioventricular ring aids the LV filling. Dumesnil et al.
showed that with a 40% decrease of LVEF (M-mode) in disease, there might be only 15-20% corresponding decrease in the circumferential fiber (short-axis) shortening (59), highlighting the significant contribution of longitudinal fibers in overall LV function.
Figure 5
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Figure 5. Off-line color M-Mode analysis
of strain rate of the antero-septum from
the base to apex. (dotted line on 2D color).
S= Systolic strain rate; E= Early diastolic
strain rate; A= Late diastolic strain rate;
D= Diastasis. (Courtesy of TP Abraham MD)
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Since the introduction of the
concept of mitral annular descent by echocardiography
in 1967, it has been shown that the peak systolic
mitral annular amplitude and total excursion correlate
well with LV stroke volume (60-63). Its amplitude
and velocity have been used as an index of ejection
fraction (EF) and been shown to correlate with
the LVEF obtained by radionuclide ventriculography
in humans (64-66).
The systolic MA amplitude also
predicts mortality in patients with chronic heart
failure (67). Decreased MA excursion was demonstrated
during balloon angioplasty (68) and was normalized
within 48 hours of a successful procedure (69).
The asynchrony of a particular annular site correlates
with reversible defects on thallium myocardial
perfusion (70), and with distribution of coronary
stenosis by angiography (71). Additionally, the
MA motion shown to be abnormal just before vein
grafting in coronary artery disease normalized
within four hours of operation (72). The regional
asynchrony as reflected by the timing, amplitude
and velocity of the MA motion is further aggravated
by dobutamine stress (73). The asynchrony can
occur in the absence of symptoms and ECG changes
and thus provides sensitive, non-invasive and
highly reproducible evidence of ischemia.
Tissue Doppler not only defines and measures
the mitral annular movement, but also gives high
temporal relationship. Decrease in peak systolic
descent velocity at a mitral annular site with
corresponding longer time to peak correlates with
LV asynergy and infarct regions in patients with
previous myocardial infarction (74). Henein et
al demonstrated that a combination of systolic
and
diastolic long axis disturbances
at rest in patients with peripheral vascular disease
can be used to predict peri-operative surgical
risk as assessed by adenosine thallium emission
tomography (75). They proposed a long axis score
that could stratify these patients into two categories
of high or moderate/ low risks. However, general
application of this score in other population
groups with different pre-test likelihood of coronary
disease is still unknown. The sensitivity and
specificity of the scoring and whether it could
further stratify lower risk group require further
study.
The mitral annular velocity has also been shown
to be a sensitive marker of alteration of LV contractility
induced by inotropic stimulation. In studying
12 normal volunteers, Gorcsan et al. showed that
peak mitral annular velocity increased significantly
with corresponding decrease in time to peak velocity
at very low dose (1mcg/kg/min) dobutamine. A further
linear dose-dependent incremental increase of
the velocity was observed up to the target infusion
of 5mcg/kg/min (76). In contrast, regional peak
velocities did not change until the 2mcg/kg/min
dose and no change of myocardial wall thickening
and ejection fraction was observed until 3mcg/kg/min.
These data support the mitral annular velocity
as a sensitive marker of global systolic function,
even when the endocardial definition is suboptimal
for estimation of LV volumes and ejection fractions.
The MA velocity provides important insight in
terms of amplitude, velocity and timing in relation
to the cardiac cycle.
For detection of induced myocardial
ischemia, assessing abnormal regional function
within each vascular territory may be more important
than the global function. Measurement of the annular
displacement reflects abnormality in each wall
and does not allow a segmental evaluation pertaining
to a vascular territory.
Segmental TDI can quantitate
the extent of abnormal myocardium and also detect
regional delays in the onset of motion, which
has been shown to precede changes in regional
myocardial systolic amplitude of motion (77).
TDI assessment is more accurate and objective
than human visual assessment, which can, at best,
detect motion delays of 89 ms (or about
70 ms if abnormal image is viewed side-by side
with the normal)(78). By comparison, Derumeaux
et al. demonstrated that TDI can detect a 30 msec
prolongation of isovolumic relaxation time during
acute animal ischemia which correlates with >70%
stenosis of the culprit artery (79). Regional
delay in myocardial motion is, therefore, an important
early marker of ischemia. The accurate identification
and quantification of delays, amplitude and velocity
of regional wall motion during both rest and stress
echocardiographic studies should improve both
the sensitivity and specificity of ischemia detection.
