What does strain and strain rate actually measure?
The relation between function imaging and physiology - contractility, load, work and phases of the heart cycle.
Faculty of Medicine,
NTNU Norwegian University of Science and Technology
|Any imaging modality, including strain and strain rate only shows muscle shortening, and thus only tells half the truth about cardiac contractility and work.||Function is contractile force,
and shortening is force versus load. Work is the
amount of shortening times load.
The spatial derivative of flow is
Pressure increase of 100 MMHg in 100 ml blood (LVEDV) = 13.3 J.
Ejection of 50 ml blood (at an EF of 50%) at a velocity of 1 m/s at
constant pressure, is about 0.025J. Thus, in terms of work, most of
it is generation of pressure, and thus isometric rather than
isotonic. The greatest great
part of the ventricular work - the isometric work, cannot be
described by deformation analysis (or any imaging modality) at all
as all functional analysis by cardiac imaging is about deformation. Load independent imaging
modalities doesn't exist. The full description of LV
work need to incorporate a measure of load,
either by invasive measures, or by externally measured pressure
(eventually pressure traces) in combination with mathematical
|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 in
the section on dioastolic function. Image courtesy
of Ph.D. Tomas
exercise research group (CERG), Dept. of
Circulation and Medical Imaging, Norwegian University of
Science and technology.
|Looking at various definitions, all taken
from medical dictionaries:
”a capacity for shortening in response to suitable stimulus.”
”capacity for becoming shorter in response to a suitable stimulus.”
- Total confusion of shortening and contraction
”the inotropic state of the myocardium”
- As inotropy is defined as change in contractility, this dfinition is absolutely circular: "contractility is contractility", which is correct, but useless
”the ability of muscle tissue to contract when its thick (myosin) and thin (actin) filaments slide past each other.”
”The ability or property of a substance, especially of muscle, of shortening, or developing increased tension.”
- The last two are better, but has no quantitative connotations, it is simply the ability to.... (ability is non qyantitative, capacity is quantitative) , and no consideration of load
"a measure of cardiac pump performance, the degree to which muscle fibers can shorten when activated by a stimulus independent of preload and afterload"
- Close, but no cigar, load independence, but still confusion of shortening and contraction
It could be argued that contractility don't need a definition, being hard to describe, but instantly recognizable when spotted, which is the elephant test: I can't define an elephant, but I know it when I see it, or the equivalent duck test: When I see a bird that walks like a duck and swims like a duck and quacks like a duck, I call that bird a duck (James Whitcomb Reilly). However, this is insufficient:
This is not a duck, it's a penguin!
|Isometric twitch i.e. contraction
without shortening, showing the tension. Peak tension,
rate of force development and time to peak tension are
all measures of contractile function.
||Isometric twitches, showing the
effect of inotropy (in this case noradrenaline), showing
an increase in both peak tension, RFD and a shortening
of time to peak tension.
|Stretching the muscle before
stimulation, increases tension. The increase in passive
tension will be present at rest, before twitch, and is
equal in baseline and inotropic state. During twitch,
there is an increase in total tension with increasing
pre twitch length. The increase in contractile tension
is then the diference between the passive and the total
curve. This effect is additional to the effect of
||Isometric twitces with increasing
pre-twitch length. In can be seen that as opposed to
inotropy, time to peak tension do not increase, even
though peak tension does, and, as a consequence of this
the rate of force development (as the rise to higher
peak during the same time gives higher rate).
|Hypothetical length tension
diagram, based on the sarcomere hypothesis, that by
increased fibre length initially will increase the
overlap between the myosin head regions and the troponin
regions on actin, optimising the number of cross bridges
that can be formed, and thus the peak tension
obtainable. In this model there is an optimal length,
then the available number of cross bridges, and thus the
peak tension decline again. This seems to be in
accordance with (208), as far as active tension is
||The Frank- Starlings law. Acute
increases in end diastolic filling, will increase the
stroke volume along the curve shown. This effect was
observed with both increased venous pressure, but also
with decreased stroke volume in previous beat, resulting
in an increased EDV. Within physiological limits there
is an increase, but with increasing dilatation, there
will be less response. However, at least in normal
hearts, there is little evidence for a descending limb
of the curves.
|Illustration of the preload. If a
weight is attatched to the unloaded muscle, this muscle
will be stretched, increasing the peak force the muscle
can develope. But the preload is also part of the force
the tension has to overcome in the contraction.
||In an intact ventricle, the preload
is also a function of size. In addition to the size
being a measure of the pre stretch of the muscle, the
intraventricular pressure acts on a larger surface, and
thus the force that has to be generated must be
proportional to the 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 × × r2).
|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 difference between pre- and
afterload is illustrated here. After preload is added, a
support is placed, preventing further stretch of the
muscle when another weight is added. This second weight
is the afterload. When the muscle contracts, it has to
develop a tension that is equal to the total load,
before it can shorten. If the peak force is higher than
the total load, the muscle will then shorten without
generating more tension, in an isotonic
||Isotonic isometric twitches tension
diagrams above, length diagrams below, after (208).
From the diagrams, it is evident that shortening only
starts after tension have reached load, and then, the
tension is constant while the muscle shortens. Thus the
first part of an unloaded contraction is also
shortening, while the first part of a loaded contraction
is isometric, becoming isotonic after tension equals
load. Peak rate of force generation (RFD), occurs during
the isometric phase (except in the unloaded phase, where
there is no tension development). Peak rate on the other
hand occurs during the first part of the shortening,
after tension = load, and is thus later than peak RFD.
The figure also shows that shortening decreases as load
increases, as more of the total work is taken up in
tension development. This affects both peak maximal
shortening and peak rate of shortening.
contraction, the muscle will increase tension, but
resulting in no shortening as long as the tension is
below the total load (isometric contraction). When
tension equals load, further contraction will result in
shortening at constant tension (isotonic contraction).
