Clinical use of deformation imaging

Is deformation imaging useful?

A practical guide to clinical use.

Making friends with the method and sniffing out extra information

Making friends with Danny, a Greenland dog working in the Sirius Sledge Patrol in North East Greenland.
Sniffing out something useful. Arctic fox hunting under Auk mountain, Spitsbergen.
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This section updated: April 2016.                                                       

This section is intended as a quick introductory guide for those who want to start using deformation imaging, but who don't want to go into the basic theory of deformation, display and physiology/pathophysiology first. 
The other sections can be used as reference over time. This section is meant to be self contained, but of course, links are provided to the relevant more in depth chapters in the other sections. To understand more about the curves and colour M-mode, I recommend the section on displays.

The intention of this section is to shown how to become friends with the method. It is usually possible to sniff out extra information not visible to the eye. n this section I will try to show that the use of deformation imaging not necessarily needs to be very complicated or time consuming, as well as suggesting how to interpret the findings in a quick, and hopefully easy way, and then giving some more information for those who wish to go further. The chapter is illustrated illustrated by examples both of pathology and artefacts. It is an integrated approach, using both velocity curves and colour SRI, in addition to strain rate and strain curves.

For reference is included links to tables of normal values from the HUNT study.

List of tables of normal values. As the normal value tables are located in the relevant sections, this list of links is provided for those who want a quick reference.

However, my main philosophy is that the approach to deformation imaging should be qualitative, looking at the curve shapes and time courses rather than peak values.

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Deformation imaging has never reached the popularity it deserves.

Being principally a method for measuring regional myocardial function, the main interest for both clinical use and clinical research have been in global function (global strain). While this seems useful, it is mainly a normalisation of longitudinal shortening (which could be measured as MAPSE by simple M-mode) or annular systolic velocity, for heart size. Whether this normalisation is actually important, remains to be proven.

Deformation imaging, however, is absolutely necessary to assess changes in regional function. Not using modern methods, limits regional assessment to Wall motion score by B-mode. As I will show below, there is additional information to be gained.

I think much of the reason it never became popular was that the tissue Doppler method was:
Speckle tracking should attempt to solve this,  by presenting a more user friendly interface, making processing quicker, and by making interpretation easier by presenting only segmental peak systolic strain. However, this approach discards much of the extra information inherent in deformation imaging, and due to the very heavy spatial smoothing in speckle tracking, it is very dubious if the diagnostic sensitivity is better than visual wall motion score by B-mode, meaning that the results by speckle tracking will be unequivocal only where they are obvious by B-mode directly, as for instance seen below. Also, due to the lower frame rate, it is not very useful in stress echo (302).

Make friends with strain rate imaging in an easy way:

To start with:

Don't bother with peak values (or any values at all).

One of the main points about assessing regional function by deformation parameters, however, is that peak values is not the most important thing at all. As seen below, the colour M-mode and the shape of the curves gives almost all information qualitatively in a quick and easy way:
This can be seen very easily below.

But remember:

However, instead of trying to extract curves for measuring peak values of strain and strain rate, using curved M-mode with colour display of strain rate, is:

A curved M-mode is very quick to generate,

either in one wall at a time, if so usually from apex to base, orienting the CAMM image the same way as the B-mode image
or through both walls, in that case enabling comparison between the timing of walls, important in assessing asynchrony as in left bundle branch block. In that case customary from the right sided base (septal in 4ch, inferior in 2ch or inferolateral in ALAX) through the apex to the left (lateral, anterior or anteroseptal) base. In that case the first wall is oriented upside down.

The curved M-mode will then give the possibility of assessing both if regional shortening is normal, and to look at the timing. Actually, the curved M-mode has better spatial resolution that strain rate or strain curves.


