Department of Circulation and Medical Imaging,
Faculty of Medicine,
NTNU Norwegian University of Science and Technology
|Ummanaq (the heart shaped mountain), national mountain of Greenland||Snøhetta (Mount Snow Hood),
by many regarded as the national mountain of
Norway. Not quite as heart shaped, but at least situated
at the heart of both Norwegian geography (grensen mellom
det nordenfjeldske og søndenfjeldske - Gerhard Schøning)
and history (enig og tro til Dovre faller).
|An academic discussion. Northern fulmars in New Ålesund, Spitsbergen||Professor and
student. Blue eyed shag and adelie chick-
Peterman Island, Antarctica
|Motion. Floating iceberg in
hurricane, Antarctic sound.
||Deformation. Calving glacier in Marguerite Bay, Antarctic peninsula.|
|Strain. Thingvellir, Iceland is situated on the rift between the Eurasian and American continental plates, which are sliding apart. Thus the area is expanding (positive strain), which can be seen by the ground cracking up.|
|An object undergoing strain.
In this case there is a 25% elongation from the original
length (L0). The Lagrangian strain is
Thus, according to the Lagrangian formula there is positive strain of 25% or 0.25.
|Strain rate. Both objects show 25% positive strain, and both corresponds to the object to the left, but with different strain rates, the upper has twice the strain rate of the lower. If the period is one second in the upper object, the strain rate is 25% or 0,25 per second, giving a strain rate of 0.25 s-1. The lower object has twice that period, i.e. half the strain rate, which then is 0.25 / 2 seconds = 0.125 s-1 . In these cases, the strain rate is constant.|
Strain rate. In these four cases there are different instances of deformation and motion. Object A does not move, none of the end points has motion (V1 = V2 = 0), and thus, there is no motion and no deformation (SR = 0). Object B has motion, but the two points 1 and 2 move with the same velocity. Thus there is motion, but no differential motion, and thus no deformation. (SR = 0). No elongation of the object can be seen. In object C point 1 has no velocity (V1 = 0), but point 2 has velocity, thus the two velocities are different, the object has differential velocities and motion, and thus there is deformation (SR does not equal 0), elongation is very visually evident. There is little motion, although one might argue that the midpoint does move a little. Object D shows velocities at both end points, thus there is definitely motion, and in addition V1 and V2 are different. Thus there are differential velocities and differential motion, and there is deformation, visually, elongation in addition to the motion is evident.
| Looking at
displacement instead of velocity, the change in
length of the objects is the difference in
displacement of the two end points:
L = L0 + (D2 - D1), L = D2 - D1, and = (D2 - D1)/L0
|Systolic velocity plot through
space, from the septal base to the left through the apex
in the middle to the lateral base to the lateral base to
the right. The velocities seem to be distributed
along fairly straight lines, i.e. there seems to
be a fairly constant velocity gradient (in space, but
not in time).
||Longitudinal velocity gradient,
where v1 and v2 are two different velocities measured at
points 1 and 2, and L the length of the segment between
|Lagrangian strain (top) and
Eulerian strain (below). Visually, it is evident that
both objects undergo the same strain at the same strain
rate. Thus, the physical reality is the same, but the
two figures show the two different ways of describing
the deformation, as the Lagrangian strain shows an
increasing deformation relative to the constant baseline
length, while Eulerian strain describe the deformation
(in this case constant, as the strain rate is constant,
but this is not a condition), relative to the
continually changing length.
||Lagrangian strain (top) and
Eulerian strain (bottom). Only four point in time is
shown, to illustrate how this means that by Lagrangian
strain at any time is the sum of
all length increments up to that time, divided by the
baseline length, while Eulerian strain at any time is
calculated as the sum of all ratios of length increments
and the instantaneous length up to the actual time.
|If speckle tracking is used to
track the relative positions of two kernels, the strain
will be derived form the relative displacement, divided
by the distance between the kernels. If the denominator
is the initial (end diastolic) distance, this gives the
Lagrangian stran, if it is the instantaneous distance,
it will be the Eulerian strain.
strain by speckle
tracking, applying the principle shown to the
left. In this application, it uses
the instantaneous distance, so in order to acquire the
Lagrangian strain, the conversion below
has to be used.
|Lagrangian versus Eulerian strain.
Lagrangian strain will give slightly higher values, i.e.
negative values are lower in absolute values, while
positive values are higher.
||Lagrangian and Eulerian strain
curves. As myocardial strain in general is negative, the
Eulerian strain curve lies below the Lagrangian.
|Longitudinal M-mode through the mitral ring,
displaying the displacement of the mitral ring. The total
systolic displacement (MAPSE; mitral annular Plane
Systolic excursion) can be measured. If the
MAE is divided by the end diastolic length of the
ventricle (which, in fact is a spatial derivation), it
will give a measure of the strain of the wall. The global
strain of the left ventricle is an average of more points
of the wall.The longitudinal (Lagrangian) strain during
systole is thus MAPSE /LD.
||Pulsed tissue Doppler of the
mitral ring. These are the velocity traces of the
longitudinal motion, while dividing by the end diastolic
length results in the Lagrangian strain rate (Which is
different from the Eulerian strain rate that is
customarily used in ultrasound.) This is discussed below.
|Strain rate from velocity curves. Spatial derivation process is illustrated above. Velocities at two points, v1 (yellow) and v2 (cyan), and the area between them shown in red. Strain rate is (v1-v2)/L. In the figure in the middle the velocity differences are shown by colouring the area between the curves, they become negative (red) when v2 > v1, and positive (blue) when v1 > v2. To the right the resulting strain rate curve (negative red, positive blue) from the area between them.(Thus, strain rate do not equal the area between the curves, but the instantaneous offset between them divided by the distance. The area between the velocity curves divided by the distance is the strain).|
|Temporal integration of velocity to
displacement. The displacement is the cumulated
distance, which is equal to the area under the velocity
curve (temporal integration). Positive velocities are
shown in solid red, and corresponds to an increase in
displacement, negative velocities are shown in solid
blue, and corresponds to a decrease in displacement.
||Temporal integration of strain from
strain rate. Strain is the cumulated strain rate, equal
to the area under the strain rate curve (temporal
integration), from the definition shortening is negative
strain / strain rate. Negative strain rate is shown in
solid blue, corresponding to a decrease (numerical
increase) in strain, positive strain rate in solid red,
corresponding to an increase (numerical decrease) in
|Strain from displacement. Spatial derivation: Motion (displacement) is first acquired by integration of velocities, and strain can be derived from that (although usually acquired from integrating strain rate). Motion (displacement) at to points d1 and d2. The differences between the two points is shown in the middle. Strain is (d1 - d2)/L. The difference between the curves is again shown in the middle. (In this case, the strain is the instantaneous offset between the two displacement curves divided by the distance, not the area.) In this case, almost all of the area is red, and thus strain is negative, except a small overshoot at end diastole.|
|A patient with an apical
infarct, especially evident in the inferolateral
||By colour M-mode initial
akinesia apically, hypokinesia in the middle segment
and basal normal shortening.
|Reduced strain rate in an
infarct visualised by tissue velocity. The systolic
velocities can be seen to decrease normally in the
basal segment (white to lilac curve, red interval),
while the middle segment (lilac
to orange curve, cyan interval), and almost no
difference in the apical segment (orange to green
curve, yellow interval). The intervals correspond to
the strain rate, showing normal shortening in the
basal segment, hypokinesia in the middle segment and
akinesia in the apical segment In fact, inital
systole, shows reversal of velocity curves, thus
signifying positive strain rate (initial
||Strain rate curves from the
segments between the measurement points in the left
image. Thus, the amplitude of the strain rate curves
correspond to the width of the intervals between the
measurement curves, and for clarity, the curves have
the same colours as the intervals to the left.
Here is apical: initial dyskinesia, reduced peak strain rate, but also post systolic shortening, midwall hypokinesia and basal normal strain rate.
|Velocity and displacement
curves with some noise in the velocity curves, the
integration in obtaining displacement curves tend to
eliminate random noise.
||Top: strain rate curves
obtained by spatial derivation of
the velocity curves to the rigth. Bottom, strain
curves by integration of the strain rate curves
above. Again, integration tends to smooth the random
noise. However, that makes it especially vulnerable
to non random noise (clutter).
|In this video the rocking motion of the left ventricle is evident, the whole heart rocks toward the left in systole. (However, this is NOT due to conduction delay).||However, looking at
deformation (wall thickening - transmural strain) in
this cross sectional recording, the wall thickening can
be seen to be normal and symmetric in both onset and
|Apparent asynchrony: Looking at mitral valve velocities, the lateral wall (cyan) seems to have a delayed contraction compared to the septum (yellow), both looking at onset and peak velocities, indicating either asynchronous activation or initial akinesia of the septum||Looking at multiple sites in the lateral wall, it seems that the delay in early ejection phase corresponds to positive velocity in the base (yellow), zero velocity a little more apical (cyan), and increasingly negative velocities toward the apex, i.e. possible apical initial dyskinesia (which might be ischemia).||The curved M-mode from the base of the septum through the apex to the base of the lateral wall shows the same effect, normal timing of the velocities in the septum, inverted velocities in the apical two thirds of the lateral wall.|
|Comparing tissue velocity
with strain rate in the base and apex, however, , we
see that the apparent delayed motion in the lateral
wall has no corresponding delay in deformation,
wheteher looking at onset of, or peak negative
strain rate. All four parts shortens
synchronously and normally. Thus, it illustrates
that the rocking motion velocities are added to the
velocities, the subtraction algorithm of the velocity
gradient subtracts these velocities again,
showing the true timing of regional deformation.
Tethering: The basal and midwall segment is infarcted, and is akinetic and being pulled along by the active apical segment. The whole inferior wall seems stiff.
shows all segments to move similarly, thus there is
little differential motion, and at least below the
apical point , little strain.
||Strain curves, however,
show that the findings are more differentiated,
showing akinesia basally (yellow), hypokinesia in
the middle (cyan) and hyperkinesia in the apex
|Velocity images showing
motion towards the apex in red, away from apex
in blue. Left, systolic 3D reconstructed
image, showing normal motion in the septum and
inferior wall, and paradoxical motion in the
inferolateral, lateral and anterior wall. Right, o
top are bull's eye from systole, showing the same,
as well as early diastole showing inverse motion
during the e-phase, i. e motion of the whole wall
towards the apex in diastole. Apparently, the whole
anterolateral half of the ventricle is ischemic .
||Strain rate images from
the same recording, left systole, right early
diastole, showing that the ischemia is due to a
smaller ischemic area in the inferolateral, lateral
and anterior apex, where there is stretching during
systole (blue). This stretching, results in
the midwall and basal segments moving away from the
apex, despite contracting normally. In early
diastole there is recoil in the ischemic area
(yellow), resulting in anterior diastolic motion in
the whole of the wall. In this case, the
ischemia is obviously limited to a part of the apex,
the rest of the motion abnormalities being due to
|(Motion (velocity), The
diastolic phases of early and late relaxation are seen
as being simultaneous from base to apex.
Protodiastolic downward motion can be seen befor AVC
(aortic valve closure) in the tow basal segments.
||Deformation (strain rate)
shows both early and late relaxation to be biphasic,
and in addition the peaks are not simultaneous in
the different levels of the myocardium.