This is what we see in imaging.
an increasing load will both delay onset of
shortening, as the development of higher tension takes
longer time, but will also result in less shortening, as
well as a lower initial rate of shortening. The
effect of increased load in slowing relaxation (224)
is not shown in this simplified diagram. This would have
shown up in slowing the tension downslope, but the
lengthening would still be shortened by increased load.
will give a slower tension development and lower peak
tension. However, this has the same effect as increased
load on shortening, resulting in delay in onset of
shortening, lower rate of initial shortening and less
total shortening. The
relative incr4ase in load due to reduced contractility,
would still slow relaxation, (224),
but this is not shown here.
|Shortening curves related to
afterload, modified from the figure above. The
shortening in percent, is equivalent to the longitudinal
strain of the muscle.
||Strain curves from a normal
subject. The strain curve is fairly similar to the
shortening curves to the left.
|Shortening velocity and total
shortening, Relation to preload and total load.
Both shortening and velocity can be seen to decrease
with increasing afterload (total load), but increase
||Shortening velocity and total shortening, Relation to total preload and inotropy. Both can be seen to increase with inotropy, but decrease with load.|
|Effect of load on work and power.
With increasing total load the muscle increases the work
and power, despite decreased shortening, but only up to
a peak. After that, increased load will decrease work
and power by decreasing shortening. Increased preload
increases shortening at all afterloads, and will
increase both work and power.
||Effect of inotropy on work and
power. Inotropy will increase work at any given total
load, by increasing shortening. It will also increase
power, by increasing velocity of shortening.
|Simplified pressure volume
diagram (Wigger's diagram) of a whole heart cycle. The
diagram shows the atrial, ventricular and aortic
pressure curves, the ventricular volume curve and the
ECG on a time axis. Mitral valve opening (MVO) and
closing (MVC) occurs about the crossover between
atrial and ventricular curves, aortic closure (AVC)
and opening (AVO) occurs near the ventricular and
aortic valve closure, while aortic valve closure
occurs at the aortic dicrotic notch pressure curves
having crossed much earlier during ejection.
Isovolumic contraction (IVC) is between MVC and AVO,
there being no volume change, this is a true isometric
contraction. Isovolumic relaxation is between
AVC and MVO, this is the isometric phase of
relaxation. The three peaks of the atrial pressure
curve, are a (atrial contraction), c (closure wave)
and v (ventricular contraction).
Below is shown the analogous isotonic - isometric twitches. As seen there is initial preload increase during atrial contraction, increasing passive tension as well as the subsequent tension and ate of force development. Then there is isometric contraction, during IVC. In the isolated muscle, there is isotonic contraction (shortening). In the working ventricle, there is less increase in tension (Systolic load can be considered more or less equal to central pressure during ejection for acute changes), but pressure continues to increase during first part of ejection due to aortic elastance, and then drop during last part of the ejection due to aortic run off. Thus, in the intact heart, the contraction is far from isotonic. The corresponding shortening curve as it would have been in an isolated muscle is shown in dark blue, pre stretch during atrial systole, peak shortening early in the isotonic contraction with lengthening still during isotonic contraction, returning to baseline length at the start of isometric relaxation. The true curve as it is in a working ventricle is, of course, parallel to the ventricular volume curve and shows continuous shortening during the whole ejection (isotonic analogy) and only partial return to baseline length even after completed relaxation.
The Wigger's diagram is fairly common in this form, but is incomplete, as rapid filling is shown as a passive event, and as valve openings and closures are shown at pressure crossover.
|Pressure volume diagram of a
heart where pressure is plotted against volume, a
pressure-Volume loop (PV-loop). The top version shows
the cardiac phases, with the same simplifications as
the Wigger's diagram to the left; rapid
filling is shown as a passive event, and as valve
openings and closures are shown at pressure
crossover. Time runs around the loop in a
counterclockwise direction. The width of the loop is
equal to the stroke volume. The top of the diagram
shows the pressure curve during ejection.
The red, dotted line touching the loop is the end systolic pressure - volume relation. The slope of the tangent is P / V, which is the common definition of elastance. In filling, the elastance is usually taken to mean how much (counter-) pressure a given volume generates, but end systolic LV elastance is a function of emptying. Thus this must be taken to mean how much volume reduction a given pressure has generated. The blue dotted line, the left ventricular end diastolic pressure relation, is the passive tension that the diastolic filling generates, i.e. at atrial filling.
The bottom diagram shows the LV work, which is the area within the PV-loop (cyan).
During isovolumic contraction pressure rises, with no change of volume. During ejection, volume is ejected, reducing ventricular volume from end diastolic volume to end systolic volume. During isovolumic relaxation, the relaxation reduces pressure from LVESP to LVDP, and during diastolic filling the volume increases from LVESP to LVEDP. The area within the loop is P × SV. The equivalent area with mean pressures is shown as the dotted rectangle, to give an intuitive visualisation of the P × V. The Ees is shown to increase with positive inotropy (red dotted line) and decrease with negative inotropy or failure (blue dotted line). The potential energy delivered to the remaining (end systolic) volume, which is not converted into ejection work, is the yellow shaded area.
As we have seen, work is load
× shortening. In the intact heart, this is equal to
the area of the pressure volume loop, as shown above.
Systolic load is more or less equal to central pressure
during ejection. This is a simplified model, excluding the
volume and wall thickness part of the Laplace equation, and
not taking into account the LV diastolic pressure, which may
be important if elevated. But it is valid for acute load
changes, being proportional to pressure changes. But
the ejection phase occurs with a non-constant pressure as
seen above, so the contraction during ejection is not
|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 correspond to contraction
- relaxation. The temporal resolution of MUGA is
low, and the isovolumic phases are poorly defined.
||(Longitudinal) strain (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. It is evident that the longitudinal shortening describes most of the volume changes. Again the shortening might seem to be contraction, and the (early) elongation relaxation.|
LV end systolic elastance is defined as Ees = P / V, which is the slope of the line through the end systolic pressure-volume point in the PV loop as shown above. The relation of the PV loop to load and contractility, is illustrated below:
|Effect of preload. Increased
preload (increased LVEDV), will, through the
Frank-Starling balance increase stroke volume.
This increased stroke volume will be ejected at
the same pressure, thus returning to the same
point on the ESPVR line. Myocardial work, bing
BP×SV, will increase.
||Effect of afterload.
Increased afterload (increased SBP), will reduce
the stroke volume, This can be easily seen here,
as the end systolic point moves up the ESPVR line,
shortening the width of the loop, i.e reduced SV.
