Case presentations on Norwegian DICE
session Euroecho 04.
Tissue Doppler should mainly be seen as an additional tool for decision
support, not as an independent diagnostic tool. It is important to
emphasise that:
- The utility of tissue Doppler depends on the quality of the
images. Artefacts such as reverberations, drop outs and angle deviation
between the direction of motion / deformation and the ultrasound beam
may reduce the data to rubbish.
- The more processed methods such as strain rate and especially
strain is even more prone to artefacts.
- The variability is high, due to the high variability.
- Studies often present differences between means, which is group
data, and not directly relevant for clinical decision making if
reproducibility is low.
- Presentations and illustrations are often the best examples
(including here), not what one will see in the average patient.
- Finally, the additional value of tissue Doppler is limited if the
pathology is obvious from standard echo.
Thus: Tissue Doppler should be considered an additional aid in decision
making, where there is uncertainty, and where recording quality is
good. Then one will have the benefits of the higher temporal and
spatial (axial) resolution of tissue Doppler.
Tissue velocities are least processed, and least prone to artefacts. It
is especially useful for timing.
Strain and strain rate have higher variability, but is tethering
independent, and thus will aid further in the correct location of the
pathology.
A more detailed information about the background of deformation
imaging, interpretation of findings and problems and pitfalls can be
seen in strain rate imaging.
Case 1: Patient with
Chest pain.
By Stig
Slørdahl,
Asbjørn Støylen and Siri Malm,
department of Circulation and Imaging, NTNU and department of
cardiology, St. Olav Hospital.
The patient was a 37 year old man, Smoker, no family history or other
risk factors. He presented with acute chest pain and nausea at 8:30 in
the morning. The pain persisted for about one hour. He was
admitted at the hospital at 10:00, and was at that time free of pain.
The initial ECG was described as normal. Initial Echocardiography was
performed as shown below. Before progressing further, it is advised to
try to assess if there are pathological findings, and if so, the
location and extent. Also try to be honest, is this easy or difficult
to see, without being primed that there may be something.
Initial echocardiography. of the three apical views; top
left four-chamber, top right two-chamber and bottom apical long axis.
This echocardiography was initially perceived as no certain pathology.
Findings of hypokinesia are most pronounced in the apical septum as
shown in larger format below:
The echocardiography was initially perceived as normal, at least
without specific findings. With hindsight, one can see a hypokinetic
area in the extreme apex, most pronounced in the apical septum of the
four chamber view. The finding, however, is subtle. In the actual case,
the patient were monitored in hospital, without treatment. The
recordings were
made with tissue Doppler data acquired in the background. The analysis
of the tissue Doppler data was not performed initially, but in
retrospective post processing. In this case, for those who are unsure
about the pathology, the analysis of tissue Doppler may give more
decision support.
Recordings from the apical septum, cyan and basal septum,
yellow. Tissue velocity (top left) is lower in the apex than the base,
but this is a normal finding as the apex is stationary while the base
moves back and forth. Thus there is a velocity gradient form the base
to the apex. It is difficult to ascertain that the apical
velocity is pathologically reduced. Strain rate (bottom, left),
however, is normally fairly the same from apex to base. In this case
there is reduced systolic strain rate to between -0.25 to -0.5 s-1
, and there is a marked post systolic shortening. These findings
are supported by strain (bottom right) showing apical systolic
strain of -5%, with an additional 4% post systolic strain, a
marker of ischemia). The values in the base are i the upper normal
range with systolic strain rate of -1.5s-1
and systolic strain of -25%.
In this case the suspicion of apical hypokinesia would be supported by
strain and strain rate, but not by velocity imaging. The findings are
consistent with ischemia, but as there is marked hypokinesia, there has
to be an additional component of necrosis or post ischemic stunning.
After two hours, the patient developed new chest pain, this time with
concomitant ST-elevation in ECG. At the same time, the answer of
initial laboratory tests were available, and showed an initial CK-MB of
34 microgram/liter and Troponin T of 0.36, consistent with a
necrosis. a coronary angiography was performed:
Angiograms , showing a tight LAD stenosis successfully treated
with acute PCI with stent. (Pictures courtesy of Dr. Kaare Bonaa
, St. Olav Hospital, Trondheim)
A follow up was done at day two and day 7 to see assess the initial
amount of stunning as opposed to necrosis. Consider the following two
chamber view, at first trying to remember back, but without looking at
the initial recordings.
To get a better assessment of this, it is not necessary to go to tissue
Doppler, a simple side by side comparison of loops in synchronised mode
will be helpful:
Initial presentation top left, day two; top right and day seven,
bottom left. all in four chamber view. The improvement from day one to
seven is easier to assess in this viewing mode.
Improvement is easier to see in this mode. however, tissue Doppler will
still give additional information, due to the ability to quantify
deformation.
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Strain rate curves from
day 1 (top) and day 7 (bottom). The initial apical hypokinesia (yellow)
is nearly normalised. In the 7 day image, the apical curve (cyan) shows
near normal peak strain rate of -1s-1 (even though it may be
a little slow in onset), and a post systolic shortening of less than
0.5.