Both pulsed-wave and color tissue
Doppler velocity have been used to quantify regional
wall motion changes with dobutamine stress echocardiography
and exercise echocardiography. However, it has
been shown that dobutamine results in greater
regional systolic myocardial velocities than maximal
exercise, and enhances the differences between
ischemia and normal zones (80).
In experimental settings, myocardial
velocity has been shown to accurately reflect
changes in regional and global LV function induced
with dobutamine, esmolol, and ischemia (81,83).
In humans, differential changes of the systolic
velocity during stress have correlated with normal,
ischemia, and scar responses interpreted by standard
wall motion scoring. The ischemic segments have
lower resting systolic velocity than the normal
segments while scarred segments are even slower
than ischemic segments. Both scar and ischemic
segments have lower peak systolic velocity with
blunted incremental response to stress than the
normal segments. Furthermore, these velocity changes
correlate well with abnormalities on myocardial
perfusion imaging. Heart rate, functional capacity
and regional dysfunction (scar or coronary ischemia)
are independent determinants of peak exercise
myocardial velocities (86-87).
It is recognized that there is
a gradual decrease of the longitudinal myocardial
velocities from the base to the apex. This results
from a relatively stationary apex and differences
in myofiber orientation. Having established good
correlation between regional LV dysfunction and
peak systolic myocardial velocity, the next step
toward clinical application is to identify normal
ranges for different myocardial segments and then
apply these as diagnostic criteria for the identification
of significant coronary artery disease.
Katz et al. studied 60 patients, aged 56 ± 10
years to determine the normal and abnormal segmental
velocity response to dobutamine stress
and the sensitivity, specificity
and accuracy of TDI in detecting abnormal wall
motion at peak stress (83). Two groups of patients
receiving comparable dobutamine and atropine dosages
were identified: 21 patients had normal stress
echocardiography and reached target heart rate
at peak stress and serve as control, whereas 19
had abnormal wall motion at peak stress. Apical
segments in the long axis were excluded because
of significantly lower myocardial velocities and
unfavorable wide angle of incidence with respect
to the transducer. A peak of systolic velocity
of 5.5cm/sec or less with the peak stress was
found to have an average sensitivity of 96%, specificity
of 81% and accuracy of 86% for identifying abnormal
segments at peak stress as defined by routine
2-dimensional criteria.
Cain et al. studied 242 patients
undergoing standard dobutamine stress echocardiography
and recording myocardial velocities using TDI
at rest and peak stress and establishing site-specific
normal ranges for basal and mid-ventricular segments
(88). 114 consecutive patients underwent coronary
angiography within 2 months of the stress echocardiography.
128 patients had a normal dobutamine stress without
angiography, including 57 patients with a low
(18 ± 15 %) pretest probability of coronary artery
disease. The 2-dimensional stress echo was interpreted
by an expert reader blinded to patients clinical,
angiographic, and the myocardial velocity data.
Sensitivity and specificity of wall motion scoring
and myocardial peak systolic velocities were obtained
by comparison with angiographic evidence of coronary
artery disease (>50% diameter stenosis). The
wall motion scoring and peak systolic myocardial
velocity yielded comparable sensitivity (88% vs
83%) and specificity (81% vs 72%) and similar
overall accuracy (86% vs 80%) (all p-values not
significant). Interestingly, inexperienced users
measuring the myocardial velocities obtained high
intraobserver as well as interobserver concordance
with an expert. Similar to previous reports of
interobserver variation of 10% or less (84), this
study confirmed high reproducibility of TDI measurements.
This is an important advantage if integrated into
stress echocardiographic interpretation. In a
subsequent study, these same authors have suggested
a hybrid approach of combining wall motion scoring
in the apical segments and myocardial velocity
assessment in other segments for eventual clinical
application of this technique (89). The multicenter,
crossover study of 77 patients who underwent harmonic
dobutamine stress echocardiography and subsequent
coronary angiography, showed that integration
of regional myocardial velocity data into stress
echocardiographic interpretation would improve
accuracy of novice readers, of interpreting basal
segments, and in interobserver variability.