The effect on work is more uncertain, as SV
decreases while BP increases.
||Effect of inotropy. Inotropy
shifts the ESPVR line to the left, thus increasing
the force and thus LV emptying, increasing stroke
volume through reduced LVESV.
|In reality, an increased SV
will cause increase in SBP, causing an increased
afterload on the same beat, thus reducing
the effect on SV somewhat, through interaction
between pre- and afterload.
||In reality, an acute increase
in afterload, will reduce emptying (increased
LVEDV), so on the next beat, the preload
is increased, partly offsetting the effect of
afterload on SV.
||In reality, decreased LVESV,
without increased venous return, will in the
next beat result in reduced LVEDV, thus
offsetting the effect of inotropy somewhat by
Thus, as seen, above the ventricular elastance is a measure
of contractility, as it seems to be load independent (400),
and it has achieved a "gold standard" status for measurement
of contractility. In reality, this index is not easily
obtainable in the clinic, even in continuous invasive
monitoring, as volume measurements are not available in
routine monitoring. But in animal experiments, using
conductance catheters, where multiple pre- and afterload
manipulations can be done, and where the ESPVR can be
obtained by linear regression, it serves as a reference
method, to test other contractility indices.
However, the LV elastance may not be a perfect gold
- Firstly, using end ejection for end systole, means that measurements are done at a point in time where the myocardium is in relaxation (but not relaxed) phase.
- Secondly, as we see below, the true end systolic volume is not easily defined due to the protodiastolic volume decrease as discussed below.
Peak systolic pressure volume relation might be closer to
the real thing, but is not easily discernible.
Finally, however, of course these volume considerations are only related to acute changes. In inter individual differences in healthy individuals, as well as in LV dilation, the EDV is not a measure of preload, and the PV-loops can only be interpreted in relation to the individual. PCWP, on the other hand, is a measure of preload, that is relatively standardised and thus a more universal measure of preload when applied across individuals, although it does not take the Laplace effect into consideration.
The total of the arterial effect can be described by the
arterial elastance: Ea = P / V and ventriculo arterial coupling
The main intervals of the heart cycle is defined by the
valve closures and openings. That means start and end of
flow, but with the right positioning of the sample volume
/beam, it can also capture the valve clicks.
Valve opening and closures then will define the main
intervals of the heart cycle, IVC, LVET, DFP and IVR.
As seen, a lot of phases can be seen in the motion and deformation curves. To understand their relation to the phases of the heart cycle, it is necessary to go into the heart cycle in a little more detail. Already Wiggers (402) was clear that the phase pattern was more complex than the original six phases depicted above.
But, again, there are
manu things happening during each of the main intervals,
as will be seen
The pre ejection period (PEP) is defined as the period from
the start of the first deflection of the QRS, to the start
of ejection, as defined by the aortic valve opening, or the
onset of flow in the LVOT (235).
Onset of ECG happens before active contraction, and also
before the MVC, meaning that the IVC is only the last part
of PEP, as shown below.
Even PEP is sub divided into periods.
To start with, there is electrical conduction of the signal
from the AV-node through the His' bundle and the anterior
and posterior left hemi-bundles.
Early experimental and invasive studies seemed to show that
there is initial endocardial activation almost
simultaneously in mid septum and mid lateral wall, after 10
- 15 ms after onset of ECG (350,
but this will be partly concomitant with EMD at the cellular
|Mapping of earliest
endocardial electrical potential in normal
subjects. Numbers show time after earliest ECG
deflection in QRS, and the earliest endocardial
activation can be seen in mid septum and laterally
||- corresponding to the two
parts of the left bundle, as indicated here.
Thus, electrical activation occurs earliest in mid septum
and inferolateral base through the left anterior and
posterior bundles, delay 5 - 15 ms.
Then, there is electromechanical delay at the cellular
level, the action potential generating Calcium influx, again
generating release of more calcium form the SR, resulting in
onset of cell shortening as shown here.
This process takes about 30 - 40 ms (234),
and leads to onset of local shortening.
Active contraction could be expected to start in the mid septum and mid lateral wall after about 50 ms; i.e. before the end of ECG.
short duration event of apical displacement as
seen by M-mode
||- and tissue Doppler|
|Pre ejection spikes
evident bt tissue Doppler, both septally and
||By colour tissue Doppler
they can be seen to be simultaneous
||And they correspond to a
very small pre ejection displacement of the
annulus, which stops abruptly, presumably at
|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
ejection spike thus occurs BEFORE MVC, as seen here
(valve openings and closures from Doppler flow -
||MVC is concomitant with
the stop of apical motion.
|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. (This is a highly trained, healthy subject, the AV block is physiological)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).|
Schematic representation of the findings in (173), showing that as onset of contraction results in shortening, this is interrupted by MVC (onset of IVC), when mitral valve is stented (red curve), this results in a smooth non-interrupted transition to ejection velocities.
Thus it's the MVC that is actually terminationg the pre ejection
longitudinal motion /volume reduction.
|At the end of late filling (atrial systole), there is again equal pressures in atrium and ventricle, and no flow. The start of contraction will then lead to closure of the mitral valve, as they move in a stationary blood column, they will be pushed toward the base and toward the middle. The motion of the leaflets is mainly lateral, i.e. towards the middle, and thus may be greater than the longitudinal displacement of the annulus.This motion of the nitral ring would tend to displace the mitral eaflets towars the middle, and thus be a part of the closing mechanism. The mitral leaflets move towards the middle, and thus the displacement of the ring towards the apex is far less than the motion of the leaflets towards the base.||Volume reduction due to pre ejection shortening. This volume reduction is also evident from displacement and strain traces.This volume reduction is not due to flow, but the fact that the mitral annulus excludes part of the blood volume by , sliding along a stationar column of blood that then is "atrialised", illustrated by the light red cyllinder in the image above.|
Even if one study found a fair correspondence between isovolumic
periods using colour tissue Doppler and Doppler flow (369).