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Strain curves from
day 1 (top) and day 7 (bottom). The initial apical
hypokinesia (yellow) shows partial normalisation. In
the 7 day image, the apical curve (cyan) shows a systolic strain of -8
to -9%, and an additional post systolic shortening of only -1 to - 2%.
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Case 2. Stress
echocardiography.
The patient was a 64 years old woman with hypertension, diabetes type
II, who for the last months had developed pain in both axillae and arms
while walking, especially uphill, and with worsening in cold weather.
Exercise test had been positive, with pain and ST-depression in V4
- V6. The point in this case is mainly to demonstrate
whetther stress echo can diagnose and locate ischemia. Dobutamine
stress echo was performed, 40 microgram/liter gave heart rate 136.
Recordings are shown below.
Stress echo recordings from the
apical long axis view. Top left, baseline, top right 10 microgram/l,
bottom left 20 microgram and bottom right, peak dose.
Try to assess whether there is ischemia, and if so, which area is
dysfunctional. With experience, the findings are obvious, but with less
experience findings are less obvious. To render findings more
objective, tissue Doppler can be analysed from the same loops. The
first thing is to look at the peak velocities. The application contains
the cut off values for stimulated peak velocities friom the Brisbane
database. At peak stress, if segment are scored normal in WMS, they
will be coloured green if peak velocity is above normal stimulated
velocity. This is shown below.
Peak velocity analysis. The green colour shows that peak
velocity is above normal cut off level for stimulated velocity, both at
20 and 40 microgam/l. Thus no evidence of ischemia.
Looking at the contraction paqttern, the most striking finding is
asynchronous motion, with a delay in the motion of the inferolateral
wall compared to the anteroseptal. This will not show up in peak
velocities, but in the timing that can be analysed from the
velocity traces. However, looking closely there is a delay of the
inferolateral wall even at baseline. This has to be analysed first:
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Tissue
velocities at baseline. It is evident that there is delayed onset of
motion in the inferolateral wall (yellow) compared to the anterior
septum, as perceived in the cine-loops. However, the simultaneous
diastolic waves indicates this to be a delay entirely within systole.
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Placing
a sample volume in the aortic ostium will identify end ejection by the
spike showing the rapid motion of the aortic cusp. Thus motion in the
lateral wall is shown to be entirely systolic.
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Strain
and strain rate shows the same, delayed onset of deformation in the
inferolateral wall, but all shortening within systole (ref. the AVC at
about 1.5 in the horizontal scale shown in the upper right panel)
without any sign of post systolic shortening.
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Having seen that the wall motion and
shortening is entirely systolic, we look at the recordings at peak dose:
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Tissue
velocities at peak stress. As at baseline, a sample volume in the
aortic ostium can identify the rapid motion of the aortic cusps, in
this case both AVO and AVC. The inferolateral basal velocities (yellow)
show a downward motion in early systole, and a upward motion in late
systole, continuing into post systole, compared to a normal
velocity curve in the anterior septum. However, peak velocities are
normal, as the algorithm identifies the high velocities in the peak of
the isovolumic contraction, not during ejection. Peak systolic velocity
during ejection
is indeeed reduced according to the Brisbane database. Thye failure to
identify this is in the application, because start systole is set by
ECG, not by stat ejection.
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Tissue
velocities comparing the basal inferolateral, the apical inferolateral
and the midwall anteroseptal wall. The curves show exactly the same
motion pattern in the apical and basal inferolateral wall. These
velocity curves show the same as the visual assessment, the wall motion, with paradoxical
motion at start systole, and apical motion continuing out in diastole.
However, by velocity (motion) analysis alone, both apex and base seems
to be ischemioc to the same degree.
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Strain
rate (left) and strain (right) from the same regions as top right. We
see that there is initial dyskinesia only in the basal inferolateral
wall, and with a pronounced post systolic shortening. The strain cirve
especially show that in the base there is only stretching and return to
baseline longth during systole, net shortening occurs only in post
systole. (Ref AVC at top left). In the apical inferolweteral wall,
there is reduced contraction and some, but less post systolic
shortening, and no systolic stretching (dyskinesia) at all. Thus, the
motion pattern seen in top right, in the apex, seems to be partially
due to tethering.
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Angiography data (courtesy of Knut Hegbom). Top left; LAD, which
is normal. Top right; Right coronary, which shows wall changes, but no
significan stenoses. Bottom left; cicumflex arterey, showing stenoses
distal to the obtuse marginal (this is a slightly late image, thus
there is little contrast left in the left main. Bottom right, the
result afdter PCI with stent.
Thus, there is evidence of ischemia only on the circumflex area. The
apparent reversibility in the apical area is due to a slight rotation
misalignment between the stress and rest images, so the area of reduced
uptake in the apex is not exactly aligned. This demonstretes taht SPECT
has a vulnerability to processing artefacts as well, and that the
diganosis should also in this method should be done in the least
processed mode. The review images are given below.
Editor:
Stig Slørdahl, Contact address: isb-post@medisin.ntnu.no,
Updated: December_04.