Colour WMS (A larger variety can be seen below). The colour WMS seemed to equivalent with B-mode WMS both in feasibility and accuracy (6, 7), but no better. This is hardly be surprising, as the expert WMS is a fairly precise method, an colour WMS is still semi quantitative. However, looking at the colour images, one can se both delayed onset and hypokinesia in 2, as well as post systolic shortenng. In 3, there is aknesia and PSS, and in 4 there is dyskinesia and PSS. From this, it seems that there is extra information in doing deformation.
This is evident in this case, where there is little pathology; colour M-mode offers more information, as can be seen in this image from a patient with a small apical infarct, there is initial stretch in the apical segment, before systolic shortening, the systolic shortening is reduced, and then there is post systolic shortening after ejection. Thus, colour strain rate shows more information compared to B-mode WMS.
Even with heavy clutter noise (blue bands during ejection and red fields during filling phases), the timing information is still evident. Also, clutter (reverberations) are very easily identified in the colour image, by their horisontal time course.

Curved M-mode from speckle tracking, however, have both less spatial resolution due to smoothing, as well as lower temporal resolution due to lower frame rate in B-mode as shown below.

Another point is that also the curves can add information just by visual, qualitative assessment, even if no values are measured.

It is a main point that deformation imaging gives added value, on top of a basic echo. This is not always very necessary:

Case 1: In this case the pathology is evident, there is an acute, large apical infarct, with reduced global function.
However, with strain rate imaging, there are more details, showing initial stretch in the septal apical and midwall segments(1), hypokinesia (2) and post systolic shortening (3) in the apical half.

The rocking motion is evident both from B-mode and TDI, but the global function can be measured by the (mean) peak systolic velocity of 5 cm/s and displacement of of about 7.5 mm.
Strain rate and strain gives more or less the same information as the colour M-mode above. Thus details in timing is supplementary information.

In this case, deformation imaging is no additional evidence for diagnosis, but still gives additional information.This should be the basic approach, deformation imaging being part of the total evidence, and can serve as an aid to diagnosis. This means that it will be a help, and part of the total evidence in selected cases, not the obvious ones. But used this way, the added value, used with discrimination, is  difficult to document scientifically in studies. This means than even without documentation for added information value, one might always find something for use in the total echocardiographic assessment.

In other cases, the added value may give more assurance that the diagnosis is right:

A small infarct in the septal apex
In the curved M-mode (apex to base in the septum) it can be seen that there is both initial stretch, as well as post systolic shortening in the infarct area, important information in addition to the peak strain rate.

Both strain and
strain rate curves from the apex shows the same: initial stretch and post systolic shortening, as well as reduced systolic shortening. Thus, the full time course gives much more information than only a simple peak value or index.

Thus, in most instances, using strain rate colour imaging in this way, it is quick (quicker that speckle tracking), and gives extra information that can be assessed visually in a qualitative way, just as B-mode. The visual comparison between affected and non affected segments shows the hypokinesia as evident, even without having to measure peak values.

One of the main points about assessing regional function by deformation parameters, however, is that peak values is not the most important thing at all. The colour M-mode and the shape of the curves gives almost all information qualitatively in a quick and easy way:

Both initial delay in shortening of a segment, reduced peak values and post systolic shortening are all phenomenons that tells about the relative reduction in rate of tension development (strain rate) and total tension, all measures of relative reduced contractility of a segment or region, as well as delay in relaxation, another assessment of both ischemia and contractility.

Thus, looking at strain rate imaging as a penguin that is not able to fly, seems unfair, and contraproductive.

Molting gentoo penguin, Port Lockroy, Antarctica. During molting the penguins cannot even go into the water.
But even penguins may fly, but only for a short while. Paradise Harbour, Antarctica.

Wandering albatross has difficulties in taking off from water. Drake Passage. However, this bird is fully able to fly.
Storm petrel in full flight. Drake Passage.

It is a basic fact that doing deformation imaging is always done with access to the B-mode images. This means that some of the information is always present when deciding on the validity of the deformation data we extract from post processing. This may help in separating artefacts from pathology. On the other hand, it may also be used to support a foregone conclusion, where the interpretation of B-mode is dubious, thus resulting in biased post processing,  giving the result that are expected, but this does not add information. It is equivalent to using a lamppost as support, rather than enlightenment.

Albert Engstr÷m 1869 - 1940

In clinical use, the main point is whether they give added diagnostic value, compared to basic echocardiography. It's important to realise that all ultrasound, including B-mode has limitations. A thorough understanding of the mechanisms for the limitations and artefacts should always be part of that evaluation, some of the main points are set out in the section on "Measurements of strain and strain rate by ultrasound". This, however, is also true when evaluating clinical studies.