Others, using the same assumptions that the spikes represented the
isovolumic periods did not find good correspondence between tissue
Doppler and Doppler (370),
mainly due to discrepancies in isovolumic periods. This is
consistent with mesurements being right, but premises being wrong.
|Vortex image during pre ejection. The A wave is seen as the orange flow column, inflow is ended, but the column propagates toward the apex. in addition, there is flow towrds the LVOT, behind the anterior mitral valve, turning towards the mitral commisure.||Colour M-mode. Left, in the mid ventricle, showing the inflow during the A-wave (orange), with propagations towards the apex. Right, the M-mode from tyhe LVOT, showing flow towards the base (blue) during the same period, both in pre ejection and IVC.||pw Doppler, capturing both inflow and outflow. Both the E and the A waves can be seen to give a reverted flow towards the LVOT, with a delay due to the vortex flow. The flow after the A.wave is the J-wave.|
|Pre ejection spike
can be seen to be lower than peak ejection
|-by spectral tissue
||by colour tissue
||and by speckle
|By tissue Doppler,
although this might seem closer to the reality of bing
higher (absolute) than peak systolic SRI,
||THis is also the
method giving the highest variability due to noise.
||Also in speckle
tracking pre ejection peak is less than peak systolic
SR, although in ST, there is substantial undersampling
|The geyser Strokkur at Haukadalir, Iceland at 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, building up heat in a delayed boiling, when it boils, the pressure builds up and the column of steam will rise through the water, causing the water above to bulge (no isovolumic, then). To the left, the steam can be seen within that bulge, steam just breaking 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 the start of an eruption (ejection).|
The true isovolumic contraction
time (IVC) is defined from MVC to the start of
ejection. Thus, in this phase there is no volume change, and, hence,
no deformation. This phase it on the other hand, the period of most
rapid pressure rise, peak dP/dt, which occurs during IVC, close to
the AVC (241).
represents the most rapid rate of force development (RFD).
|Muscle twitches, showing
that the most rapid rise of tension occurs during
||Peak rate of pressure
rise, which is the closes correlate to the rate of
force/tension development. This occurs during IVC
|dP/dt can be meastured by the velocity increase, if there is a small MR, too small for generating a pressureincrease in the atrium. It is customary measured between 1 and 3 m/s, which is equivalent to a pressure increase of 32 mmHg, and the dP/dt becomes a function of the time interval between then, and is used as proxy for peak dP/dt (463)|
|Comparing a tension length
diagram of an isotonic/isometric twitch, and a
pressure/volume (Wiggers)diagram. I've added the
division of pre ejection into protosystole and IVC as
discused above. The ejection period is not isotonic, as
pressure increases and then decreases, and the
myocardial tension must follow a similar course. Thus
the tension increase is only during the first part of
ejection, and then tension decline so last part of
ejection is relaxation.
pressure/flow recordings, the peak pressure / tension is
around mid ejection, but looking at flow, peak flow
through aortic ostium is much earlier. Peak flow must
mean peak rate of volume decrease, and occurs early
|Flow velocity of LVOT.
This is closely related to flow, showing an early peak
during the ejection time.
||Tissue Doppler of the
mitral annulus from the same subject, showing early peak
annular velocity (a measure of peak longitudinal
shortening rate), a proxy of volume reduction rate.
||Colour tissue velocity
from the same subject, with transferred valve openings
and closures, showing how early the meak annular
velocity is in the ejection time.
|As flow is afterload
dependent, the increase in afterload reduces flow
compared to the continued tension increase.
||Both strain and strain
rate are afterload dependent, as described above.
||And as annular velocity is
a reflexion of wall strain rate, as discussed below,
this means the same is true for the annular velocity.
The apex beat is well known as a clinical event. The apex is pressed forwards and collides with the chest wall during systole, and marks the location of the cardiac apex on clinical examination.
|The apex beat, shown here in a normal apexcardiogram demonstrating that the beat is a systolic event. (Image modified from Hurst: The Heart). AS can be seen, in this case the impiulse wave starts before the 1st heart sound, i.e. before MVC and the start of IVC.||
The collision. Musk oxen, Grønnedal, Greenland
The apex beat has been characterised by apexcardiography, placing a pressure transducer above the apex, and recording the pressure trace, which then will be a function of the movement of the chest wall. The contraction, however, results in ventricular shortening. Unbalanced, this should logically tend to pull the apex away from the chest wall, being kept in place either by tethering or suction. In both cases this would result in an inverted apex curve. This is discussed above. Thus, it seems that the main force responsible for pressing the apex toward the chest wall is the recoil from ejection.
|The systolic motion of
the apex towards the chest wall, even displacing the
tissue overlying the apex is visible in this normal
||....and can be visualised by the
reconstructed M-mode from the same loop.
The shape of the curve resembles the apexcardiogram
|Using tissue Doppler, the initial
velocity of the apex towards the chest wall, and the end
systolic velocity away from the chest wall are both
evident. Forward velocities can be seen to start
about at the peak of QRS.
||...and the integrated displacement
curve shows the same shape as the M-mode above.
However, timing makes the situation more complex. As the anterior
apical motion starts before ejection, the recoil mechanism cannot
be the full explanation.
|Doppler LVOT flow from the subject above. The ejection starts later than the QRS, and thus later than the start of apex beat.||Doppler mitral flow. The apex
motion starts close to the end of the A-wave.
||Reconstructed colour M-mode from
the same person. The inflow
during atrial systole can be seen to propagate all the
way to the apex, and may be assumed to deliver an impact
to the apical myocardium.
Thus it seems that the initial impetus for the apical anterior
motion may be atrial filling. Thus, the effect may vary according
to the atrial part of the total filling volume, the PQ-time, and
factors affecting the flow propagation of the A-wave. However, as
the atrial impetus is an event of short duration, the recoil of
ejection may still be the main force that presses the apex towards
the chest wall as seen below:
Combined image from another patient. In this patient apical motion starts before the QRS, and stops abruptly when the apex is pressed into the chest wall as far as it can go. The apex then stays pressed to the chest wall during the whole of the ejection phase.
|Resolving the motion, we see that
the anterior motion in this case starts even before the
start of QRS (A). (The motion seen in the displacement
curve starts below zero because the tracking is set at
zero by the ECG marker). Peak forward velocity (B1)
is just after the QRS, while the motion stops in
systole (B2), but the
apex remains in the anterior position. At end
systole (by T-wave in ECG), there is the start
of backward motion (C), and the apex returns to the
diastolic position at D.
||Comparing the apex tissue velocity
with LVOT flow (aligned by ECG), both start and peak
apical velocity occurs before start ejection,
but continues into ejection. In this case, even a second
peak may be seen starting at start ejection, indicating
a second impetus from ejection recoil.