Protodioastolic elongation can be seen to be present
in the midwall segment only, the protodiastolic
motion of the basal segment being a tethering
|As the apex is stationary, while the base moves toward the apex in systole, away from the apex in diastole, the ventricle has to show differential motion, between zero at the apex and maximum at the base. Longitudinal strain will be negative (shortening) during systole and positive (lengthening) during diastole (if calculated from end systole).||M-mode lines from an M-mode along the septum of a normal individual. These lines show regional motion. It is evident that there is most motion in the base, least in the apex. Thus, the lines converge in systole, diverge in diastole, showing differential motion, a motion gradient that is equal to the deformation (strain). This difference in displacement from base to apex is also evident in the displacement image shown above.|
|AS motion decreases from apex to base, velocities has to as well. Thus, there is a velocity gradient from apex to base, which equals deformation rate.||Spatial distribution of systolic velocities as extracted by autocorrelation. This kind of plot is caled a V-plot (247). It may be usefiul to show some of the aspects of strain rate imaging. The plot shows the walls with septal base to the left, apex in the middle and lateral wall base to the right. As it can be seen again the velocities are decreasing from base to apex in both walls. There is some noise resulting in variation from point to point, but the over all effect is a more or less linear decrease. The slope of the decrease equels the velocity gradient. (Image courtesy of E Sagberg). However, this shows only one point in time, and all values are simultaneous.|
|Velocity, displacement, strain rate and strain from three different points, apex, midwall and base, in the septum of a normal person. These curves all represent the same data set. It is evident that motion (velocity and deformation) increases from apex to base, showing a gradient, while deformation (strain rate and strain) is more constant, in fact a direct measure of the motion gradient. Diastolic deformation is far more complex, and is discussed below.|
|Motion (velocity and
displacement - left) and deformation (strain rate and
strain - right) traces from the base, midwall and apex
of the septum in the same heart cycle. It is evident
that there is highest motion in the base (yellow
traces), and least near the apex (red trace), and this
is seen both in velocity (top - actually both in
systolic and diastolic velocity) and displacement
(bottom). The distance between the curves are a direct
visualization of strain rate and strain, but the curves
are shown to the left, showing no difference in systolic
strain rate or strain between the three levels.
|Good quality V-plot shows
velocities as near straight lines, and
thus, a constant velocity gradient. This seems
to exclude that there is a strain rate gradient from
base to apex.
||A nearly straight line. Blue eyed
shags (cormorants) at Cabo de Hornos (Cape Horn), Chile.
|Left: Real velocity curves from
two points at a distance of 1.2 cm, right strain rate
calculated from the velocity traces as the
velocity gradient SR= (v(x) - v(x+x))/x.
It is evident that both velocity curves have a much
steeper initial slope, an earlier maximum and a
steeper decline. Peak velocities, however, are
not always simultaneous.
|This, of course, is due to the
strain rate being the difference between the curves.
Her the difference between the two velocity curves is
plotted without the length correction, (which then
will be equal to SR*1.2). As can be seen, the
early steep sloe of both curves will result in a much
less steep slope in difference, as the difference
curve is the divergence of the two velocity curves.
From the peaks of the velocity curves the two curves
seem almost parallel, despite both dipping sharply,
this results in a near horisontal strain rate curve,
and finally the slow
convergence of the curves give a much slower reduction
of the difference.
|Tissue velocity curve from the
base of a normal heart. The curve shows a pre
ejection spike (due to contraction before MVC as
and an early spike during ejection, and a negative
spike which ends with AVC (as discussed below).
||Alignment with valve closures is
shown in this registration with phonocardiogram,
although in this recording the early ejection spike is
||Apexcardiogram. The curve shows a striking resemblance to the systolic tissue Doppler curve to the left. Valve closures are given by the phono recordings. (Image modified from Hurst: The Heart).|
||8.3 (1.9)||8.8 (1.8)
|Top: Pulsed wave recordings from
the mitral ring, peak systolic velocity can be seen to
be highest in the lateral wall. Below; the same can be seen
in the M-mode recordings of the left ventricle, lateral
systolic annular displacement is seen to be higher than
in the septum.
||Top: Colour tissue Doppler
recordings from the same subject. Mark how colour
Doppler recordings are analogous to, but slightly
different from the pulsed wave recordings to the
left. This is discussed more in detail in the ultrasound
section. The difference is also evident from the normal
values of the HUNT study. Below: Motion of the
mitral ring, can be shown by integration of the
velocity, and both peak systolic velocity (top) and
displacement (bottom) can be seen to be higher in the
lateral wall than in the septum. The effect seen
in motion measurements may vary, due to the difference
of insonation angle.
|Deformation of the walls, both peak systolic strain rate (top) and strain (bottom) can be seen to be equal in the two walls (the small peak in the strain of the septum is post systolic, and in addition only amounts to 1% absolute or 5% relative). Thus the higher motion of the lateral wall is not reflected to the same degree in deformation.||The shape of the heart. As can be seen in the top image, and is illustrated in the bottom, the curved lateral wall is longer than the septum. Thus, strain rate (velocity difference per length) and Strain (shortening per length) is more similar between the walls than just the total shortening or velocity of the wall.|
|Velocity imaging. Velocities toward the probe is coded red, away from the probe is blue. Thus the ventricle is red in systole, when all parts of the heart muscle moves toward the probe (apex) and blue in diastole.||Strain rate imaging, strain rate is coded yellow to orange for shortening, cyan for lengthening but green in periods of no deformation, and is thus yellow in systole, cyan in the two diastolic phases early and late filling and green in diastasis.|
|Curved M-mode showing
velocities. In this case, the curve is drawn from
the apex to the base, showing one wall. The shifts
between positive (red) and negative (blue) velocities
are clearly demarcated.
||Curved M-mode showing strain
rate ( the curve is the same as in the image to the
left, but the mode is shifted to display strain
rate). The pattern is different, due to the better
spatial resolution when deformation is imaged, as shown
and discussed in details below.
|The same curved M-mode showing displacement during the heart cycle.||However,
In order to display data for the whole ventricle. one
need to display an array of CAMM recordings. 4-cnamber plane (top),
2-chamber plane (middle) and apical ong axis (bottom).
For each plane the curved M-mode is drawn from the base
through the apex and back to the base in the opposite
wall, thus displaying the base at the top and bottom of
each M-mode, apex in the middle.In this display, all six
wall are displayed.
|Curved M-mode from base of
the inferolateral wall through apex and back to base of
anterior septum. In this image it is evident asynchrony,
the septum having anterior motion (red velocities before
the inferolateral wall). Here the point is comparison of
walls, but the difference in onset of motion can be
||Strain rate curved anatomical
M-mode from one wall only, of a normal person. The point
in thois image is the measurement of the propagation
velocity of the stretch waves during early relaxation
and atrial systole that only can be measured in the
parametric image, due to it's display of distance-time
|Bull's eye plot of velocities in systole (left) showing velocities toward the apex in red, and early diastole (right) showing velocities away from the apex in blue.||Strain rate data from systole (left) showing longitudinal shortening in yellow, and early diastole showing longitudinal elongation in blue/cyan.||Systolic strain rate data
from two different patients with an apical (left) and
inferior (right) infarcts, respectively. The area of
dyskinesia is shown in cyam, contrasting with normal
shortening in the rest of the ventricle. Data are
|The curved M-mode is a line
(one dimensional) that curves through the two
dimensional plane (left). The curvature gives
information about the spatial relations between the
pints on the line.
||Keeping the curvature
information enables the mapping of the points of the
line in two dimensions (middle).
||Using three standard planes, it is possible to
reconstruct a grid with the true curvature of the surface,
in this case a curved plane, that curves through three
|3D velocity display in
systole and diastole, the same dataset as in the bull's
||3D strain rate display in
systole and diastole, the same dataset as in the bull's
eye images above.
|The area distorsion in bull's
eye is evident comparing these strain rate images of the
same infarcts in bull's
eye and 3D. All images are from mid systole, the infarcted
area is shown in cyan, showing a- to dyskinesia, while
normally shortening myocardium is shown in yellow.
|Strain rate 3D mapping. The 3D image can be rotated in space showing that it contains a full reconstructed 3D dataset. Stopping the scrolling will allow closer inspection, but scrolling in space will show only one instance in time. (In this case it's mid systole). (Image courtesy of E. Sagberg.)||Strain rate 4D mapping. The image can also be scrolled in time, showing the full time course of the data. Stopping the scrolling will allow closer inspection. The problem with the moving loop is the same as in 2D display, and in addition it won't show all of the surface simultaneously. (Image courtesy of E. Sagberg.)|
Still preaching my personal litany: Strain is geometry. (Cormorant seen in Galway, Ireland).
The basic direction in three dimensions are given by the coordinate system given. In a Cartesian coordinate system, the directions are x, y, z, somewhat randomly chosen. In relation to the ultrasound system the coordinates of the ultrasound system are often used: Axial (depth - i.e. along the ultrasound beams also often called radial), lateral (In-plane angle or distance - i.e. across the beam; also called azimuth) and elevation (out of plane distance or angle), while in relation to the ventricle, the coordinates are longitudinal, circumferential and transmural (also confusingly called "radial").
|Strain in three dimensions. All three-dimensional objects
can be deformed in three dimensions (along all three axes).
In this case there
is deformation along the X axis,, the strain is:
strain. In this case the cube is deformed along the X
axis, and the shear strain is:
|The cylinder shows strain (compression along its long axis) , which can be described as Lagrangian strain from L0 to L. However, the figure also shows simultaneous thickening or expansion in the two transverse directions. This also illustrates the principle of incompressibility. An incompressible object must maintain an unchanged volume, thus compression along one axis has to be balanced by extension along at least one other. In this case both diameters increase simultaneously.||Incompressibility in the XYZ coordinate system.
Usually this comprises simultaneous strain inall three
The cube is stretched along the x axis, and compressed along the y and z axes, the three strains musc be interrelated so:
If the object is incompressible, the volume (not mass!) remains constant during deformation as shown in the illustrations above.This is the true definition of incompressibility. Thus, compression in one dimension has to be balanced by expansion in others as shown in the figures above, i.e. strain in the three dimensions in a coordinate system cancel out, in way described in more detail here. This means that strain in three dimensions are interrelated, so strain in one direction is representative of regional deformation in more than one direction, as has been shown for heart muscle where wall thickening and wall shortening gives the same information about regional function (7).
can be shown that in an incompressible object:
The radial motion of the septum in diastole is determined by the differences in filling pressure of the left and right ventricles. In systole, If the filling pressures are reasonably similar, as in the normal situation, the septum has little radial displacement in diastole. In systole, the pressure induces a circular cross section, as the most energetically feasible shape. Thus, during systole, the ventricle operates without much change in the outer contour.
Looking at the
ventricular volume curve shown below
left, it is evident how much the volume curve reflects a
curve, showing the close relation between longitudinal
deformation and pumping volume. (The volume curve shows the
remaining volume in the ventricle). Looking at the figure above,
given the invariant outer contour, the whole of the stroke volume
is described by the longitudinal shortening, as wall thickening is
simply a function of wall shortening. The total volume in diastole
is the sum of the blood inside, and the muscle wall. When the left
ventricle shortens in systole, the total volume is reduced by the
volume of the cylinder shown in grey: . But the
myocardium, comprising a part of this volume is incompressible,
thus maintaining a constant volume. Thus, the whole
volume reduction is the reduction in blood volume, in
other words the stroke volume: .
Thus, the stroke volume is given by the outer diameter and the
systolic longitudinal ventricular shortening (56).
as the myocardium is incompressible, the wall shortening and
thickening, and thus the internal diameter reduction have to be interrelated
thus both would be valid measures of stroke volume. In a newer
study, the correlation between MAE and stroke volume in healthy
adults was seen to be about 90%, corresponding to an explained 82%
of the stroke volume compared to the reference (Simpson). Thus, an
outer contour systolic reduction should be present to explain the
rest of the stroke volume (158).
The volume (and mass) being ejected, is equal to the volume being moved towards the apex as shown here.
|Recoil forces. The momentum away from the apex
is ejection of the stroke volume. The displacement of the ejected
volume is equal to the stroke velocity integral (measured
by Doppler flow in the left ventricular outflow), which is
about 15 to 20 cm. The motion of the opposite
momentum is displacement of the annular plane,
which is between 1 and 1,5 cm (30) at the same time. Thus the momentum being
generated by ejection is at least ten times the momentum
pushing in the other direction, thus generating the
forces pushing the heart into the pericardium, which is
||This can be felt as the apex
beat, shown here in an apexcardiogram demonstrating that
the beat is a systolic event. (Image modified from
Hurst: The Heart).
|Strain in three dimensions. In the heart, the usual directions are longitudinal, transmural and circumferential as shown to the left. In systole, there is longitudinal shortening, transmural thickening and circumferential shortening. (This is an orthogonal coordinate system, but the directions of the axes are tangential to the myocardium, and thus changes from point to point.)||This video shows how the apex is stationary, while the base moves toward the apex in systole, away from the apex in diastole. This ,ans the ventricle shows strain between apex and base. Longitudinal strain will be negative (shortening) during systole and positive (lengthening) during diastole (if calculated from end systole).||Wall thickening . The relatively constant outer contour and inward moving endocardium, shows clearly a displacement gradient (strain) gradient across the wall.The wall thickening is equivalent to transmural strain.|
|Ventricular strain. Diastolic
and systolic images of the heart. Systolic shortening of
the left ventricle relative to diastolic length, is the
systolic strain of
the ventricle. The longitudinal strain during
systole is thus:
However, it is also evident that as the wall shortens, it also thickens, to conserve the volume. Heart muscle is generally assumed to be incompressible.
|Strain being (L - L0)
may still not be
unambiguous, as shown below. Both the strain length, L0
and the shortening (L - L0) will be different when
measured along a skewed line (red) and even longer along a
line following the wall curvature (blue). As both strain length and shortening increase when the curved line is used,
the ratio will not be as affected, but still, L0
will increase more than than the shortening.
|Simultaneous strain in three dimensions. Relation of long axis shortening and wall thickening. As the heart muscle is generally considered incompressible, longitudinal shortening must give trensmural thickening.. Thus as the ventricle shortens, the wall has to thicken correspondingly in order to preserve wall volume, the thickening shown in blue. In this case, the outer contour of the left ventricle is assumed fairly constant, as described below.||Transmural strain is wall thickening. Wall thickening is a function of longitudinal strain (longitudinal strain given in negative values; i.e. wall thickening increases as THE VALUE of longitudinal strain increases) in a half-ellipsoid model of the left ventricle with a length of 9.5 cm, outer diastolic diameter of 6 cm (reduced by 5% in systole as discussed below and in the math section), and a wall thickness of 9 mm.|
|Different measures of
the wall thickness and thickening. As the ventricle
shortens, it will thicken. myocardium, being thinner in
the apex, will thicken less absolutely, but probably as
much relatively. (Black, gray.) However, looking at a
cross section, (as in parasternal views, or measuring
thickening in the horizontal direction (As in many MR
tags) , will give a distortion, the measures a thicker
wall and a greater absolute wall thickening.