Early attention focused on measurement of peak
systolic velocity as the parameter likely to be
most useful in assessing regional LV systolic
function with stress, but more recently other
parameters such as the time to peak systolic velocity
and the velocity time integral (i.e., total systolic
displacement) have been proposed as equally important
measures (90). The multicenter, multinational
MYDISE study (MYocardial Doppler In Stress Echocardiography)
is an ongoing study assessing the feasibility
and reproducibility of these TDI methods. Early
results indicate that TDI does enhance both objectivity
and reproducibility of stress echocardiography
(91).
There are many reports on clinical feasibility of TDI in
the setting of induced ischemia during stress
echocardiography, but fewer reports on the clinical potential
of tissue Doppler imaging in detecting myocardial viability.
Rambaldi et al. reported detection of hibernating myocardium
in 40 patients with chronic ischemic heart disease and LV
dysfunction (mean EF 33±11%) using regional peak systolic
myocardial velocity during dobutamine stress echocardiography.
F18-fluorodeoxyglucose single photon emission computer
tomography (FDG-SPECT) served as the reference (92). The
baseline regional peak systolic myocardial velocity did not
differ between viable and non-viable segments. However, viable
myocardium showed higher systolic velocities at low and
peak-dose dobutamine than non-viable segments. An increase in
regional systolic velocity low-dose of >1±0·5 cm/s
predicted viability. For the prediction of viability, the
sensitivity (95%CI) of pulsed-wave Doppler was significantly
better than standard dobutamine stress echocardiography {87%
(8292) versus 75% (6781)}, while the specificity {52%(4459)
versus 51% (4559)} was comparable.
Like many other regional quantitative
myocardial indices, tissue myocardial velocity
is affected by cardiac translation. Moreover,
adjacent ischemic or scarred segments may affect
normal segments through tethering of their
motion, thus lowering the measured velocity, and
conversely, normal segments may augment the
velocity in abnormal segments. Because of a
relatively fixed epicardial apex and a
longitudinal velocity gradient from base to apex,
apical velocities are close to zero and
differentiating normal from abnormal apical
segments based on their myocardial velocity is
difficult.
To partially circumvent this problem, the imaging window is
narrowed to a sector angle of 20-30
for imaging individual ventricular wall with tilting in an apical view so that
the whole wall is parallel to sampling cursor. In this way, the frame rate is
enhanced, and the proximal one-third of the apical segments can be measured for
myocardial velocities within acceptable angle of insonation.
Because strain and strain rate are derived from the motion of
segments relative to each other, tethering and translation will affect both
velocity vectors equally and are therefore minimized. Measurement of strain at
one site reflects function at that site and therefore might be expected to have
greater spatial resolution than tissue Doppler velocity data alone. Normally,
the longitudinal strain rates in the anterior and septal walls are comparable
but higher than those in the antero-lateral and infero-lateral walls (93).
Myocardial strain derived from color tissue Doppler data
promises to improve the quantitation of regional myocardial contractile function
in the future.
The regional strain values have been validated to correlate
with those obtained from sonomicrometry in an acute ischemic canine model (53).
The real-time color SRI was shown to have moderately good correlation (weighted
k of 0.55) with the wall motion score of standard echocardiography in 15
patients with acute myocardial infarction (94) and also in identifying infarct
related artery of 20 similar patients (weighted k of 0.64) undergoing coronary
angiography (95).
Voigt et al. compared 12 patients with history of transmural
myocardial infarction with 10 normal controls
and found that longitudinal peak segmental systolic
strain and strain rate decreased with increasing
wall motion score (96). Edvardsen et al showed
that longitudinal segmental systolic strain and
strain rate are more sensitive in detecting regional
myocardial ischemia than tissue Doppler velocity
measurements in patients undergoing percutaneous
coronary intervention (97).