|| And for illustration the relation
between apical displacement and ejection. Apical
displacement starts before ejection, and then continues
into ejection, and maximal apical displacement is close
to peak ejection velocity. The
apex remains pressed to the chest wall during most of
ejection, until the flow velocity is so low as to not
generate sufficient recoil pressure, while the full
return to diastolic position is somewhat later.
|Comparing this with basal
velocities, we see that the anterior motion of the apex
starts in the pre ejection phase. The basal pre ejection
spike, however, reaches peak before the apex velocity,
which peaks close to the
time of start ejection (B), by the tissue Doppler
curves. Backward apical motion starts a little
before end ejection (C), while end of backward
apical motion is well within the early filling phase (D)
||Relation between apical and basal displacement shows the same.||Looking at strain rate, at the time
of pre ejection, there is maximal apical velocity and
there seems to be positive strain rate (stretch) in the
apex, but negative strain rate (shortening) in the
midwall and base, consistent with there being active pre
ejection shortening, but the apex being stretched due to
the A-wave impact.
from two different normal subjects, showing basal and
midwall shortening during the pre ejection velocity
spike, consistent with active contraction during this
phase, while the apex shows stretch, consistent with
passive motion of the apex, which may originate from the
impact of the A-wave as suggested above. Looking at the
early ejection phase, there is an early velocity spike
which probably is due to recoil force as discussed above.
The early ejection velocity spike can be seen to be
progressively dampened from base
to apex, as the apex of course cannot be accelerated,
being already in contact with the chest wall. But
this means higher (absolute) strain rate during early
ejection (not to be confused with peak strain rate).
|As we see, apical velocity is close to zero.||When strain rate (SR) is taken from tissue velocities, the definition is SR= (v(x)-v(x+Δx)) ⁄ Δx where v(x) and v(x+Δx) are velocities in two different points, and Δx is the distance between the two points. If the two points are at the apex and the mitral ring, the apical velocity v(x) ≈ 0, apex being stationary, and v(x+Δx) is annular velocity. Δx then equals wall length (WL), and peakSR = (0-S') ⁄ WL= (-S') ⁄ WL.|
But this, of course, also means that the strain rate of the whole
wall, equals the negative value of the basal velocity of the wall,
as the apex is close to stationary:
|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.
|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.|
|Early lateral peak velocity, late septal; early septal peak strain rate, later lateral, mean peak strain rate later than mean peak velocity||Early lateral and later septal peak velocity, earlier lateral than septal peak strain rate, mean peak strain rate later than mean peak velocity.||Early peak velocity on both sides. Still slightly later peak strain rate in lateral wall, and thus mean peak.|
|- but even this is not absolutely perfect, as seen above, and also when comparing with peak flow as seen below.|
|During last part of
ejection, pressure decreases (at least when reflected
waves are not taken into account, and so does flow. Thus, despite afterload
decrease, there is simultaneous tension decrease and
||Peak systolic annular velocity (S'), which is early systolic, compared to peak annular displacement (MAPSE), which is end systolic. 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 fraction.||Peak strain rate, being early systolic, compared to peak strain, which is mainly end systolic, and closer even, to ejection fraction.|
|As flow is afterload dependent, the continuing afterload reduces flow during tension release.||Both strain and strain rate are afterload dependent, as described above.||And as annular displacement is a reflexion of wall strain rate, as discussed below, this means the same is true for the MAPSE.|
|The same as for velocity
vs. strain rate, of course, must then hold for
displacement vs strain.
||Likewise, strain = (d(x)-d(x+Δx)) ⁄ Δx where d(x) and d(x+Δx) are displacements in two different points, and Δx is the distance between the two points. If the two points are at the apex and the mitral ring, the apical displacement d(x) ≈ 0, apex being stationary, and d(x+Δx) is annular displacement = MAPSE. Δx then equals wall length (WL), and Strain = (0-MAPSE) ⁄ WL= -MAPSE ⁄ WL.|
This, however, may be a difference between high and low HR.
Thus, the imaging measures are all measures during ejection, and all have weaknesses, as they become afterload dependent at the time of AVO.
Again, the exact timing of AVC, and by this, the end of LVET, is precisely defined by the valve click in Doppler:
It has been assumed that the first negative spike in tissue velocities after ejection was due to isovolumic relaxation, basing it on the erroneous assumption that there is elongation during IVR. (47, 366, 369, 370, 465, 466, 467). This negative event can also be seen in colour M-modes of tissue Doppler, both in the mitral ring and the mitral leaflet. However, already Wiggers showed that the event relating to the closure of the aortic valve was a relaxation preceding the IVR, and he termed it proto diastole (402).
The peak negative dP/dt, is the transition point from convex to
concave point . This transition should be no earlier than AVC. It
has been seen to be close to the AVC (244),
and has been suggested as a marker of aortic valve closure in
pressure tracings, so some studies used this, but it seems that
this also places the AVC reference a bit early. That study,
however, used correlation between end of aortic flow and pressure
traces, with no attempt to calculate bias or significance of bias.
In an early study of high framerate (16)
we noticed the initial midwall elongation in the septum by
strain rate, bfore the AVC. Thus, the negative spike in
velocities corresponds to a protodiastolic elongation seen by
|Colour strain rate M-mode from the septum of a normal subject. It is evident that there is an elongation in mid septum, resulting in initial negative velocities in mid and basal septum before closure of the aortic valve. Notice also how the initial elongation of the mid septum occurs before the closure of the aortic valve, i.e. the initial negative velocities in the basal and mid septum are protodiastolic.||Colur TVI and SRI derived
from the same recording, showing that the midwall septal
elongation and the basal downward velocities are
corresponding. The difference in locartion is a
ejection spike thus occurs BEFORE AVC, as seen here
(valve openings and closures from Doppler flow -
||AVC is concomitant with
the stop of basal motion.