(Blue.) The effects of relative wall thickening
may vary, depending on the angle and the change of angle
during systole. Assuming equal wall (ROI) thickness
throughout the length of the wall (as in som e speckle
tracking applications), will overestimate the wall
thickness in the apex. If inward displacement at the
same time is taken from tracking data, the measure of
wall thickening will be unpredictable as compared to
the real wall thickening.
|Relation of wall thickening
(transverse or transmural strain) and circumferential
strain. As the wall thickens in systole (blue),
the midwall line moves inwards half the distance of the
endocardium. Endocardial circumferential shortening is
greater than midwall circumferential shortening, which
is greater than epicardial circumferential
shortening (which is close to zero).
(although a small reduction in outer contour will
||Endocardial and midwall circumferential strain in the same half ellipsoid model as above, as a function of wall thickening (transmural strain), given an end diastolic outer diameter of 60 mm, and end diastolic wall thickness of 10 mm and assuming a systolic outer contour reduction of 5% (Circumferential strain given in negative values; i.e. as wall thickening increases, THE VALUE of circumferential strain increases). As wall thickening increases, end systolic diameter decreases, leading to a decreased end systolic circumference, hence, increased circumferential strain. Using endocardial strain shows the same relation, but higher absolute strain values.|
|3D strain rate mapping.
Reconstructed 3/4D image with longitudinal tracking
from tissue Doppler. (This is described in detail below). Yellow
represents shortening, blue elongation and green no
strain. In this case only longitudinal strain is
tracked and displayed, as can be seen from the
diameter circumference of the grid, it doesnt change
during the heart cycle.
||Apical four chamber view with
B-mode and tissue Doppler data. Longitudinal
shortening is tracked by tissue Doppler. In this
image both sides of the LV wall are marked and
the wall thickening is tracked as well, by
speckle tracking. In this
analysis both longitudinal and transmural strains
are available, but for circumferential strain 3/4D
reconstruction is necessary, and requires three
||3/4D reconstruction from three
sequential planes to a thick walled model
analysed as shown in the image in the middle.
In this case, the endocardial and midwall
circumferences are given in the grid, and
circumferential and area strains can be calculated.
(The colours in this image, however, are
tissue Doppler derived strain rate, i. e.
longitudinal strain rate).
|Simplified diagram of how
curvature may affect longitudinal strain, showing the
wall divided into two layers. In this diagram, only the
effect due to wall thickening is shown isolated, to
avoid confusion with the effects of longitudinal
wall shortening. As the outer layer (grey)
thickens, both the mid layer (thin black lines) and
inner contour (thick black lines) of that layer shifts
inwards (dotted lines). In a curved wall, this
inward shift of the midwall line (average for the
layer), will shorten it, this is an effect that is added
to the wall shortening itself. Thus, longitudinal strain has
some effect of wall thickening, like circumferential strain.
But as the outer layer thickens inwards, the inner layer not only thickens, but also is displaced inwards. This adds tothe inward shift of the midwall line, this midawall line is thus displaced inwards both by the layer displacement and the layer thickening. And this effect is even greater, as there is less room for the inner layer as it is displaced inwards, forcing it to thicken even more, displacing the midwall line even more. This is equivalent to the effect on circumferential layers, and this effect is most pronounced in the inner layers.
In longitudinal strain the wall shortening is the most important for the over all strain, however, the layer effect may be responsible for the gradient, or else there would be torsion of the mitral ring. In circumferential strain this effect is the mechanism for both overall strain and the strain gradient.
|Global longitudinal strain.
This diagram shows how it can be measured in different
ways, giving different results.
The effect illustrated to the left will be mainly if strain is measured alng the curvature of the wall, while straight line shortening as measured by B-mode, M-mode or tissue Doppler will not show this effect. Measuring along a curved wall will increase this gradient even more, as the denominator shortens due to curvature as well.
|Hypothetical model of equal tension (orange lines), equally distributed along the layers as well as acros the wall will result in normal shortening (orange) across the wall layers and along the wall regions.||Approximation to the normal
tension distirbution of the tension, with least
longitudinal tension in the middle layer. With a
deformable mitral ring and independent layers, the
deformation would be unequal as well, causeing the
mitral ring to buckle in the middle (A). As discussed
above, this is undocumented as well as improbable, the
more probale model being homogeneous deformation across
the wall, as a resultant of the different forces.
|A: Unequal distribution of tension (red: high , orange: medium and yellow: low - reduced) across the wall. If this should result in differential deformation, (A1), there would be torsion of the mitral ring, which is improbable, and indeed undocumented. As in the discussion and example above, the more probable would be a more homogeneous deformation due to the transmural resultant force (A2). B: Unequal distribution of tension along the wall, but not across the wall will cause the segments to behave differently, the weakest may be akinetic, or even stretch (cyan) due to the pull from adjacent segments while the strongest may shorten excessively due to the reduced pull of the weaker segments, as discussed later). The total wall shortening is reduced due to reduced total force, but the mitral ring does not move less locally, but globally, as discussed later, and shown empirically (40).||Hypothetical model of unequal distribution both across and along the wall, in a model where there is some freedom for the layers to slide past each other. A; in the base and B; in the apex. This corresponds to various situations of ischemia with varying transmurality. This may cause the layers to behave differently, layers with very reduced tension in one segment may be akinetic or even stretch in that segment due to the pull from the stronger layer segments, and the reduced pull in weaker segments thus causing extra shortening in normal segments as shown here.|
|As shown above, circumferential
strain is the reduction of a
circumferential line as it is shifted inwards by the
wall thickening. The endocardial circumferential strain
is higher in value than the midwall circ strain.
||If we add another
layer with the same diastolic thickness, it becomes more
complicated as shown in this simplified model of two
layers. The outer layer is identical to
the layer shown to the left. Thus, outer
contour of the inner layer is identical with the
inner contour of the outer layer. The inward
displacement of the inner contour of the outer
layer, displaces the outer contour of
the inner layer inwards the strain are identical. But
this means that the wall thickening of the inner layer
has to be greater, in order to conserve volume, as there
will be less space for the layer in systole. This means
again that both midwall and endocardial strain in the
inner layer will have a greater value, not only as the
wall thickening of the inner layer is added to that of
the outer, but also because the wall thickening itself
is greater due to the lack of space. I e. there vill be
increasing both transmural and circumferential strain
form the epi- to the endocardium.
fibre directions are diverse, and varies throughout the
thickness of the heart, the middle layer being more
circular, while the endo- and epicardial layers being
more longitudinal, although helically ordered (62, 257). In dealing with
the principal strains, the wall is treated as isotropic,
which it is not. Thus, there may be differential strain
as well as shear strain.
Differences in longitudinal strain across the wall, as has been described by some authors, would necessitate a torsion of the mitral annulus , and thus is geometrically unfeasible, except to a very minor degree allowed by the small change to the saddle shape in systole. The studies finding large differences, are probably describing artifacts, as the lateral resolution is low, and the angle deviation may vary.
The concept "radial function" is somewhat meaningless, as there are no fibres running in the radial direction. What is called "radial function" is either wall thickening, which is a function of fibre thickening, and circumferential shortening, and the term radial function means that the transmural strain, or wall thickening is used, the term circumferential strain means that circumferential shortening is used as parameter.
Only the small contribution from circumferential shortening that results in outer diameter reduction, is the independent radial function. Fractional shortening is the reduction in cavity diameter, and is equal to * endocardial circumferential shortening.
|Transmural strain is not only due to wall thickening, but also of inward displacement of the inner layers. Simplified and exaggerated diagram showing the relation between fiber thickening and wall thickening. As the fibers shorten, they thicken. Thus, the sub epicardial longitudinal fibers will thicken, displacing the circular fibers in the mid wall inwards. In addition, as the fibre become thicker, they will need more room, thus necessitating some rearrangement of the fibres, making the layer thickening even more than the individual fibres. They will also displace the circular fibres inwards, thus making the shorten and also thicken as they contract. Finally the sub endocardial longitudinal fibers will be displaced inward. The sub endocardial fibers will also, thicken. But the circumference has been decreased at the same time due to the thickening of the outer fibers, and thus there has to be an extra inward shift of longitudinal fibers for them to have room. Assuming a systolic reduction in outer diameter will only enhance this effect. By this, it's evident that wall thickening is not equivalent to the sum of fibre thickening alone. The circumferential strain is thus mainly the shift of the midwall line inwards due to wall thickening.|
fibers, mainly contributes to the pressure increase, i.e.
isometric work, which takes place mainly during the isovolumic
contraction phase, as discussed below.
Isometric contraction cannot be measured by deformation along the
fibers. As they contract, however, there will also be a slight
inward shift, due to the displacement of the fibres, which also
results in a shortening and thickening of the fibres. In addition,
the circumferential fibers may be responsible for whatever there is
of outer contour diameter reduction . If so, they contribute to the
ejection work, and in addition slightly to wall thickening, as the
wall has to thicken even more in order to retain wall volume with a
reduced outer diameter. If there is loss of longitudinal contractile
function, either regionally (typical ischemia) or globally as in
cardiomyopathia with sub endocardial affection (e.g. Fabry), there
may be a shift toward circumferential pumping, with an increase in
the variations of outer circumference. Then there will be true
radial compensation for loss of longitudinal function. But in
hypertrophic states, there is usually loss of longitudinal function
and circumferential function both, but due to the increased wall
thickness the fractional shortening may be increased. This has been
called "radial compensation", but as explained below,
this is a total misunderstanding of geometry.
dysfunction, there is an inter dependence of the segments in
both directions, that will alter regional deformation, in addition
to the loss of tissue, that will be described below.
|Excitation-tension diagram. After Cordeiro (234). The Action potential triggers
the influx of calcium, which triggers further release of
Ca2+from sarcoplasmatic reticulum. Calcium
binds to troponin, and allows activated (by ATP) myosin
heads to bind to troponin sites on actin (cross bridge
forming) and release energy, causing the filaments to
slide along each other, as long as there is a high
calcium concentration in the cytoplasm. As the
cell membrane repolarised, this triggers the removal of
calcium from the cytoplasm, mainly by the SERCA pumping
it into the sarcoplasmatic reticulum again. Thus,
the forming of new cross bridges is inhibited, and
relaxation starts. The pumping of calcium is energy
dependent, and is the energy requiring part of the
relaxation cycle. In energy depletion (f.i. ischemia),
there will be less shortening in systole, but also
||Image of beating isolated
myocyte. The myocyte is treated with an agent that
fluoresces in the presence of free calcium in the
cytosol. We see that the cell lightens and shortens
simultaneously; stimulation causes an increase in free
calcium (released mainly from the sarcoplasmatic
reticulum), causing the cell to become lighter. The free
calcium is the trigger for the binding of ATP, and the
formation of activated ("cocked") cross bridges between
actin and myosin, and the subsequent release, which
leads to tthe buildup of tension in the cell. In the
unloaded isolated myocyte, (as in previous studies in
isolated papillary muscle), this will correspond almost
directly with the shortening, as virtually no energy is
used to overcome load. However, a small part of the
energy needs to be stored for diastolic lengthening,
even in isolated myocytes, as discussed below. Thus, even an
isolated myocyte is not entirely unloaded. Image courtesy
of Ph.D. Tomas
exercise research group (CERG), Dept. of
Circulation and Medical Imaging, Norwegian University of
Science and technology.