How to use strain and strain rate clinically

Below is showing both the quick and easy way,

Looking at:
Qualitatively rather than quantitatively, as well as doing a more comprehensive evaluation of curves. However, there is no emphasis on cut off values of numerical measurements.

But first one example where deformation imaging proves valuable:

Parasternal long axis view. Inferolateral wall looks evidently dyskinetic. (However, the normal wall thickness gives a reason to be suspicious.)
Apical two-chamber view. Basal inferior wall looks also definitely dyskinetic, although in this view out-of-plane motion is very often present. .
Parasternal short axis. Again, the paradoxical motion of the inferior wall is evident, but looking more closely, this is due to diastolic flattening, with a closer to normal normal circular cross section in systole. Thus, there is no evicence of systolic bulging as in true dyskinesia, and there is a suspicion of the phenomenon being due to compression from the outside.

In the longitudinal strain rate image apical long axis view (equivalent, as can be seen below), there is, however, no evidence of dyskinesia, which would show up as longitudinal stratch (blue).
Neither is there in the two chamber strain rate analysis.
Reconstructed M-mode through the inferior wall from the same loop. The inferior wall shows normal systolic thickening. Although there seems to be post systolic thickening, this do not correspond to post systolic shortening (even though the shortening in the long axis view has slightly longer duration in the base, the two periods don't match. )

In this case, it is evident that this is not dyskinesia. The paradoxical motion is due to diastolic inward motion, and was due to compression from the outside. In this case, however, the diagnosis of sequela of inferior infarct was made, but happily, this was not considered adequate reason for witholding potential cardiotoxic chemotherapy, as the patient had a lymphoma.

In this case, there was lymph nodes in the mediastinum. After cytostatic treatment, the pseudo-dyskinesia was gone:

The main point of this is that the lack of true deformation is shown clearly by strain rate imaging.

To look at the value of strain rate imaging, below is compared the case with a case with a real infarct sequela in the inferolateral wall.

This is the same case as shown above, confirming that the parasternal long axis and apical long axis are comparable.
Patient with true dyskinesia in the inferolateral wall, this is case 5 below.

No sign of dyskinesia in strain rate imaging.
Evident apical dyskinesia, midwall hypokinesia and post systolic shortening in both.

In this case, the strain rate imaging is useful to rule out the apparent dyskinesia in the left case, and  to localise the pathology in the right case. The dyskinesia is in the apex on the right, causing the visual dyssynchrony between the apex and the base. The patient on the right had an LAD infarct.

In regional dysfunction (coronary disease)

The main indication for assessing regional deformation is where there are differences, meaning regional dysfunction, as seen in coronary disease. Thus, the first round in this "how to" section is illustrating the approach by several examples of infarcts.

It might be useful to consider what information there is in the different display modalities:

  1. Strain rate curves give the rapid changes in deformation, and peak values of those changes in all phases of the heart cycle, but with reduced spatial resolution.
  2. Velocity curves will give information of strain rate when the differences between the curves is considered. This information is qualitative, but with the same spatial resolution as SRI curves.
  3. Strain rate CAMM gives the rapid changes in deformation qualitatively, but with better spatial resolution.
  4. Strain rate CAMM is excellent to discover the presence of clutter.
  5. Strain curves gives less temporal information, mainly peak systolic strain, but strain rate can be seen in the curves qualitatively, and is thus comparable to Colour SRI, but with lower spatial resolution.
  6. Strain CAMM, on the other hand, is of little use whatsoever

Normal values for global strain and strain rate per gender and age are provided here, and regional normal values per wall and level here. It may be assumed that there is little difference between levels (apical, midwall and basal) or between walls. With the limitations inherent in basic ultrasound and in the specific methods, the careful weighing of the evidence in terms of the methods limitations is thus an integral part of the examination, and a knowledge of the methods themselves is essential.

The previous and the following cases will be used for demonstrating features of deformation imaging.

Case 1: Large apical infarct, four chamber view.