|Apical recording of Doppler flow of the LVOT. At end ejection, the valve click can easily be seen as the short spike. This is coincident with the start of the phonocardiographic first heart sound as seen by the phonocardiogram. However, in the last heart cycle, there can be seen a small oscillation earlier in the others, a small noise spike (red arrow). Thus the Doppler is the gold standard, and the phono has to be calibrated.||Aortic valve closure seen by tissue Doppler in long axis view. The AVC is identified by the start of rapid positive velocities (toward the probe/apex) in the sample volume in teh LVOT. (Blood velocites are filtered out by the low amplitude as explained here. (The rapd upstroke is not an aliasing of the high downward velocities seen imidiately before, this can be seen as the shift from negative to positive occurs at lower velocities than the peak negative velocity in the a' wave, which doesn't aliase)|
|Proposed 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 (blue arrows). The aortic cusps then are closed due to the valve motion in 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 annulus|| Volume increase due to proto diastolic lengthening. This volume increase is also
evident from displacement and strain traces. This
volume increase is not due to flow, but the fact that
the aortic annulus includes part of the blood volume by
, sliding along a
stationary column of blood that then is
"ventricularised", illustrated by the light
red cylinder in the image above.
|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
|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
||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 line.
|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 (green curve).
|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 to
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.
|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.|
As discussed above,
there is an elongation and volume expansion at end ejection, due to
continued relaxation after the flow has stopped, but this occurs
before aortic valve closure, and is thus protodiastolic. It may be the mechanism for aortic
valve closure itself.
|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
||IVRT: Zooming in on the
images, at end ejection can se the valve click as a
vertical bar (Just as in pulsed Doppler recordings as
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.
|Strain 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.||Peak 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 Velocity/displacement traces.|
|Diastolic filling. 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 illustrated below.
||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.|
The main point is that when there is pressure drop (negative P) concomitant with
volume expansion (positive V), this means that there is negative compliance C = V / P, which means suction, as
argued already by Katz (407)
|Suction driven filling (vis a fronte; a force acting from the front), versus pressure driven (vis a tergo; a force acting from behind) filling of a chamber (B). In this simplified model, the level of fluid (and, hence, pressure) in chamber A is assumed to be constant during filling. 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 fronte, energy is applied to creating a pressure drop in chamber B, in vis a tergo, the force application (energy) is applied to the fluid in chamber A.|
|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.||Looking at LV diastolic function, seeing that flow velocity is the rate of volume change, and thus volume increase, it seems that early filling is vis a fronte (red); showing volume increase of the LV (chamber B) with simultaneous pressure drop (negative dP/dV), the driving force being left ventricular recoil, while late filling is vis a tergo (blue) showing volume increase with pressure increase (positive dP/dV), the driving force being atrial contraction.||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.|
|Revised Wigger's cycle showing the
valve closures as phono traces, with pressure crossover
and a small volume expansion before MVC, dividing the
pre ejection interval into three; EMD, proto diastole
and IVC, also the small volume reduction in proto
diastole before AVC, and also the pressure drop during
early (rapid) filling concomitant with rapid volume
||Revised PV-loop, based on the full
cycle as it is. The small volume reduction in proto
systole and the small volume increase in proto diastole
before valve closures is shown as the red shaded areas.
The two notches before valve closures is in accordance
with experimental findings (173).
In addition, the diastolic part of the PV-loop is shown
with the first part having pressure drop and concomitant
volume increase, in accordance with the established
physiology of early filling.
|While both start and peak
systolic velocities are near simultaneous, both the e'
and a' velocity waves show a progressive delay of both
start and peak from base to apex, while the ends are
||Strain rate, on the other
hand, show delay of both start, peak and end of the two
onset of velocity and strain rate during early and
late filling, seen by both velocity and strain rate,
but with a different pattern, as a triangle in
velocity plot, showing the simultaneous end of the
velocity wave, but as a tilted band in the strain
rate. Onset, however follows the same propagation
M-mode from the septum, showing the dip of the AVC
event, and the time delay from base to apex of the
initiation of downward motioning the filling phase.
|Diastolic strain rate propagation. M-mode from a myocardial wall, velocities at the top, and strain rate at the bottom. During the two diastolic phases, there is blue colour showing downward motion, which can be seen by the tissue lines as well. The elongation can be seen to propagate from the base to the apex over time.||Diastolic strain rate propagation velocity is the slope of the elongation wave.|
|Relation between diastolic strain rate propagation of the E-wave and the peak early diastolic velocity of the annulus. If the wave propagates slower, the resulting velocity wave of the annulus will be broader and lower, even with regional strain rate may be the same, but the strain rate propagation is dependent on both local diastolic strain and the properties of the wall. .||In reduced diastolic function as shown here to the right, there is a lower peak diastolic annular velocity as well as a reduced early magnitude of motion of the mitral ring.|
|As we see, apical velocity
is close to zero.
||When strain rate (SR) is taken from tissue velocities, the definition is SR= (v(x)-v(x+Δx)) ⁄ Δx where v(x) and v(x+Δx) are velocities in two different points, and Δx is the distance between the two points. If the two points are at the apex and the mitral ring, the apical velocity v(x) ≈ 0, apex being stationary, and v(x+Δx) is annular velocity. Δx then equals wall length (WL), and peakSR = (0-S') ⁄ WL= (-S') ⁄ WL.|
Velocity and displacement in the base of the septum, showing systolic motion toward the apex, protodiastolic motion away, and the the two basis diastolic phases, early (e') and late (a') motion way from the apex, separated by diastasis.
and strain rate, the pattern can be seen to be much more
complex in these tracings from the base alone. There are
at least four positive spikes (elongation) during
diastole, this is reflected by much more "steps" towards
zero in the strain curves. As
strain rate is fairly susceptible to noise, this might
have been interpreted as noise (as is the small negative
spikes between) , but integrating to strain eliminates
the random noise, and shows what is real.
|Diastolic strain rate. The strain
rate M-mode reveals that some of the diastolic phases has
the characteristics of elongation waves between base and
apex. The differences between base, midwall and apex
can be seen clearly in the traces diagram to the left,
showing that not only are there more elongation phases,
but they don't even coincide in the different levels of
|Proposed explanation of the return wave of the two filling phases, which may be a crossing over from the opposite wall. The protodiastolic lengthening is less evident in the lateral wall, but this is due to a drop out in the wall.||Diastolic
strain rate. Diastolic events seen by strain rate. Both
the curved M-mode and the traces shows the separation
1: Midwall protodiastolic lengthening
2: Apical isovolumic lengthening
3: Early filling propagating from base to apex and back
4: Late filling propagating from base to apex and back.
|Colour flow, showing how inflowboth
during early and late filling shows vortices (blue
colour to the sides of the main inflow.