|It has been shown that the re
ejection tissue velocity spike in the septum styarts
about 35 ms after start ECG (268),
thus corresponding to the electromechanical delay on the
cellular level (234)
shown above, so the start of
the pre ejection spike marks the onset of the active
contraction in the septum, startring slightly before the
mitral valve closure as discussed below.
||The pre ejection spike terminates
with the mitral valve closure and the start of
isovolumic contraction, wherte there is tension
development, but no deformation. Ejection starts with
the aortic valve opening (AVO), after this there is
ejection and volume decrease, but much slower pressure
increase. The peak
ejection rate may be a little before peak contraction,
(tension), as the ejection rate may be slowed slightly
because of arterial impedance. However,
the ejection persists both due to the tension being
reduced gradually, and due to the inertia as the blood
pool is accelerated.
|The peak velocity of annular plane
motion may differ at different sites, The earlyt peak
often only present lin the lateral wall) and the early
peak during ejection will often be earlier
than the peak ejection, this is also true for the
mean velocity cyrve between eptal and lateral
||Peak rate of deformation is later,
as the early peak is translational
|Shortening velocity (= strain rate) and total shortening (Strain) decreases with increasing load (after 208).||Thus an increasing afterload
load will result in less shortening, as well as less
initial rate of shortening in an isotonic preparation
like the one above.
|Relation of force to surface
area. Assuming that the two balloons have the same
intracavitary pressure, the total load on the wall (as
illustrated by the larger number of arrows in the larger
balloon) is proportional with the surface area, and thus
a function of the radius
(F = P × A = P × (4/3) × × r3).
|Wall stress. A force
acting on a segment is distributed across the cross
section, thus a bigger cross section gives a smaller
force per square unit as illustrated by the wider
segment with smaller arrows on each half.
|The Wiggers cycle. The
pressure changes are shown in relation to the heart
cycle. The filling pressure is the atrial pressure, and
the total filling determines the end diastiolic pressure
(and volume). The contraction starts with isovolumic
contraction (IVC), which raises the ventricular pressure
to the level of the aorta. This is the isometric phase
of conmtraction, i.e. tension (pressure) increase
without volume (muscle length) decrease.The ejection phase is during
aortic opening. From the pressure curves it
it evident that the tension decline (i.e. relaxation)
starts around mid ejection, and the last part of
ejection is during
relaxation. But as there is ejection,
there is still volume reduction. Relaxation continues into the isovolumic relaxation
(IVR) phase, where there is further pressure (tension)
release, and then into early filling (E) phase of mitral opening.
The rest of the heart cycle, the diastasis and late
(atrial -A) filling phase are phases where the
ventricular myocardium is passive.
||Volume change and flow rates related to the heart
Top, Ventricular volume curve, with the different phases demarcated. IVC starts with mitral closure (MVC). Then, there is pressure increase as shown to the left, but no volume change. During ejection, there is volume decline, corresponding to muscle shortening. Peak ejection rate, corresponds more or less to maximal tension. After that, there is ejection, due to the inertia of blood, but simultaneous tension decline as shown by the pressure traces (left). After end ejection there is further decline in pressure, but no volume change in IVR, and then further relaxation creating early (E) filling. In diastasis, there is little filling, and then there is further filling of teh passive ventricle due to atrial contraction.
Below, composite Doppler flow velocity curve showing both LVOT outflow and mitral inflow to the left ventricle. The flow velocity curve is an approximation to flow rate, and hence, similar to the temporal derivative of the volume curve, or, conversely, the volume changes are the integrated flow rate.
The end systolic pressure volume relation, is the slope of the
straight line through pressure volume loops for a given
inotropic state. As it can be seen, the slope is the pressure
volume relation, the change in pressure for a given volume.
The general definition of elastance is given by:
| PV loops are often
erroneously shown with horizontal pressure during
ejection, and equal pressure at start and end ejection,
but the pressure at start ejection, bein equal to the
end diastolic aortic pressure, and the arterial pressure
dropping during diastole, the start ejection pressure
has to be lower than the end ejection. Also, the true
pressure curve shows an increase at start ejection and
drop at end ejection. The filling period is complex. It
is often erroneously shown as horizontal or
gradually rising, but as there is pressure drop
simultaneous with volume increase during early filling,
and may be slow filling during diastasis, and
finally concomitant pressure and volume increase
during atrial contraction, the filling phase has to be a
curve more or less as shown. Also, it is a trend to
describe the filling as passive, while it actually
consists of active relaxation and atrial contraction,
only during the last, is the ventricle passive. The
dynamics of filling are discussed below.
||The effect of end diastolic
volume, load and inotropy on the PV loops. Black: Normal
PV loop. Yellow: effect of increased end diastolic
volume or preload, (e.g. volume load, or increased RR
interval) without increased afterload. The contraction
will increase through the Frank Starling mechanism, and
the stroke volume will increase somewhat, partially
restoring the end systolic volume. Blue;the effect of
afterload increase. Increased afterload will close the
aortic valve at a higher pressure, and higher end
diastolic volume, reducing the stroke volume (blue
dotted line). This, however, will increase end diastolic
volume (through reduced emptying) if filling is
unchanged, increasing end diastolic volume, which
partially will redice the effect on stroke volume.
Green: Inotropy increases contractility, and thus, the
end systolic pressure volume relation line, and thus
increases stroke volume by reducing end systolic volume.
However, even if increase in contractility may increase
cardiac output somewhat, if filling remains unchanged,
the end diastolic volume will decrease again, offsetting
some the effect of inotropy in normal ventricles (green
dotted line). Thus increased contractility without
increased venous return may lead to the ventricle mainly
workingat somewhat lower volumes, with only a slight
increase in stroke volume. Orange, in heart failure,
contractility is depressed. Venous return will cause the
PV loop to move out on the end diastolic slope, but in
time reduced stroke volume will also reduce venous
Thus, the arterial stiffness and resistance are factors contributing
to the afterload, but the compexity of the issue, (especially #3
above) means that the central aortic pressure may vary from the
peripheral arterial pressure, and thus the real afterload may not be
assessed directly by peripheral blood pressure measurement, but will
need invasive measurement or complex modeling.
|Left ventricular volume curve
from MUGA scan (gated blood pool imaging by 99Tc
labelled albumin. The total volume is proportional to
tne number of counts, thus making MUGA a true volumetric
method, but averaged from several hundred beats.) It is
evident that there is volume reduction corresponding to
ejection, then there is early and late filling. Thus
this might seem to corresond to contraction -
relaxation. The temporal resolution of MUGA is low, and
the isovolumic phases are poorly defined.
(shortening) curve from left ventricle. Note the close
correspondence to the volume curve on the left, but due
to higher temporal resolution, the isovolumic phases are
visible. Again the shortening might seem to be
contraction, and the (early) elongation relaxation.
|The Wiggers cycle:
Heart cycle in terms of pressure changes
||Volume and flow
|Classical Wiggers cycle, where events during the heart cycle is related to pressure changes in atrium and ventricle. The flow is a direct result of the pressure differences, and thus the volume changes are the result of flow. It is evident that pressure decline (relaxation) starts long before end ejection when comparing with the image to the left.||Top, Ventricular
volume through one heart cycle, with the different
phases demarcated. Below, composite Doppler flow
velocity curve showing both LVOT outflow and mitral
inflow to the left ventricle. If the orifice remains
constant, the flow velocity will be similar to the
flow rate curve. Thus, the flow velocity curve is an
approximation to flow rate, and hence, similar to
the temporal derivative of the volume curve, or,
conversely, the volume changes are the integrated
flow rate. The isovolumic phases are exaggerated.
||Strain and strain
|Top, mitral annular displacement curve, being the curve showing the longitudinal shortening of the left ventricle. Below, the tissue velocity curve, which is the temporal derivative of the displacement curve. Comparing to the volume/flow curve, it is evident that there is more complex motions, especially n elation to the isovolumic phases, than is evident from the mere volume diagram to the left.||Top, strain curve from
mid septum, showing the deformation, below the
strain rate (temporal derivative). The curves seem
to be very similar to inverted motion and velocity
curves, however, deformation will show more
regional detail as discussed below.
Remark also how the strain curve is similar to the
volume curve, showing the same pattern, while the
strain rate (temporal derivative of strain) is
similar to the flow curve (temporal derivative of
|The phases of the heart
cycle shown as basal velocities (top) and motion by
integration of velocity traces (bottom). The
velocity curve crossing the zero line corresponds to
a shift in the direction of motion. Thus, positve
velocities are motion toward apex, negative
velocities are motion away from the apex. The heart
cycle in the ventricle starts with start of QRS in
the ECG (provided the scanner ECG is properly
aligned with the disrection of the initial vector of
activation (across the septum).
The precise timing of events, like the valve openings
(strat of flow), as well as vale closures (which may be a
little later than end of flow, but can be timed with valve
clicks as shown below (168)),
may be most reliably timed as global events by Doppler flow
However, this presupposes that heart rate is fairly
constant, as tissue Doppler/B-mode recordings are taken as
End ejection can be reliably identified by Tissue Doppler
tracings from the septum, both in relation to Doppler flow
and Phono (168),
to very high frame rate B-mode (169)
in both normal ventricles, ventricles during high heart rate
and ventricles with ischemia infarct sequelae (170).
This can thus be done in the same acquisitions as the tissue
Doppler recordings, without having to transfer from a
different recording. However, in mechanical asynchrony from
other causes, this is more dubious (289)
By experience, this is probably not feasible in conduction
abnormalities nor pacing, as discussed below.
That has also recently been shown (289).
The main point in the studies (168,
however, was mainly to elicit the mechanisms for aortic
valve closure, and to correct much cited, but mistaken
suppositions that the IVC was the initial negative velocity
of the tracings, i.e. to elicit the physiology.
|The geyser Strokkur at Haukadalir, Iceland at immidiate pre eruption (pre ejection). In a geyser, the water is heated deep below the surface, at high pressures. Thus the water becomes superheated before it boils. when boiling, the column of steam will rise through the water, causing the water above to bulge. To the left, the steam can be seen within that bulge, just beaking through the surface at one point. To the left, the steam breaks through, and the water is driven out both by the steam and the pressure below, resulting in an eruption (ejection).|
|Pre ejection period, from onset of ECG (provided the ECG is properly aligned) to start of flow out of LVOT. There is a short flow into LVOT during PEP. THis may be due to delayed vortex formation from mitral inflow.||The early inflow into LVOT during PEP can also be seen by colur M-mode, but stops above the annulus.|
|In this recording, the
pre ejection spike (middle vertical marker line)
is seen to start after the onset of ECG (left
vertical line), but before the onset of the first
heart sound (right line). In the Doppler
recording, the ECG can be seen to precede the
first heart sound, which precedes the start of
|Volume reduction due to
pre ejection shortening. This movement can also be
seen in displacement traces (below).