Case 2. Small apical infarct, long axis view

Case 3. Inferior infarct, 2-chamber view

Case 4: Apical infarct, four-chamber view

Case 5: Apical infarct. long axis view.

Case 6: inferior infarct, 2-chamber view.

Assess image quality and consider the limitations of each method to evaluate which information can be assessed.

The garbage in - garbage out principle still is important.

Deformation imaging has a high variability, and the variance means that some of the findings are artificial. This also means that it is possible to achieve almost the results one wants, as changes are small from one point to another as shown in the example below, or due to the poorer lateral resolution of TDI as shown here, traces that seem reasonable, may still be artificial.

In tissue Doppler, concerning angle deviation, the main point is to exclude segments with to great angle deviation from analysis, at least other than parametric/ time course analysis.

Strain rate is a method with a high variability due to a high noise content and high susceptibility to artifacts. Some are common to all ultrasound methods, but may result in different pitfalls in different methods. A working knowledge of all problems and pitfalls is necessary to do proper post processing as well as interpret the findings.

Then, TDI and speckle tracking has different limitations, and within speckle tracking the segmental strain and the 2Dstrain again have method specific pitfalls. This means that processing may produce artifacts. A more in depth on the effects of artefacts on both speckle tracking and tissue Doppler can be found in the measurements section.The artifacts may mimic or mask  pathology, and if findings are processed to support a foregone conclusion.

Shadows and dropouts, reverberations and foreshortening will cause problem in both speckle tracking and tissue Doppler. Concerning clutter, however, it is important to know that while B-mode uses harmonic imaging, while
 (to avoid aliasing). Thus, there will be more reverberations in tissue Doppler than in B-mode.

This is relevant both in clinical practice, and also in studies. Given the high number of artefacts found in daily echo practice, studies reporting a very high feasibility may be prone to this effect. This means that not only do the studies overestimate the accuracy of deformation images, by just confirming the visual assessment, but the wall motion may in fact be the main sorce of information. However, studies reporting added information or increased accuracy in relation shows the added diagnostic value, as has been shown in some studies (128, 133). But basically a high discard rate ensures higher quality of the studies.


With a liberal attitude to excluding segments, the question becomes related to the feasibility of analysis. accuracy may be as good as it will, if there is too low feasibility.  We did a feasibility study (115) at our department, showing that the there were reverberations in more than 80% of the patients. With the high number of reverberations artifacts reported, it may well be that the real feasibility should be around 80% of segments, and that studies reporting more than 90% by manual analysis may in fact have a high number of artifacts included in the data.

A useful way of assessing the presence of clutter, is to use the tissue Doppler M-mode, where reverberations will show up very vividly. For tissue Doppler. this means that the M-mode can be used to guide the placement of ROIs, if possible, or to decide whether the wall or segments should be discarded from quantitative analysis, segments with poor data quality should be discarded entirely.

Image with shadowy reverberations. The 2D image doesn't seem too bad, as the movement of the wall is fairly well visualised.
Strain rate in the same image.  Shadowy reverberations are better visualised in this image.
Curved M-mode from the lateral wall. Apex on top, base at the bottom. The S, e and a phases can be seen, but that is about all the information that can be extracted.

Look at colour M-mode

1: To assess data quality.

Heavy reverberations will show up, and the Colour M-mode will tell about timing parameters, and say if the quality is good enough to extract  deformation curves.

All the phases of the cardiac cycle can be seen and the timing seems normal.
In this case there is left bundle branch block, with reverberations in the lateral wall. Still the septal flash with lateral stretch, the lateral wall shorteining with early and late septal stretch and the septal post systolic shortening (recoil) can be seen. The image can guide the placement of ROIs, but the information should still be used only qualitatively.