In the canine model, reduced systolic strain appears earlier
than tissue Doppler velocity abnormality and semi-quantitative visual wall
motion abnormalities in acute ischemia (98). Using closed chest animals, the
strain rate has been shown to correlate linearly with maximal value of the first
LV pressure time derivative (dP/dtmax)
and peak elastance(Emax),
both global measures of LV systolic function or contractility (99,100). In both
normal human and stunned porcine myocardium, the dobutamine-induced increase in
systolic strain rate (SR) preceded the increase in strain itself (e) and the
increase in LV systolic wall thickening (76,99).
An increase of peak systolic strain rate of more than 0.23
per sec from rest during low-dose dobutamine discriminates viable from
non-viable myocardium, as determined by 18F-fluorodeoxyglucose positron emission
tomography (FDG PET). The regional SRI compares favorably with TDI with better
sensitivity (83% vs 69%) and specificity (84% vs 64%) in the detection of
myocardial viability (101).
All these indicate that segmental strain rate analysis has a
promising and potentially superior role than tissue Doppler imaging in
quantitative assessment of regional contractility and function during stress
echocardiography.
The MVG has an advantage of being independent of translational movement of the heart (102). Secondly, it is more sensitive in differentiating ischemic from non-ischemic segments in submaximal dobutamine challenge than either endocardial velocity measurements or wall motion abnormality (103).
It detects resting regional myocardial dysfunction in post-MI patients with single vessel coronary disease (11, 103) and induced ischemia during submaximal dobutamine stress echocardiography in patients with single vessel coronary disease, prior MI and preserved LV function (104). It has been used in distinguishing viable from non-viable segments during low-dose dobutamine in patients with significant chronic triple coronary disease (>70% diameter narrowing) and LV dysfunction (LV ejection fraction <50%) (105).
Figure 6
Recently, there has been a renewed research interest in clinical significance of inward wall movement during the isovolumic contraction (IVCT) and relaxation (IVRT) period detected either by TDI or SRI in ischemic and post-ischemic myocardium. During coronary occlusion in dogs, most of the systolic lengthening occurs during IVCT and most of the subsequent shortening during the IVRT with more rapid change of LV pressure during these phases than during ejection (106). Thus, the abnormal wall motion during these periods may serve as better measures of regional LV function than peak wall motion during systole.
The delay of segmental longitudinal or radial LV contraction
until after the aortic valve closure is termed as post-systolic shortening (PSS)
or thickening (PST) respectively. PSS (or PST) represents LV asynchronous wall
motion during IVRT period (Figure 6) and has major effects on subsequent
ventricular filling (107). However, it is uncertain whether it directly causes
or indirectly worsens global LV diastolic dysfunction. It has been reported in
clinical conditions other than myocardial ischemia or stunning, e.g., activation
abnormalities as in left bundle branch block (108), syndrome X (109),
hypertrophic cardiomyopathy (110) and aortic stenosis (111). Possible mechanisms
have been postulated. It may be due to delayed active contraction after
reduction of regional wall stress and relaxation of other adjacent LV segments,
or to delayed passive inward movement caused by adjacent normal contracting LV
segments as the LV pressure rapidly falls and the regional wall stress
decreases.
However, whether postsystolic shortening and thickening might represent an
active, or passive process, its clinical implications are still in debate.
Gibson et al. noted delayed inward motion during isovolumic relaxation as a
common finding in patients with acute myocardial infarction using digitalized
ventriculography at a data acquisition rate of 50 frames/sec but that invariably
resolved after successful reperfusion (112). Using sonomicrometry in an acute
ischemic canine model, the degree of PSS correlates with regional systolic
function immediately after reperfusion and also late functional recovery 2-3
weeks after the reperfusion (113-114).
Figure 7
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Figure 7. Curve longitudinal M-mode from base to apex of the anteroseptum. Delay in transition (arrow) from contraction to relaxation (prolonged regional TCEC) during mid-LAD occlusion, indicating ischemia. (Courtesy of TP Abraham MD)
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Based on centerline method of analyzing endocardial wall
motion in 35 patients with acute myocardial infarction undergoing
ventriculography before and after angioplasty, PSS in the infarct region
predicts recovery after reperfusion (115). In 23 patients with angiographically
proven significant coronary artery disease, 98% of all hypo- and akinetic
regions with PST and only 6% of those without PST improved at low dose
dobutamine stress-echo. Furthermore, 92% of segments with PST and 38% without
PST improved after revascularization (116). All these indicate that PSS (PST) is
related to myocardial viability. Larger clinical trials are needed for defining
its role in myocardial viability.