This motion of the
nitral ring would tend to displace the mitral
eaflets towars the base, and thus be a part of the
closing mechanism, however, the displacement of
the ring towards the apex is far less than the
motion of the leaflets towards the base.
||Pressure volume loop
with a small pre ejection or protosystolic volume
reduction before IVC (P). This shape of the
pressure volume loop is in accordance with
experimental data (173).
|Ultra high frame rate tissue Doppler from the base of the septum a subject with atrial fibrillation. Even with no atrial activity, there is the same pattern of double velocity spikes, showing them to be ventricular in origin. Image modified from (268).||Ultra high frame rate tissue Doppler from the base of the septum a subject with 2nd degree AV block, as seen by the second P-wave following the first heartbeat, with no QRS nor ejection velocities. The atrial recoil can be seen as three velocity spikes (arrows), indicating that the mitral ring bounces. However, this is in a situation without LV myocardial tension. At start of the first heart cycle, there may be some fusion between atrial recoil and vetricular contraction as seen by the timing. this may be due to longer PQ time. Image modified from (268).||Ultra high frame rate tissue Doppler from the base of the septum a subject with 1st degree AV block. Three spikes are seen before ejection (arrows). Here, the initial spike must be atrial recoil, coming before start of the the QRS, it cannot be ventricular i origin. Even the second spike may be atrial, or a fusion of an atrial bounce and ventricular contractioncontraction. Both middle and left images shows that there is atrial activity i the pre ejection phase, but that the visibility of this may be dependent on the PQ interval. in shorter PQ interval, the presence of ventricular tension may modify or abolish the atrial component. Image modified from (268).|
ejection phase shows a rapid rise in both ejection
flow and tissue velocities, with an early peak,
and the slower decline. The peak ejection velocity
is the the maximal rate of of shortening,
after the AVO. This should be the peak rate of
volume decrease, although it is difficiult to alig
completely with peak systolic strain rate. The
peak rate of annular displacement (annular
velocity) is usually earlier, at least in the
lateral wall, due to the early over all motion
towards the apex.
|Stroke volume by
Doppler flow velocity integral (VTI) and LVOT
diameter. The diameter gives the area, and the
velocity time integral gives the distance that an
object travels if it follows that velocity curve
(v =ds/dt, means that s = v
dt. Multiplied with each other, the area and VTI
gives the volume of a cylinder, equal to the
||Relation of stroke
volume and LV shortening. The volume reduction is LV shortening * LV area
at the mitral plane. As area is far higher, the
distance is far smaller than the VTI.
|Strokkur during ejection and immediately after. During ejection there is a water column that is ejected due to the pressre. At peak height, all the pressure is converted into potential energy. Afterwards, the height of the column decreases, water is still flowing due to inertia, but decelerating, and the flow rate and height decreaseing, at the end there is only the remaining steam column, active ejection is finished.|
|The peak ejection velocity is the the maximal rate of of shortening, shortly after the AVO. This is also the peak rate of volume rediction of the ventricle.||The peak annular systolic velocity seems to be another measure close to peak rate of shortening, as annular motion is a global measure. In this case, septal and lateral velocity are simultaneous, however, this may not always be the case.|
|A fairly common pattern is a sharp peak in the lateral annulus (cyan), and a more rounded curve with a later peak velocity in the septum (yellow). Thus, the divergence of the curves in the initial ejection phase may represent a light tilting (rocking) of the apex toward the septum.||A slightly different normal
pattern where the initial peak in the lateral wall
decelerates slightly, the accelerates again,
giving a later second peak. The septum shows an
even curve, but with peak velocity between the two
peaks of the lateral wall.
||In this case peak annular velocity is early and simultaneous in both walls.|
|IN this case with
simultaneous peaks, peak ejection velocity is
later than the tissue
velocity peaks, even when they are simultaneous.
||Mitral annular velocities
from the basal septal (yellow) and lateral (cyan)
parts. The two curves can be seen to have
different shapes, and the peak systolic values do
not coincide. The peak ejection velocity from the
LVOT of the same patient (aligned by ECG) do not
coincide with any of the peaks.
||In the latter case, the mean
velocity curve can be seen to have an early peak,
and the peak mean annular velocity do not coincide
with peak ejection velocity (which is at the
crossover of the septal and lateral curves, as can
be seen to the left).
|Examining one normal subject
with early velocity peak in the lateral annulus:
||Looking at velocities within
the wall in base an apex, the biphasic pattern
with an early peak can be seen in
both points in the lateral wall.
||Examining the strain rate
from the entire walls between the apical and basal
points no sign of a biphasic shortening can be
seen, indicating that the lateral peak is only due
the peak being subtracted. The peak strain
rate is much later than peak velocity in
both walls, as discussed above.
|In this case, the peak
ejection velocity seems to be simultaneous
with peak septal velocity, but this may be
coincidental as this was not the case in another
subject shown above.
||relation to apical and basal
septal velocities may again be coincidental.
||But the main point is that
peak ejection velocity is earlier than peak strain
rates. As has been shown earlier,
timing of peak strain rate may differ between
segments, but in this case the ROI occupies a much
larger part of the wall, being more representative
of the global strain rate,
and thus the timing of the peak.
|Velocity curves. It can be seen that the two velocity curves have an early maximum, showing that the myocardial acceleration occurs early, and is an early event. Peak systolic velocity is seen at about 100 ms into the heart cycle, starting with ORS. After this, there is a period of nearly constant velocity difference, before the velocity difference decreases again.||Strain
rate curve from the segment between the two ROIs
in the left picture. It can be seen that peak
strain rate is a later event.
Wall thickness 17 mm, EDD 40 mm, Fractional shortening was 35%, however, wall thickening only 28%
which is confirmed, systolic mitral annular
excursion is 5 mm and peak systolic
annular velocity is < 3 cm/s
|LV length (cm)||9.5
|LV outer diameter (cm)||6.0
|Wall thickness (cm)
|LV Inner diameter (cm)||5.1
|Wall thickening (%)||50
annular velocity (S') compared to MAPSE.
S' is actually the peak rate of annular
displacement, and is thus closer to
contractility, while MAPSE is end
systolic and thus closer to ejection
||However, in many
cases the peak velocities of septum and
lateral wall are not simultaneous.
Averaging peak values is then a slight
approximation, compared to the peak of a
mean curve, although in this case the
dufference is slight.
|Systolic strain is normalised MAPSE. The normalised MAPSE for this ventricle with an end diastolic length of 9.2 cm and an MAPSEE of 15 mm is 15 / 92 = 16.3. THis corresponds to a longitudinal strain of -16.3%.||Compare with global strain, in this case the global strain was 16.1%, giving a good comparison. However, the two methods are different, as this method normalises for the length of the curved wall, and the actual values are dependent on the curvature (especially in the apex) of the segments.|
|MAPSE by M-mode. In
this case the MAPSE was 14 mm in the septal
site and 16 mm in the lateral, giving an
average of 15.
||MAPSE by tissue
Doppler showing an MAPSE of about 15 mm.
systolic images of the heart. Systolic
shortening of the left ventricle relative to
diastolic length, is the systolic strain of
the ventricle. The longitudinal strain
during systole is thus:
However, it is also evident that as the wall shortens, it also thickens, to conserve the volume. Heart muscle is generally assumed to be incompressible.
|Strain being (L - L0)
may still not be
unambiguous, as shown below. Both the strain
length, L0 and the shortening (L - L0) will be different
when measured along a skewed line (red) and even
longer along a line following the wall curvature
(blue). As both strain length and shortening
increase when the curved line is used, the ratio
will not be as affected, but still, L0
will increase more than than the shortening.
|Dividing the end
systolic mitral annular displacement (MAPSE)
by L0 (end diastolic length) gives
the end systolic Lagrangian
strain. (Dividing the MAPSE by end
systolic length do NOT give the Eulerian
strain, which must be summed up by the ratios
of each time frame length change to the
instantaneous length as discussed above. )
annular systolic velocity by L0,
gives the Lagrangian
strain rate, the velocity
gradient on the other hand, equals the
Eulerian strain rate. (Dividing the peak
velocity by the end systolic length, however,
do not give the Eulerian strain, this is
obtained by dividing the velocity difference
in each frame by the instantaneous length in
the same frame).
ventricle, mean of 4 walls
ventricle (free wall)
|< 40 years
|40 - 60 years
|> 60 years
|< 40 years
|40 - 60 years
|> 60 years
|End systolic strain (%)
||Peak systolic strain rate
||End systolic strain||Peak systolic strain rate|
- 60 years
|Parasternal long axis of
the aortic valve, Due to the longitudinal motion of
the base of the heart, the valve has moved out of the
M-mode line at end ejection, and the AVC cannot be
||But this recording was
done with tissue Doppler superposed, and turning on
the colour reveals the valve click as a vertical
blue line (marked by the yellow arrow). The
visibility in tissue Doppler is due to the broader
beams and different filter setting of tissue Doppler
compared to the B-mode.
|Short, negative velocity
spike at end ejection. This ha erroneously been
assumed to be isovolumic relaxation, and hence, AVC
at the start of the spike.
||The negative spike
corresponds to the vertical narrow blue band (blue =
negative velocity) and perpetuating the mistake, the
AVC would be at the start of this blue band as
marked by the black arrow.
|Well known finding of a
systolic "notch" in the septum in systole. This
corresponds to a slight thinning of the septum with
an abrupt stop.
||Displacement curve of the
septal mitral ring. (The same can be seen in septal
M-mode). It can be seen that there is a short motion
away from the probe, corresponding to the negative
velocity spike at end ejection. The motion stops
abruptly, and there is a slight "bounce" before
mitral opening leads to another downward motion.
Thus, end ejection can be reliably identified by Tissue
Doppler tracings from the septum, both in relation to Doppler
flow and Phono (168),
to very high frame rate B-mode (169)
in both normal ventricles, ventricles during high heart rate
and ventricles with ischemia infarct sequelae (170).
This can thus be done in the same acquisitions as the tissue
Doppler recordings, without having to transfer from a
different recording. However, in mechanical asynchrony from
other causes, this is more dubious (289)
|Placing the AVC event
marker, shows the protodiastolic negative velocities
to be present in the basal and midwall segments
(yellow and cyan curve), but not in the apex (red
curve). Converting the dataset to
a curved M-mode, the spike corresponds
to the narrow blue band, and the zero crossing to
the shift from blue to red.
||Keeping the event marker,
but converting to displacement, wee see the "notch"
in the basal (yellow) curve, and the AVC is the
bottom of the notch where there is an abrupt change
from downward to upward motion, thus the change from
negative to positive velocities.
|Propagation of mechanical wave along septum, as visualised by ultra high frame rate TDI. The wave is identified by the peak positive acceleration in each point, showing this to be earliest in the base, lowest near the apex. The orange frame shows the velocity curves, the blue frame the acceleration curves. Image courtesy of Svein Arne Aase, modified from (172).||Point of peak acelleration can also be shown by this method to be later in the lateral wall than in the septum. Image courtesy of Svein Arne Aase, modified from (172).|
|Keeping the event marker in place, but converting to strain rate and strain. Now it can be seen that there is an elongation only in the midwall (cyan curve). The finding of negative velocities in the base as well, is due to tethering, and shows how deformation imaging has a better spatial resolution in separating events in space. The protodiastolic phase cannot be seen in the traces from the base, only in the mid wall and in the M-mode as seen below.||Strain rate traces shows a generally complex pattern and are little suited to location of AVC. In strain curves, however, AVC can again be seen as a "notch" (as in displacement), most evident in the midwall (cyan) trace.|
|Strain rate M-mode. If
AVC should be placed by strain rate traces, it can
only be located from the M-mode or the midwall
trace, just after the initial elongation, but strain
rate traces shows a generally complex pattern and
are little suited to location of AVC. M-mode is far
mechanism for the aortic closure. During
ejection the ventricle can be seen to shorten,
and there is ejection (arrow), keeping the
cusps open. Ejection is decreasing
towards the end of the ejection period, as
shown by the decreasing length of the arrow.
At end ejection, there is no flow, and the
relaxation that started during ejection as a
reduction in tension, leads to a slight
elongation. The aortic cusps then are closed
due to the action of the now stationary blood
column, similar to what happens if a scoop is
put into the water (opening forward) from a
boat that is moving forward. In this case, the
motion of the cusps are mainly lateral, i.e.
towards the middle, and thus may be greater
than the longitudinal displacement of the
The aortic valve stops when the cusps close, there being no further room for backward motion. This leads to an abrupt stop in the motion of the base of the heart, and a small "bounce", which is what's seen in the motion traces above. (The "bounce" is not depicted in the animation.)
|But this mechanism
also should lead to there being a small volume
increase of the LV at end ejection,
protodiastolic volume increase (P); due to the
motion of the AV plane. This, again is not due
to regurgitation, just the point that the aortic
annulus "grabs" a small volume by moving around
a immobile column of blood. This shape of the
pressure volume loop again is in accordance with
experimental findings (173).
||S' (cm/s pwTDI)||S' (cm/s cTDI)||Segmental SRs (s-1)
|Mean intra subject variation (max - min)
|MAE(mm)||S' (cm/s pwTDI)||S' (cm/s cTDI)||Segmental SRs (s-1)||Mean SRs (s-1)
|The AV plane. It consists of a fibrous plane connecting the rings of the pulmonary artery (PA), the aorta (Ao), the Mitral (MV) and the tricuspid (TV) valves, and surrounded by the muscular base of the heart. The sections of the mitral ring cannot be seen as indepndently moving structures. Thus, segments will interact within this framework.||And both ventricles
move the AV plane. (It might seem to be slightly
flexible, as the motion of the tricuspid corner
(tapse) is higher than the mitral motion, but
still the palne will move as a whole, even if
there is some deformation. The velocities of the
lateral left wall are higher than the septum,
but this is due to the longer wall, as discussed
The overall systolic motion
is not so different.
|Diagram of longitudinal segment interaction. the longitudinal shortening of one segment results in shortening of the segment itself (orange arrows), but also in motion (red arrows) of the segments basally to it. (In this illustration, the red arrows show the motion of the middle of the segment, meaning that it also included the effect of the shortening of the apical half of the segment itself.)and the motion of each segment is equal to the summation of the shortening of the segments apically. However, the primary effect is force generation. And this means that contraction in one segment results in a force applied to the neighboring segments. This force has different effects, as the apex is considered anchored (by the recoil force), while the midwall segment has force applied from both sides, and the basal segment is freely movable. The main point is that the force from neighboring segments may be considered part of the load of each segment, and that motion is secondary to deformation, but deformation is secondary to force and load.|
|Deformation patterns in apical loss of contractility. A: normal pattern as in the diagram above. B: partial loss of contractility, as shown by the shorter black arrow pulling on the midwall segment. In this case several things may happen: If the residual contractility is just about to balance the force from the two other segments, no deformation occurs, thus the segment will be akinetic, but not due to a total loss of force. Thus, akinesia does not necessarily mean total loss of function. If the contractility is a little better, there will be shortening, i. e hypokinesia. If the contractility is a little too small, there will be stretching, i.e. dyskinesia as in C. In the case of akinesia shown here, there will be a little motion of the middle of the midwall segment, due to the shortening of the apical part, but not much, and the basal segment will have substantially reduced motion as well, despite both segments having normal shortening. C: Total loss of contractility. (Of course, in this case normal function of the midwall is improbable, this is just an illustration of the mechanics. In this case, as the apex is anchored, there will be stretching of the apical segment. The midwall segment may then have no motion, as the stretching of the apex and the shortening of the basal segment may cancel out, as depicted here. Or there may be net motion in the apical direction, as the stretching may require more force than moving the (more freely moving) basal segment. Also, especially in infarction, the picture may be complicated by fibrosis. Heavy fibrosis in scarring may render the segment totally un-stretchable, thus mimicking situation B.||Apical infarct. In
LAD infarcts, the whole of the apex is usually
affected, the infarct sits as a "cap" over the
apex, although the extension towards the base
may vary in the various walls. Thus, the
reasoning in the illustration to the left holds
for the whole ventricle.