The reverberation is easily identified in the M-mode, and the timing of the phases of the heart cycle is evident despite the reverberation. In the traces, the yellow curve shows dyskinesia, the cyan shows hyperkinesia (in strain rate), the red is apparently normal, and the green shows initial dyskinesia and then some shortening. From the traces alone, it's not possible to identify what's correct. Thus, any attempt to use the curves to determine what is correct, will result in getting the answers you want. Even the normally appearing curve (red) should be discarded.  The image shows also clearly how meaningful information can be taken from the parametric image (curved M-mode), both in terms of identifying the artifact as well as the timing and phase information. The mechanisms for the artifacts is discussed in the measurements section

  This will also show:
    - If abnormal findings have a spatial extent, thus not being a finding of only one point. A curve that changes much from one pixel to the next, is unreliable, as shown above, although especially drop outs have spatial extent as well as seen in the methods limitations paragraph). But the main point is that with poor quality, curves and qualitative measurements sghould not be done, but still, the time course and timing information might be gleaned from the CA;;:

2: To assess deformation and time course qualitatively

Colour strain rate is robust, as quantitative data are reduced to semi quantitative. This means it is less vulnerable to noise.

The colour (parametric) imaging can be translated into a wall motion scale, equivalent to wall thickening (6, 7) :

Curved M-modes from apex to basedifferent walls. All are drawn from apex (top) to base (bottom) as shown in the paragraph on parametric imaging. Green shows areas with no deformation. On top, normal systolic function, the shortening phase (orange) can be seen as fairly even in colour and starts and ends at about the same time in all segments of the wall; WMS=1. Below that, the two basal segments are hypokinetic. The orange colour starts later, and is mottled, this is due to a lower  mean (absolute) value, in combination with variations due to noise. WMS=2 - hypokinetic. In addition, the shortening can be seen to extend into the diastolic phase; there is post systolic shortening. Below that, the two basal segments are totally green throughout systole; akinetic, WMS=3, although post systolic shortening is evident. 4: Bottom, there i dyskinesia (systolic stretching - blue) with post systolic recoil. WMS = 4.

In addition, the timing information is present.

The following M-modes are from the cases above.

Case 1 septum. initial apical and midwall stretch (1), apical and midwall hypo- to akinesia (2) and post systolic shortening (3).
Case 2. Septum. Apical tardokinesia with initial stretch, midwall hypokinesia and apical and midwall post systolic shortening Case 3. Inferior wall. Basal dyskinesia, midwall hypokinesia. The blue line between the apical and midwall segment is an artefact, as it is moving, probably a side lobe. This is a very old registration, so the strain rate data are much more noisy, and the spotted orange and yellow pattern signifies an area with hypokinesia and noise.

Case 4. Septum. Apical near akinesia, midwall hypokinesia (again an old recording, the hypokinesia is seen seen by the spotted pattern signifying noise). The noise is evident in the strain rate curves below.
Case 5.
Inferolateral wall. Apical dyskinesia, midwall hypokinesia and post systolic shortening in both.
Case 6. Inferior wall. Akinesia in basal segment (seesn by the noise fluctuating between blue and orange, so there is not much net deformation), although there seems to be an overweight of blue at the start ejection, indicating initial stretch, and yellow at the end, indicating some shortenng at the end. The orange colour in the most basal part is due to angle error.

Look at velocity (and displacement) curves to assess deformation, not only deformation curves directly.

The more processed a method is, the more artefacts there will be. Both tissue Doppler and many speckle tracking methods start with generating a velocity field, tissue Doppler directly by autocorrelation, speckle tracking by tracking small acoustic markers and calculating velocity from displacement of each marker and the frame rate (time between frames). Thus, the velocity data are the primary data, which then are integrated to displacement, or derived to strain rate (which again is integrated to strain). The derivation induces both noise and is vulnerable ti artefacts, the integration induces drift, especially where there is clutter. As strain rate and strain can be assessed by the offset between curves, this will give a semi.quantitative ides of strain and strain rate.

Tissue velocity gives increased temporal resolution, and will show presence of synchrony / asynchrony, presence of post systolic motion and diastolic function. Data are quantitative. Displacement shows more or less the same as velocity, but mainly in systole. Also look at the difference between the curves from basal, midwall and apical segments, to see if the velocities decrease in an ordered way, (i.e. the velocity gradient being evenly distributed). Strain rate is the spatial derivative of velocity, and has increased spatial resolution compared to velocity. It will discern better between hypo- and akinesia, and give a more precise location of pathology. If there is much random noise, integrated strain will eliminate this, but still give the same spatial information.