||Still picture from the loop to the
left at the time of early filling, showing the negative
velocities (blue) to the sides of the positive main
Inflow during early filling in a normal subject. The E wave can be seen as a fairly steep wave from base to apex (I), followed by a more "smeared out" wave arriving later in the apex, representing the vortex following the initial flow velocity propagation.
|Inflow in a dilated ventricle
ventricle of a patient with heart failure. Flow
propagation is reduced, not due to the reduced
propagation of velocities in the early phase, but
because most of the flow propagation is vortex
||Strain rate prop (cm/s)
||flow velocity prop (cm/s)
|Inflow during early filling in a normal subject.||Inflow in a patient from the study,
showing much more rapid flow propagation, as well as
reduced vortex propagation.
|Pulmonary venous flow can
be seen to have three main phases: A; retrograde flow
from the atrium backwards into the pulmonary vein, S;
Forward flow from pulmonary vein to atrium during
ventricular systole and D: forward flow during early
||Sometimes the S-wave can
be seen to be split into two peaks, the S1 and S2 waves.
venous flow, with retrograde flow into the pulmonary
vein during atrial contraction.
from the same subject with antegrade flow into the
ventricle during atrial contraction.
|Pressure gradients from PV to LA from the figure above, compared to a standard flow velocity curve. The pressure gradient is negative (magenta) during the a wave, driving flow backwards (A), and positive during the rest of the cycle (violet), driving flow forward. Looking only at the arial curvem, however, this very closely mirrors the pulmonary flow velocity profile.||Looking at the atrial
pressure alone, it can be seen that pulmonary venous
flow is almost perfectly mirroring the atrial pressure
curve alone. Pressure peaks correspond to velocity
nadirs, pressure troughs to velocity peaks, pressure
decrease to acceleration and pressure increase to
|Pulmonary venous flow
showing termination of the A wave at start of QRS in the
||Mitral flow showing premature termination of the A wave before start of QRS in the ECG.|
|Atrial strain. It is very evident
that the atrial expansion during ventricular systole is
simply a function of LV shortening, i.e. the same
AV-plane motion that describes the ejection.
||The same shown schematically in colour. Shortening is yellow, stretch is cyan, and here the reciprocal nature of the strain in atria and ventricles is shown. In diastasis, there is no deformation, both are green.|
|Strain rate curved M-mode going through both ventricular and atrial septum shows the reciprocal colours of the atria and ventricles.||Strain and strain rate in atrium (yellow) and ventricle (cyan) are seen as almost mirror images of each other. However, the absolute values in the atria are higher, as the atrioventricular plane motion is a greater percentage of the smaller atria as illustrated below. Strain rate curves are also basically mirror images of each other. As deformation is active in one chamber and passively transmitted to the other, the peak values may be higher in the active chamber, and there will be a time delay of events as waves propagate as shown in the ventricle during diastole.|
|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
is due to the longer wall. The overall systolic strain rate
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 from ejected blood), 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.|
contraction, the muscle will increase tension, but
resulting in no shortening as long as the tension is
below the total load (isometric contraction). When
tension equals load, further contraction will result in
shortening at constant tension (isotonic contraction).
This is what we see in imaging.
an increasing load will both delay onset of
shortening, as the development of higher tension takes
longer time, but will also result in less shortening, as
well as a lower initial rate of shortening. In
these diagrams, the effect of load in slowing
is not shown. This effect would show up in prolanged
duration of the downslope in the tension diagram.
However, the lengthening phase would still be shortened
by the load.
||Reduced contracility will give a slower tension development and lower peak tension. However, this has the same effect as increased load on shortening, resulting in delay in onset of shortening, lower rate of initial shortening and less total shortening. Thus, reduced contractility would also have effect on relaxation (224), seen in the tensin curves, but this is not shown here.|
|Symmetrical forces in all segments,
will result in symmetrical shortening. Thus, all
segments shorten equally (orange colour), which means
that the base moves most (the sum of shortening of all
segments), as the apex is stationary.
||Loss of contractility in a basal
segment (smaller black arrows in the left basal
segment), results in less shortening in the affected
segment. However, this means that the load on
the more apical segment is reduced, and thus, this
segment will shorten more Red colur9 , not due to
hypercontractility, but to less load. Also, the
total force acting on the base is reduced, resulting in
reduced total shortening (smaller red arrows in the
||Even more reduced tension in a
basal segment will result in the segment actually
stretching, while the apical segment shortens even more
in response to the basal segment stretches. This will
not result in reduced motion of the regional
mitral ring point, mainly a shift in the distribution of
shorteningbetween segments, and a reduced global
||Reduced tension and stretch of an
apical segment may result in increased shortening of the
opposing wall, as well as the basal segment, but
this may result in a rocking of the apex toward the
||Symmetrical weakening of the apical
segments, may result in increased shortening of the
basal segments, but as the apex stretches, the motion of
the AV-plane is more reduced.
||S' (cm/s pwTDI)||S' (cm/s cTDI)||Segmental SRs (s-1)
intra subject variation (max - min)
|MAE(mm)||S' (cm/s pwTDI)||S' (cm/s cTDI)||Segmental SRs (s-1)||Mean SRs (s-1) per
is no regional reduction of mitral motion in
||Only global reduction of mitral motion, and segmental hypokiesia with resiprocal hyperkinesia.|
The full deformation pattern in acute ischemia was shown early in
the experimental work of Tennant and Wiggers (46):
|Figure modified from (46), the time course of segmental myocardial deformation after acute LAD occlusion. The deformation (myogram) curves have been inverted to orient them as customary for strain curves today. Thus, the sequence starts at the bottom with A, and progression of ischemia is upwards, following the letters to the left. The numbers to the right, denotes the number of heartbeats after occlusion. As we see, in A there is a normal strain curve, the first change is an abbreviation (B) of the duration, and then delayed onset and reduction of the magnitude systolic strain (D), followed by initial systolic stretch and an increasing post systolic shortening peak (E-G). At the end, the systolic stretch lasts through systole - i.e. holosystolic stretch, but with post systolic shortening that exceeds the amount of systolic stretch )H-J), and finally there is virtually only passive stretch and recoil (K).||Myocardial ischemia in the LAD area
during dobutamine stress echo shown by the strain
curves. The different colours
of the curves correspond to differently placed ROIs in
the lateral apex (cyan), septal apex (yellow) and
basal septum (red). To correspond to the image to
the left, the time course of ischemia is from bottom to
top, so the four panels are baseline (bottom, then 10ug
dobutamine/kg/min, then twenty, and finally 30 at the
top. The different regions have different
degree of ischemia during the stress. At
baseline there is slight post systolic shortening in the
apical lateral part, increasing ischemia at 10 ug where
there is initial akinesia (even a little stretch),
reduced systolic shortening and finally post systolic
shortening. This is similar to stage F at the left. At
20 ug there is initial stretch, systolic akinesia and
post systolic shortening in the apicolateral segment,
increasing to holosystolic stretch and post systolic
shortening at peak, corresponding to stage G-H to the
left. The two other segments showing less ischemia,
although the septal apex shows hypokinesia and post
systolic shortening at 20 ug awhich is increasing at
peak, while the basal septum shows slight ischemia at
It is evident that in a segment being stretched in systole, if
there is any elasticity at all, the segment will recoil in
diastole, i.e. as a function of the elastic force stored in the
segment. (also, if the segment had not returned to the original
shape, the whole heart would have been turned inside out in the
time of a few minutes. Thus, stretch / recoil is a mechanism
for post systolic shortening. In ischemia, post systolic
shortening develops before there is systolic stretching (46,
), i.e. while there still is systolic shortening as shown in the
stress example. This this can be explained by the timing of the
tension interaction between segments.