A: Normal function. (The arrows indicating
normal shortening are smaller, to give room
for the hyperkinesia in the infarct situation
in B.) B: Total loss of force in the basal
segment. Even with total loss of force, the
segment can be pulled along, due to the tethering effect,
the fact that the mitral ring, as opposed to
the apex, is movable. A perfect example of
this can be seen here. Thus the
probability of any great degree of stretching
is less probable. A small amount of
stretching my be present, depending on the
interaction with the other segments pulling on
the mitral ring. There is thus no force
from the basal segment acting on the rest of
the wall, and thus the load on the two other
segments are reduced, leading to increased
shortening, which may be interpreted as
"compensatory hyperkinesia". However,
this follows as a function of reduced
load, not hyper function. AS
the mitral ring moves around the whole of the
circumference, the shortening normally
distributed to three segments, in the
infarcted wall is only distributed to two.
There is slight stretching, but the main point
is the fact that the infarct only affects the
base and midwall of the inferior wall, and the
base of the septum. Thus only the basal part
of 1/3 of the circumference is affected.
|Strain rate of an inferior infarct at day 1, showing akinesia in the basal segment (yellow curve) and hyperkinesia in the apex (blue curve). The hyperkiesia can be explained by the load reduction due to the lack of force from the infarcted segment. (Image courtesy of Charlotte Björk Ingul).||The same patient
at day 7. Function in the basal segment
(yellow curve) can be seen to be nearly
normalised, and the shortening of the apical
segment (blue curve) is correspondingly
reduced. (Image courtesy of Charlotte
|Apical myocardial infarct
in the inferolateral wall. Inward motion after
systole can be seen in the apex.
||That post systolic
shortening in the infarct area is simultaneous
with elongation (relaxation) in the normal
basal part, is very evident from the colour
|Looking at tissue Doppler,
there is post systolic motion of the borders of
the midwall segment (lilac and orange curves),
but very little in the apex (green) or the
mitral annulus (white).
||But this of course means
that post systolic deformation happens
in the apical segment (yellow coloured
interval between green and orange curve).
|The post systolic
shortening is thus in the infarcted apical
segment (yellow cirve, negative deflection) as
seen from the strain rate .....
||.... and strain curves.
|The post systolic
shortening of the apex can in this instance be
seen to cause an ejection of blood from the apex
towards the base after normal
||This is evident in the
still frame from early diastole (top), and from
the colour M-mode where the duration and extent
of the jet cab be seen (arrows) just before
onset of early filling.
|Normal strain rate curves. Note that there is a little shortening of the lateral wall (cyan curve) after AVC (green vertical line). This is normal, and related to the shape change in IVR.||Reduced systolic shortening and presence of post systolic shortening in the apical segment (cyan curve), with normal systolic shortening and no post systolic shortening in the basal segment (yellow curve).||Two different instances of post systolic shortening. Apicolaterally, there is stretching and then recoil after AVC (cyan curve). There is little indication of active contraction at all (except possibly a little overshoot, but that may be elastic). However, the stretchability and recoil indicates that the tissue has not lost it's elasticity. Apicoseptally there is systolic shortening and then further post systolic shortening (yellow curve), which thus has to be active. It also shows the mechanism for PSS to be different than recoil. In fact, these curve is very similar to the curves in the original work of Tennant and Wiggers from 1935 (46).|
|Colour SRI M-modes
from septum of the same examination, showing
clearly at 20 µg/kg/min the
development of a prolonged shortening period in
the apex, but still systolic shortening as
well. During peak stress, there is virtually no
systolic shortening, only post systolic.
||Strain curves at 20 µg/kg/min (top) and peak stress (bottom),
showing systolic hypokinesia at low dose
with PSS and akinesia in septum / dyskinesia
laterally with PSS. Thus, PPSS are seen also
with hypokinesia, and is not only a recoil after
stretch. The dyskinetic segment
(cyan) shows post systolic shortening in excess
of recoil, so it there must be some active
tension as well.
|Strain rate bull's eye and three dimensional reconstructions of a ventricle in systole (top), showing an area of dyskinesia (blue) in the apex, and diastole (bottom), showing a larger area of post systolic shortening (yellow).||Strain rate bulls eye from systole and early diastole (top, left) , below 3D reconstruction (bottom, left) in systole and M-modes from all six walls (right), showing an inferior infarct with slight dyskinesia and more extensive akinesia in systole and post systolic shortening in the infarcted wall.|
ischemia in all walls in a patient with severe
three vessel disease (among other things
stenosis left main, occluded LAD filled from
RDP, even with occluded RCA filled from
collaterals) . Visually, the most striking
finding is fall in EF with increasing stress.
rate colour M-mode. No significant PSS
can be seen (Except possibly apicolaterally).
Thus at first glance, the M-mode looks normal,
at least concerning synchrony.
|Strain rate curves (left) and strain (right) of the ventricle at peak stress. Again, no significant PSS can be seen (Except possibly apicolaterally), demonstrating clearly that there are little PSS when there are no segments with normal contraction-relaxation cycles. The AVC is evident from the phono traces. The strain curves show delayed and prolonged shortening, but more or less in all segments. This is equivalent to the balanced ischemia of scintigraphy.|
|Recording from a patient with apical hypertrophic cardiomyopathy. During systole there is virtual obliteration of the apical cavity. Ejection can be seen in blue, and there is a delayed, separate ejection from the apex due to delayed relaxation. There is an ordinary mitral inflow (red), but no filling of the apex in the early phase (E-wave), while the late phase (A-wave) can be seen to fill the apex. Left, a combined image in HPRF and colour M-mode. The PRF is adjusted to place two samples at the mitral annulus and in the mid ventricle just at the outlet of the apex. The mitral filling is shown by the green arrows, and the late filling of the apex is marked by the blue arrow. In addition, there is a dynamic mid ventricular gradient shown by the red arrow, with aliasing in the ejection signal in colour Doppler. The delayed ejection from the apex is marked by the yellow arrow (the case is described in (87).|
|Strain rate from the same patient, showing PSS in the apical part of the septum, and nearly the whole of the lateral wall. (images were made in a very early software, but yellow is still shortening, blue lengthening.)|
|Patient with "septal beaking" in M-mode, seen as a short inward motion starting at the onset of QRS, and peaking about at the same time as the onset of inward motion of the inferolateral wall.||The septal flash consists
of a short inward and then outward motion of the
septum, the outward motion start about
simultaneously with inward motion of the lateral
||The "septal flash" evident in both parasternal long axis and short axis.|
chamber view shows both septal flash and rocking
||"Rocking apex" as seen by
tissue Doppler. The apex moves first towards
the left. This is
evident as the left side of the apex moves
downwards (yellow curve - initial downward
velocity) and the right side moves upwards (cyan
curve, initial positive velocity). After this
initial rocking, the apex rocks back towards the
right, as seen by the reversal of the velocity
curves. the initial right rocking is seen during
the duration of the QRS, then there is reverse
rocking starting early, but with a peak late in
To understand the mechanism of the septal flash, the normal pumping physiology has to be considered. Normal electrical activation starts in mid septum. The whole of the left ventricle is then activated within 80 - 100 (120) ms (the duration of a normal QRS). Electromechanical delay at the cellular level is 20 - 30 ms (234, 268). Thus, the start of the contraction of the lateral wall should be within 80 - 100 ms after start of septal contraction. The normal mechanical sequence vill then be as follows:Delayed intraventricular conduction, on the other hand, will lead to delayed activation of the lateral wall. Thus, the septum will contract for a longer time alone, with no balancing tension in the lateral wall, meaning that the septal contraction is free to stretch the initially passive lateral wall as seen by the rocking apex. This again means that the initial contraction of the septum actually results in shortening of the septum, and not isovolumic contraction, there is septal deformation (shortening) earlier than in the normal ventricle. The septal contraction may then lead to stretch of the passive lateral wall rathere that leading to pressure increase. If so, there will be no pressure increase either, and presumably no MV closure. At the time of initial lateral wall contraction, this will be the time of pressure increase, and this will presumably give pressure increase, which presumably will be the time of mitral closure, and continuing pressure increase which will push the septum back. Thus the peak of the septal beaking on M-mode is close to both onset of lateral wall shortening and MVC.
Initial contraction gives a small pressure rise which closes the mitral valve (236) about 30 ms after initial septal contraction (and thus without help of the lateral wall), and then the lateral wall will have to start contraction only about 50 ms after MVC. AS the walls contract in parallel, they will give rise to isovolumic contraction where there is pressure increase without deformation, and then ejection when ventricular pressure exceeds aortic, the ejection phase is characterised by longitudinal shortening and wall thickening.
However, active contraction is in terms of force, and cannot be seen by deformation, as the continuing ejection will result in continuing shortening despite tension decrease. The development of active contraction do not continue during the whole of the ejection, tension decrease starts around mid ejection, probably at the time of peak pressure / peak strain, after this there is tension release. Thus, the tension buildup is an event of much shorter duration than ejection. After this there is still tension, although decreasing, during the last part of ejection the ejection is partly driven by inertia.
The most important point is that active contraction is an event of short duration. Thus increased delay in the lateral wall may result in lateral contraction simultaneous with a decreasing, and thus, much lower tension in the septum, leading to the septum being either apparently passive (no deformation) or it may even stretch, depending on the remaining tension. This will lead to the lateral wall carrying most of the load of ejection, and thus more mechanical inefficiency. Even so, the septum may shorten during ejection, due to the volume reduction.
|During pre ejection,
the septum contracts, but as the passive lateral
wall is not activated, is is stretched, thus the
apex is pulled to the right, and there is no
pressure buildup, only a shifting of the
walls and apex. This is the septal flash.
||AS the lateral wall is
activated, there has to be remaining tension
in the septum (or else there would be no pumping
at all, only a rocking of the heart back and
forth as the septum and lateral wall
alternate between contracting and
stretching.) Thus, the isovolumic
contraction where pressure builds, happens only
after lateral wall activation. The increased
pressure forces the septum back. However, there
must still be active tension in the septum, or
else, there would not be any pressure increase
at all, just rocking back
and forth, as the lateral wall contraction would
only stretch the septum.
||In the last part of
ejection, the ejection is again driven by
inertia, resulting in volume reduction, as well
as passive shortening of both walls.
|Adding sample volumes in
the base as well (it is the same recording as
the one shown above,
only the scaling is changed as curves with
higher amplitudes are added), shows that basal
velocities seem nearly synchronous. Also,
looking at the offset between the curves, the
deformation of the walls can be visualised by
the offset between the curves as shown initially in
this section. During QRS there is
shortening of the septum (yellow to red), and
streching of the lateral wall (green to cyan).