One of the potential clinical applications using SRI in
detecting PST is differentiation of ischemic from reperfused yet stunned
myocardium during dobutamine stress echocardiography. In closed chest porcine
model, total and graded ischemia results in delayed onset and decrease in
regional systolic strain and strain rate but increased post-systolic thickening
(117-118). Dobutamine infusion causes a further decrease in maximal regional
strain and concomitant increase in postsystolic thickening in persistent
ischemic segments, whereas it normalizes regional PST gradually with further
increase in systolic strain and strain rate at higher stimulation in the stunned
myocardium (99).
SRI can also depict segmental PSS as a prolonged transition from myocardial
compression to expansion i.e., prolonged time from peak R wave on ECG to
compression/expansion crossover (TCEC)
(Figure 7). Using this new parameter, prolonged TCEC
correlates with and spatially quantifies ischemic myocardium measured from both
stained porcine myocardium (119) and perfusion defects from myocardial contrast
echocardiography (120). An initial study of 40 patients suggests that this new
parameter is feasible with additional 5 minutes of SRI to standard dobutamine
stress-echo time. In normal myocardial segments, TCEC
at peak stress decreases significantly from
baseline but this response is attenuated in ischemic segments. Using a 20%
reduction of TCEC as
cut-off based on receiver operator characteristic curves, sensitivity and
specificity for detection of ischemic segments were 77% and 55% respectively
with corresponding values of 62% and 88% for standard dobutamine stress-echo
(121).
Figure 8
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Figure 8. In event of acute coronary ischemia, there is a marked decrease of inward wall movement with predominant negative velocity during the isovolumic contraction (arrow), indicating paradoxical outward wall movement. TDI images from a phased-array intracardiac ultrasound catheter. (Courtesy of C Pislaru MD)
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ntraction represent asynchronous and rapid myocardial
contraction after ventricular activation but before aortic valve opening,
resulting in minor changes in the LV volume and wall thickness. Similar to
postsystolic thickening in the IVRT period, they are also sensitive to acute
myocardial ischemia and correlates with transmural myocardial infarct (Figure
8). It has been shown in acute ischemic animal models that segmental IVCT
velocities decreased to zero when >20% transmural necrosis was involved in
the corresponding segment after staining. The IVCT velocities also correlated
better with extent of transmural infarct after reperfusion than segmental peak
systolic and early diastolic velocities (122). Thus, the resting segmental IVCT
velocity potentially provides a rapid clinical, non-invasive bedside technique
of quantifying transmural extent of viable myocardium after reperfusion in acute
myocardial infarction.
Strain and strain rate measurements have their technical
limitations. Similar to any Doppler techniques, they are highly dependent on
angle of insonation. Every effort is made to ensure the tissue direction is less
than 30o
from the beam direction but this is technically challenging in the apical
segments as the angle becomes wider. The narrow sector angle approach on
individual wall obviates some of the above problem. But it lacks of concurrent
comparison of regional wall motion with contralateral segments. Like myocardial
Doppler velocities, strain is markedly load-dependent (53).
Further clinical trials will be needed for determining
sensitivity, specificity and accuracy of using individual segmental strain and
SR parameters or in combination, for detecting induced ischemia by either
exercise or pharmacological stress, and also their clinical role in assessing
myocardial viability either at rest or with low-dose dobutamine. Furthermore,
whether delayed onset of regional asynchrony is better than strain and SR
indices in detection of induced ischemia will require further clinical
validation.
Current TDI and SRI have the advantage of high temporal and
spatial resolution but depend heavily on data postprocessing of these images,
which will likely increase computative demands in future. With future advance in
image acquisition and postprocessing, it is hoped that the imaging techniques
could become easier to use and apply clinically. The rapid assessment of
regional myocardial velocities and strain could play a useful role in standard
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TECHNOLOGY- A