|1: Two segments with equal tension
(red and blue) will shorten equally and symmetrically.
||2: If one segment becomes ischemic,
this will lead to:
1: slower tension buildup, leading to initial stretch,
2: lower total shortening, and concomitant increased shortening of the healthy segment as the load on this is reduced
3: prolonged tension in the ischemic segment, leading to increased shortening as the two tension curves cross, the ischemic segment shortens as the healthy relaxes. This is post systolic shortening.
|3: As ischemia progresses and
tension becomes lower, the initial stretch increases,
and shortening becomes less and later, while post
systolic shortening remains.
||4: At one point, there will be only
stretch during systole. However, the remaining post
systolic shortening after normal contraction, is a
sign that there is still active tension
||5: Finally, with total loss of
tension, there is only stretch. The post systolic
shortening is still present, but only as a recoil
phenomenon, with no sign of active tension.
from a real stress echo, as described in full below. The
cyan curve is apicolateral segment, which is maximally
ischemic, and shows conformance to the model above. The
red curve is basal septal, which conforms bst to the
non/ischemic segment, while the yellow curve is
apicoseptal, and ischemic, although to a lesser degree.
The white vertical line shows the AVC.
Severe 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
||Strain rate curves (top) and strain (botom) 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.|
|Circumferential strain in a symmetrical ventricle model. For simplicity, the wall is divided into two layers. As the wall thickens, there is thickening and inward shift of the midwall line of both layers, but the innermost layer is in addition shifted inwards, cusing both a greater wall thickening (due to lack of room), and a greater midwall circumferential strain, both due to this, and due to the inward displacement of the innermost layer due to thickening of the outer layer.||Akinesia of the inner (sub endocardial) layer. In this case there will be normal wall thickening and cicumferential shortening of the outer layer, and almost no thickening of the inner layer. Still, there will be inward shift of the inner layer due to thickening of the outer, this will reduce the space and may cause some thickening even without function. Mainly due to inward shift, there will still be midwall circumferential shortening of the inner layer.||Reduced
circumferential strength in a segment, will result in
the normal segments contracing more (due to reduced
regional circumferential load, and the affected
segment may stretch. In that case this will also
result in thinning, as the segmental volume stretches.
Changes in timing of different segments may occur without
concurrent reduction in contractility. In especially left bundle
branch block, there is different inset of contraction in different
segments or walls, leading to some segments (or walls) contracting
while others are passive, both at the start and end of the
contraction-relaxation cycle, and where both intraventricular
pressure and elasticity contributes to specific patterns of
shortening that are quite different from the normal patterns. In
this case, it is differences in timing, that leads to
different segments or walls having different tension.
left bundle branch block may have very different mechanical
effects. This is due to the very large variability in how much,
and which parts of the left bundle that are affected, and to what
Basically, left bundle branch block means a reduced conduction velocity in the left bundle, below that of the right bundle, causing the septum activation direction to shift from left-right to right-left, but also meaning that parts of the left ventricle are activated later than the right, and later than normal, causing a widening of the QRS. The mechanical effects of the LBBB may be quite various, however:
|The "septal beaking" in M-mode , a short inward motion starting at the peak of QRS, and peaking at the same time as the onset of inward motion of the inferolateral wall. The contraction of the lateral wall is the force terminating the septal flash, so the time from onset of septal flash to onset of inferolateral wall thickening is the true mechanical delay between the walls.||The same phenomenon is seen in B-mode of the same patient as "septal flash", which consists of a short inward and then outward motion of the septum, the outward motion start about simultaneously with inward motion of the lateral wall. The "septal flash" is evident in both parasternal long axis and short axis. Images from patient with normal systolic function.|
After mechanical activation, there is an intial shortening seen in the velocity traces as a positive spike of short duration - the pre ejection spike. This initial contraction gives a small pressure rise which closes the mitral valve (236) about 30 ms after initial contraction (268).Delayed intraventricular conduction, on the other hand, will lead to delayed activation of the lateral wall.
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 rate, 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.
|Septal activation alone. leading to
septal shortening and thickening, with concomitant
lateral stretch - the septal flash. No pressure
||Lateral wall activation, ending the
septal flash which peaks) with remaining septal tension
(or else there would be only rocking, no pumping). In
this case there is pressure buildup, MVC,
IVC and probably start ejection.
||During most of the ejection there
will be shortening, but part of this may be partly
passive due to volume decrease, especially in the
||In the last end of the ejection
there will be little or no remaining tension in the
septum, which then will stretch, due to the remaining
tension in the lateral wall (which have been activated
later). Thus, there will be stretch of the septum and
shortening of the lateral wall. As the septim now causes
little load, the lateral shrtening will increase.
||Finally, there is no tension in the
lateral wall, which relaxes. In this phase there will be
elastic tension in the septum due to the previous
stretch, which will shorten in
post systolic shortening, while the lateral wall
stretches (due to both septal
shortening, and also in the course of normal early