This is the septal flash. The peak o0f the
septal flash is seen early in the QRS. It
probably marks the time of MVC and onset of the
IVC. The next period shows shortening of both
septum and lateral wall, and thus, there has to
be active ejection. The septum shows less
shortening than the lateral wall, which may be a
sign of decreasing tension a little earlier in
the septum. Finally, there is more shortening of
the lateral wall, and concomitant stretch of the
septum, which seems to sart a little before end
It is also evident, that in this case there is almost no offset between the initial peak positive velocities in the base, so the septal flash and rocking apex is not sufficient to assess the amount ofasynchrony, although being a marker tath there actually is asynchrony.
|The findings from tissue
Doppler is confirmed by this curved M-mode,
showing the phases of septal shortening and
lateral stretch, then the IVC, (there is little
deformation, but the pattern is noisy so
it is difficult to discern the phases, and there
is also some near field clutter in the apex).
The phase of simultaneous deformation is is
evident, as is the phase of continued shortening
of the lateral wall together with stretching of
the septum. End ejection is seen to be during a
small part of the period of lateral
shortening/septal stretch, but most of this is
after end ejection. There seems to be no post
systolic shortening in the septum.
Interpretation of this is somewhat difficult, but it may seem that this means that there is little work inefficiency during ejection.
As CRT now has been a well established treatment modality
for heart failure with Left Bundle Branch Block (291,
much interest has been vested in eliciting how mechanical
asnchrony may affect pumping efficiency. It seems that the
mechanism may in many cases be through mechanical
inefficiency, due to asynchronous work by the left
ventricle. Resynchronization may result in improvement due
to more efficient work.
As only about 70% of CHF patients with LBBB respond to
cardiac resynchronisation therapy (CRT), the need to
elicit the effect on mechanics in rder to see which
patients that are potential resonders, seems
obvious. However, so far, the search for echocardiographic
markers of mechanical inefficiency that may predict
response, have only beeen moderately successful (286).
It may be that in some patients the LBBB is a marker
of cardiac disease, without being a worsening factor.
Of course, simplistic approaches such as using dispersion
of "time to peak systolic velocity" would be far too
simple. Especially, as the peak systolic velocity in many
cases is the effect
of recoil, not of deformation per se, and may be differently
directed in the two walls, this is not a function of
only electrical activation. Time to peak strain rate (and
especially strain) is dependent not only on the onset
of contraction, but also on the rate of force development,
which is a function of contractility. Uneven contractility
would thus be expected to be a factor in timing of peak
Septal flash is a marker of
mechanical asynchrony per se, but not necessarily of
|There is septal flash seen
in the M-mode, start of the septal flash is
slightly after start of QRS, septal peak is
about simultaneous with onset of inferolateral
thickening, and then there is a slight septal
inward motion simultaneous with the
inferolateral wall thinning.
||Septal flash is evident
form the parasternal view.
||And both septal flash and
rocking apex in the apical 4-chamber view.
|Looking at apical
velocities, the apical rocking to the left
during septal activation (A - C) is evident,
while there is a period with
little rocking, and then rocking to the right
during the last part of systole (E-F).
||Adding basal curves (again
the apical curves are the same, amplitude is
inly due to autoscaling), it is easy to see
septal shortening and lateral stretch during the
septal flash, with the peak (B) more or
less at the same time as in the M-mode. The
peak of the septal flash (B) is not easily
seen in colour M-mode, but must more or less
correspond to the onset of lateral contraction
(tension), which is the force (through
increasing pressure) that forces the septum
Then the two septal curves cross, indicating a short period of septal stretch (C - D), while there is little offset between the curves during most of the ejection, and then a new period of septal stretcing. There is shortening of the lateral wall from A - F. From the basal curves, it is evident that there is more asynchrony seen in the velocity traces compered to the previous case, as the basal velocities peak at a different time.
at strain rate, the same can be seen,
both in the M-mode and the
traces, there is septal shortening and lateral
stretch from A to C. The peak of the septal
flash (B) is not easily seen in colour M-mode,
but must more or less correspond to the onset of
lateral contraction (tension), which is the
force (through increasing pressure) that forces
the septum back.
Then there is lateral shortening and septal stretch from C to D (here, the duration is more clear from the M-mode than the traces that are taken only from a small ROI). This may represent a period of declining tension in the septum, concomitant with increasing tension in the lateral wall, indicating a higher degree of asynchrony (more delay) than in the previous case. The period D-E represent septal shortening, but may still be passive (it ptobably is, as there was stretch during first part of ejection), due to the inertial driven ejection and hence, volume reduction. During end ejection (E-F), there seems to be lateral shortening and simultaneous septal stretch again, and part of this is well within the ejection period, indicationg again a higher degree of mechanical inefficiency during ejection. Thus, there is no evident indication that the septum actually contributes actively to ejection at all. Finally, there is post systolic shortening i the septum as opposed to the previous case, which most probably is recoil from the previous stretch, also indicating a higher amount of wasted work. The ejection period is identified by the LVOT flow curve below.
|Finally, looking at true
ejection, it can be seen to start at (or even
slightly after) the end of
the septal flash, indicating
that IVC occurs during the last part of the
flash (probably from the peak).
But ejection is still during lateral wall
||This is partly confirmed in
the mitral flow curve, the end of flow and
mitral valve closure as seen by the valve click,
occurs at nadir QRS, nearly
simultaneous with peak septal flash, indicating
that IVC starts at that point.
(equivalent with septal flash can be seen by
tissue velocity curves in the apex.
|Looking at another
example, cardiomyopathy with CHF, LBBB and
septal flash, asynchrony is evident, even
without tissue Doppler.
||Adding the velocity
curves from the base shows very little
dyssynchrony assessed by the time to peak
annulus velocity, in fact by that criterion it
seems fairly synchronous. Also, assessing the
strain rate by the offset between the velocity
curves (septum yellow and red, lateral wall
cyan and green), there seems to be a fair
strain rate in both walls.
|Although the septal flash, with septal shortening and lateral stretch is visible (before the red marker line), surprisingly, in this case there seems to be more shortening in the midwall septum than the lateral wall, both in strain rate,||and strain.This seems to
be counter intuitive as the mechanical
inefficiency is a function of septum
contracting before lateral wall, which the
does most of the real work.
||Looking at the velocity
curves from apex, midwall and base, the points
in each wall seems to be fairly synchronous,
but the offset between the curves from
neighboring points are variable.
|In the septum, the offset
between the apical curve and the midweall
curve (strong orange) is
greater than between the midwall and
basal (strong green), where there even are
some periods of systolic stretch weak green).
||Strain rate curves from
the segments between the curves to the left,
shows shortening in the basal half (orange),
while the septal half (green) has stretch,
slight shortening and then stretch again
||In the lateral wall the
situation is opposite, there is very little
shortening, and even a little systolic stretch
in the basal half, and better shortening in
the apical half.
|The response after 1 year
shows reverse remodelling, increased EF, and
abolished septal flash.
||The same is evident from
the apical view.
synchronicity of shortening can be seen by
|Dilated cardiomyopathy with left bundle
branch block. Early contraction of the septum
with short duration (septal flash and apical
rocking) is visible, and there is
delayed contraction of the lateral wall.
The septum is thinner than the lateral
wall, which may indicate that only the lateral
wall carries load.
||Looking at the strain rate colour
M-mode, the same is evident, even despite the
heavy reverberations in the lateral wall.
In this case the septal flash represents the
whole of the septal shortening, with
simultaneous lateral stretch. Septal stretch
is evident during most of the main lateral
wall shortening. In this case, however, it can
be seen that the most vigorous (rapid) lateral
shortening starts before ejection, because the
pressure buildup (IVC) has to be done by the
lateral wall while some of the work already
during this phase is wasted by stretching the
During ejection, there is a period of simultaneous shortening, which probaly represents volume reduction during ejection, but the evidence is that this shrtening is passive, at least in the septum. Finally, there is post systolic shortening (recoil) of the septum during lateral wall relaxation.
(This also goes to show that the colour M-mode may be more robust in discerning real findings from artefacts.)
|Looking at the ejection, it can be
seen to start during the period of the most
vigorous lateral shortening, and then persist
during the phase of bilateral shortening.
The ejection phase is
||End of mitral flow (MVC) can be
seen just before the peak of the
septal flash on the M-mode to the left.
There is also E-A
fusion, at normal heart rate, indicating an
AV-block. In this case the PQ time is
normal, but there is a functional block to the
left ventricle due to the bundle branch block.
|Looking at strain rate curves, the
information is the same as the colur M-mode
above. Start ejection is marked by the white
line. We see that the most vigorous lateral
wall shortening occurs before start ejection,
and is balanced by septal stretch. This
represents isovolumic contraction period, but
as can be seen from the curves, much of the
work seems to be wasted on stretching the
septum instead. There is little shortening
during the ejection period itself. Finally,
there is post systolic shortening, but this is
after end ejection.
||The mechanics may be more intuitive by
strain than by strain rate, when looking at
the traces, showing a brief shortening of the
septum (septal flash), and then stretch. The
ejection is again seen to start after the most
vigorous lateral wall shortening, indicating
that much of the work during IVC goes into
stretchingthe septum. During ejection there is
a slow decrease in septal stretch (i.e. a
little shortening, and a greater stretch in
the lateral wall. After ejection there is
reversal of lateral shortening and septal
stretch (post systolic shortening).
|The same patient 6 months after CRT. Reverse remodeling and increased EF is evident. Now, the septal flash can no longer be seen, although the overall motion is not completely normal, in fact the apical rocking has reversed, there is now an inverse rocking to the right at early systole. . Also, the septum has thickened as a response to carrying more load.||Now, there is early
shortening of both walls during Pre ejection,
ending with MVC as seen below. During the whole
of ejection there is simultaneous shortening of
|Ejection is earlier,
compered to ECG, as is IVC.
|However, the strain rate
curves look much more normal as well as
synchronised. In fact, the lateral wall seems to
activate slightly before the septum.
||This is also evident from
the strain curves, both
wall shortens simultaneously, although the onset
is earliest in the lateral wall. And
looking at the programming, the lateral wall was
actually programmed 40 ms before the septum.
|Looking at velocities, there sis an earlier peak velocity in the septum than the lateral wall, indicating asynchrony although not very much more than the previous case when looking at peak velocities). The mechanics is not evident from this image, especially as this shows higher velocities in the septum.||It is not very evident from the tissue velocities image that the left ventricle has been resynchronised.|
|Stress echocardiography with development of ischemia in the inferolateral wall. At peak stress, the whole of the wall can be seen to move paradoxically, moving inwards (and towards the apex) after end of septal contraction. Again, in a clinical situation, the interpretation can be facilitated by stopping and scrolling.|
|The velocity (motion) confirms the visual impression, the whole inferolateral wall moves downwards in systole, and upwards after end systole (Yellow and green curves), while the septum shows normal apically directed velocities giving a total asynchrony between the two walls. This asynchrony is also evident by the curved M-mode, starting a the inferior base, going through the apex and ending at the septal base.This might be due to both apical and basal ischemia.|
|The strain curves
below, separates the effects of the
segments, showing systolic dyskinesia
(lengthening) with some net post
systolic shortening in addition to the
recoil in the base (yellow curve), and
systolic hypokinesia in the apical segment
(green curve) with post systolic shortening,
compared to a fairly normal strain curve in
the septum. Thus, deformation imaging
showing most severe ischemic reaction in the
basal part, giving highest probability of a
Cx ischemia, which was confirmed
In this peak stress image, the tissue Doppler confirms the presence of initial asynchrony: The whole of the inferolateral wall seem to show dyskinesia (Yellow and cyan curve), with early motion (after IVC) away from apex. It seems to be most pronounced in the apical part.The septal base moves normally, toward apex (red curve). By placing the sample volume in the aortic ostium, the high velocities of the aortic closure is identified, giving the timing of end systole. This timing can then be transferred to the deformation images below.
|Stress echo. In this case, the image is suspect of a delayed inward motion of the base of the wall at start systole at medium and peak dose.|
|Strain rate (left) and strain (right) showing that there is a slight reversal of shortening in the early diastole, but only in the base (cyan) . The delay, however, is shown to be entirely within systole. The clinical meaning of this is uncertain, but it was not due to ischemia, as the coronary angiography was completely ("super"-) normal.|
|The whole heart can
be seen to be rocking. This might indicate
asynchrony, or dyskinesia of the septum.
||However, looking at
the short axis view, the wall thickening
(transmural strain) can be seen to be
Doppler left shows delayed onset and peak
velocity of motion of the lateral wall, but
this is due to the rocking motion of the whole
heart. Strain rate shows symmetric timing of
onset and peak shortening. This
difference between motion and deformation
imaging was evident already in B-mode, when
knowing what to look for.
|Motion of the mitral
ring, mitral leaflet and mitral tip.
Bottom; zoomed to the time period of interest.
The septal mitral ring (yellow curve) can be
seen to "bounce" after AVC, meaning that it has
apical motion during IVR. This motion is
of course imparted also to the mitral leaflet,
and means that the start of apical motion do not
mark the MVO.
||Velocity traces of the
same points as seen to the left. The start of
apical motion of the mitral ring (yellow curve)
corresponds to a shft from negative to positive
velocities after the protodiastolic negative
velocity spike (i.e. the crossing of the zero
|A sample volume at the
middle of the mitral leaflet (green curve), will
have the same motion as the ring, although with
some delay. However, we see that apical motion
starts around the middle of IVR, before MVO.
||This corresponds to
positive velocities in the last half of IVR
|The sample volume at
the mitral tip (red curve) shows no apical
motion during IVR, rater motion in the opposite
direction, but an abrupt start of apical motion
at the end of AVR, at the same time as the
mitral ring shifts to motion toward the base.
Thus, this is an independent leafet motion, and
marks the MVO, and it can be seen that during
IVR, there is ballooning away from the apex of
the mitral leaflets.
Both mitral valve traces can be seen to deflect sharply downwards at a later time point (white markers) , this is due to aliasing of the tissue velocity when the velocities reaches the Nykvist limit.
|The mitral tip (red
curve) can be seen to have negative velocities
(moving away from the apex) during IVR, and to
cross from negative to positive velocities at the
same time as the mitral ring crosses from positive
The points of aliasing can be seen at the abrupt downward stroke in the traces from the mitral leaflets (White markers), which is earlier at the tip than in the middle of the leaflet. Only in the mitral ring can AVC be seen with certainty.
from the mitral ring (left), middle mitral
leaflet (in terms of distance from ring to tip -
middle image) and mitral tip (right image),
corresponding to the traces above. The
traces show only systole and early diastole, as
above. As in the traces there is shift from
negative (blue) to positive (red) at AVC and
from positive to negative at the event taken to
be closest to MVO. In the middle mitral
leaflet, however, this is less well defined,
only in the lowest part can these event being
identified. At the mitral tips, the transition
marking AVC is absent, (as above), while the
second transition from blue to red is visible in
a short part of the M-mode.
|Looking at the mitral ring, which would reflect the overall volume changes, there is concomitant negative velocities (basal motion during the protodiastolic event in both parts of the mitral ring. But after AVC, we se negative velocities continuing in the lateral part, while there is a positive motion (bounce) in the septal part. This is consistent with no volume change, but a tilting of the left ventricle during the IVR. Mitral opening thus possibly corresponding to the start of basal motion as seen by the septal curve. Only after MVO do the septal part start basal motion concomitant with the lateral part. And only then will there be overall elongation (volume increase). This do correspond to s shioft in the septal velocity curve from posisitve to negative. It is the second zero crossing after the protodiastolic dip.|
images of velocity (left) and displacement
(right), showing that there is a peak apical
mitral ring displacement at the event
taken to correspond to MVO. This is equivalent
with the second
zero crossing of the velocity trace after
negative strain occurs later in base and
midwall. AVC can be seen best by strain curves
in the midwall segment. No definite deflection
can be seen to correspond to the event assumed
to be MVO transferred from the
|Colour M-mode in
normal subject. The mitral valve is included,
and to the left the colur is removed from the
same two cycles in the same recording, to locate
the point of mitral valve opening better.
Zooming in on the images, at end ejection can se
the valve click as a vertical bar (Just as in
pulsed Doppler recordings as seen above) thus, the
IVR is very easily defined, and apically
directed flow (red) above the mitral valve, i.e.
intraventricular can be seen during the IVR.
rate tracings in this subject show positive
strain rate (lengthening) during IVR in the
septal apical and lateral apical and midwall
segments, concomitant with negative strain rate
(shortening) in the basal segments. (In the
apical area, there are near field
reverberations, which have to be excluded.
These, however are evident by the abrupt shift
in direction between high strain rates. )
|The Wiggers cycle:
Heart cycle in terms of pressure changes
||Heart cycle in terms
of volume changes ( =flow)
|Classical Wiggers cycle, where events during the heart cycle is related to pressure changes in atrium and ventricle. The flow is a direct result of the pressure differences, and thus the volume changes are the result of flow. It is evident that pressure decline (relaxation) starts long before end ejection when comparing with the image to the left.||Top, Ventricular volume through one heart cycle, with the different phases demarcated. Below, composite Doppler flow velocity curve showing both LVOT outflow and mitral inflow to the left ventricle. If the orifice remains constant, the flow velocity will be similar to the flow rate curve. Thus, the flow velocity curve is an approximation to flow rate, and hence, similar to the temporal derivative of the volume curve, or, conversely, the volume changes are the integrated flow rate. The isovolumic phases are exaggerated.|
There are three distinct phases. Early
filling (E - wave), where there is inflow from the
atrium to the left ventricle (red curve and
arrows), the ventricle increases the volume,
evident by the velocities of the annulus away from
the apex (dark blue arrows. Diastasis, with little
or no movement. There may or may not be some
passive flow into the left ventricle in this
phase. Atrial systole (A - wave), where
there is atrial contraction, pushing blood
into the ventricle again (light red) and a new
motion of the mitral ring away from the apex
(light blue), due to pressure increase, or direct
pull from atrial contraction, or both. The
resulting flow and tissue velocity curves are
||Mitral flow curve. The conventional measures of diastolic function are shown: E: Peak flow velocity of early filling phase; a measure of rate of relaxation during this phase. Dec-t: Deceleration time of early flow; measured from peak E along the slope of velocity decline to the baseline. IVRT: Isovolumic relaxation time; the time between end ejection and start of mitral flow. It's conventionally measured from the valve click at AVC to the start of mitral flow. A: peak flow velocity of atrial systole. The E/A ratio shows the relative contributions of the two phases to filling, and is a more sensitive index of reduced early filling.|
|A: Relation between
mitral flow indices and pressure in the normal
situation. Mitral flow (red curve) is dependent on
the pressure gradients between the left ventricle
and the atrium, which is created by left
ventricular relaxation. The decline in pressure
gradient during IVRT ( = relaxation constant tau)
after AVC determines the length of the isovolumic
relaxation time. The decline in the pressure difference
between atrium and ventricle as the ventricular
pressure increases, determines the deceleration
time. This again is dependent on the
relaxation rate, as the active relaxation,
creating a quick pressure drop in the ventricle, a
high gradient and a short deceleration time.
Atrial pressure increases during atrial systole,
forcing blood to flow again in the A wave.
||B: Slower relaxation
leads to a decrease in the tau, and thus a longer
IVRT before the mitral valve opens; Increased IVRT.
In addition, the slower relaxation leads to a less
profound but longer drop in LV pressure, leading to
a reduced E amplitude and a prolonged dec-t.
The lower filling volume leads to a higher atrial
volume at the start of atrial contraction, and thus
a higher atrial stroke volume (perhaps by the
Frank-Starling mechanism), and a higher A- wave. The
E/A ratio is reversed. (Light gray flow curve is
from A, for comparison).
||C: Decreased LV compliance due to fibrosis or dilation, leads to a higher increase in LV pressure from the injected volume from the atrium. This leads to an earlier equilibration of LV and LA pressure, and an abbreviated A-wave, which can be seen by comparing with the duration of the reverse A wave in the pulmonary veins. Decreased LV compliance shows up first in end diastole, as this is the phase where the ventricle is at the highest volume. (Light gray flow curve is from B, for comparison).||D: Increased filling pressure (Left atrial pressure) due to filling problems, will decrease IVRT as shown here, as the pressure gradient between LA and LV is less. In addition, the gradient is higher in early filling, due to the higher LA pressure, with a subsequent higher E-wave. But then LV pressure increases faster in response to the filling from the LA, due to both the increased filling rate, slower relaxation and finally less compliant ventricle already during diastasis. The filling time and dec-t is shortened. Finally the A wave is blunted, due to the higher LV pressure at the start of LA systole, and the E/A ratio reverses back. When the mitral flow looks normal due to delayed relaxation compensated by higher pressure it is called pseudonormalisation, when the E/A, ratio is higher than normal, and the IVRT and Dec-t is shorter than normal, it is called restrictive filling. Restrictive filling is usually a sign of reduced compliance already in early diastole; i.e. severely reduced compliance leading to early pressure increase. (Light gray flow curve is from CB, for comparison).|
|Pressure driven (vis a
tergo; a force acting from behind) filling of a
chamber (B), versus suction driven filling
(vis a fronte; a force acting from the
front). In this simplified model, the level
of fluid (and, hence, pressure) in chamber A is
assumed to be constant during filling.
|In pressure driven
filling, the force driving the piston is the
pressure in chamber A (actually the pressure
difference between chamber A and B. The force,
F (black arrow), is the pressure * area, and the
pressure is a function of the height of the level of
A over B, and the density of the fluid. Thus, the
energy for the movement of the force is potential
energy of the pressure difference. Flow (Q) is driven by the
pressure gradient between A and B. In this case the pressure
increases in chamber B up to the level of A. This
transmits the force to the piston expanding the
chamber B by the pressure.
||In suction driven
filling, there is a force, F, applied to the
piston, expanding chamber B. This creates a
pressure drop in the chamber, and a pressure
gradient between A and B. Thus, the energy is
applied to the creation of a pressure drop in
chamber B. Flow (Q) is gain driven by the pressure
gradient between A and B.
|In both cases the flow
is driven by the pressure gradient between A and B
(i.e. there is a potential energy in A versus B
that drives the flow, shown by the blue arrows),
but in vis a tergo, the force application (energy)
is applied to the fluid in chamber A , in vis a
fronte, energy is applied to creating a pressure
drop in chamber B.
|Feasibility N (%)||657 (99%)||657 (99%)||657 (99%)||657 (99%)||653 (98%)|
|<40 years, N=208, mean (SD)||80 (16)||48 (15)||1.85 (0.76)||212 (55)||85 (16)|
|40-60 years, N=336, mean (SD)||74 (15)||59 (15)||1.32 (0.40)||220 (66)||95 (20)|
|>60 years, N=119, mean (SD)||69 (16)||75 (18)||0.96 (0.32)||244 (79)||105 (23)|
|All, N=663, mean (SD)||75 (16)||58 (18)||1.42 (0.62)||218 (66)||93 (21)|
|Feasibility N (%)
|<40 years, N=126,
|40-60 years, N=327,
|>60 years, N=150,
|All, N=603, mean (SD)
|A: Patient < 30 with
normal diastolic function. E/A > 1, Short Dec.T
and IVRT, high e'. In this patient it is normal
for age, but might have been severe heart failure
with restrictive filling, even given the patient's
age. Compare with patient F. In this case
the tissue Doppler helps to discern.
||B: Patient about 50 years with near normal diastolic function. for age. E/A = 1, somewhat longer Dec-T and IVRT.|
|C: Slightly impaired relaxation. Patient at about 70, with slightly delayed relaxation due to a history of hypertension. Prolonged IVRT, dec-T, reduced E and E/A ratio < 1. Also reduced e'.||D: Severely impaired relaxation. Patient with heart failure (and normal EF and LV EDV), but with normal filling pressure due to diuretic and ACE inhibitor treatment. Severely reuced relaxation with prolonged IVRT, dec-t, decreased E and E/A ratio <<1. Very low e'.|
|E: Pseudonormalisation. Patient age 69 with history of hypertension. Mitral flow (top left) shows normal values for E, A and Dec. time, and the IVRT (top right) is also normal. Tissue Doppler (bottom) shows impaired relaxation, (E/e' about 15), indicating that the atrial pressure is elevated. This is demasked by doing a mitral flow acquisition during Valsalva manouver (decreasing venous return and hence, atrial pressure) below:||F: Patient with restrictive pattern (actually same patient as in C, but before treatment, and then with increased LVEDV and low EF), due to high filling pressure. Short IVRT, dec-t, high E and E/A ratio. e' still low showing that there is delayed relaxation, despite the high E and E/A. Compare with A, little difference, but taking the patient's age into consideration, it is actually evident that this is restrictive filling, even without tissue Doppler showing a low e'.|
|Left ventricle, mean of 4 walls||Right ventricle (free wall)|
|< 40 years
|40 - 60 years
|> 60 years
|< 40 years
|40 - 60 years
|> 60 years
||40 - 60
|e' (SD) cm/s
|Mean of four points