Normal strain rate as seen by the even offset between velocity curves.

and normal strain as seen by the offset between displacement curves.

Case 1: There is positive strain rate (stretch) in apex the first period after QRS, as seen by the green curve lying higher than the red (and by the positive spike in the orange curve), but the stretch has a longer duration in the midwall segment (red velocity curve above cyan curve - orange strain rate curve).

Case 2: Apical hypokinesia evident both by velocity curves (offset between yellow and cyan curves) and by the strain rate from the apical segment (orange).


Case 3: Inferior basal infarct. Both velocity and displacement curves show no difference, thus there is no differential motion between the three points, the wall is nearly stiff, akinetic in the basal part. The velocity curves can be seen to be somewhat noisy, in this older recording, there is little temporal smoothing, so the noise when calculating the velocity gradient from velocity curves dramatically increases noise. Distances between velocity curves may be a better assessment of strain rate. In this case the curves are all from the same points, which is imprecise, the motion (velocity and displacement) curves should be from segment borders, deformation (strain and strain rate) curves from mid segment, for the offset and deformation curves to correspond perfectly. Also here, the inferior wall which seems stiff, differentiates between segments in the deformation curves, akinesia in the base, hypokinesia in the midwall and hyperkinesia in the apex.

Case 4: Apical infarct. In this case there is normal offset between basal velocity curves (although reduced velocities), but little offset between apical curves.  Again the motion curves should be segemnt borders. not mid segments. Also this is an old recording, showing much noise in the strain rate. Stil the apical hypokinesia is vey evident from strain rate and strain, but can be seen already from the velocity curves.

Case 5: Apical infarct- inferolateral apex. In this image there is substantial offset between velocity curves in the basal segment, less in the midwall and none in the apex. This can also be seen by the strain rate and strain curves from the corresponding segments (interval between the velocity ROIs). However, strain and strain rate are able to resolve the information a little further, as the initial stretch and post systolic shortening is more evident.

Case 6: Basal inferior infarct. Basal hypo- near akinesia (distance between green and red velocity curves, grey strain rate and strain curve).

This is case 6 again. Here much less smoothing has been used, but the basal akinesia and post systolic shortening is still evident in strain rate, and the noise disappears in strain curves.

Look at the whole time course (curve form or colour M-mode), not only peak values

In fact, why look at peak values at all? Compare curves from affected segments with curves from non-affected segments, and the diagnosis of hypokinesia can be made visually qualitatively.

One of the main points about assessing regional function by deformation parameters, however, is that much of the point lies in the time course of the deformation, not only in simple peak values. Thus, both initial delay in shortening of a segment, reduced peak values and post systolic shortening are all phenomenons that tells about the relative reduction in rate of tension development (strain rate) and total tension, all measures of relative reduced contractility of a segment or region, as well as delay in relaxation, another assessment of both ischemia and contractility.

A small infarct in the septal apex, B-mode diagnosis alone may not be entirely convincing. (this is case 2 above)
In the curved M-mode (apex to base in the septum) it can be seen that there is both initial stretch, as well as post systolic shortening in the infarct area, important information in addition to the peak strain rate.

Both strain and ...
strain rate curves from the apex shows the same: initial stretch and post systolic shortening, as well as reduced systolic shortening. Thus, the full time course gives much more information than only a simple peak value or index.

Case 6 was a patient admitted with a history of chest pain, but free of pain and with normal ECG, at admittance. He had elevated Troponin (analysis results not ready till recurrenjce of pain) at the time of admittance.  This Echo at admittance was initially considered normal, even though by retrospective evaluation there is a small area of hypokinesia with delayed onset in the apex.  This is very evident in strain and strain rate analysis, with both delayed onset, hypokiesia and post systolic shortening. He then had recurrent pain after a few hours, with ST-elevation. Angiography showed a tight LAD stenosis, right the result after PCI.

The incremental value of any method, used in this integrated approach, may be difficult to document in studies. Clinical studies will document the value of single measurements, but not the integrated evaluation.

Quantitation may also make it easier to follow the function in a regional dysfunction as in an infarct, as shown below.

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 Bj÷rk 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 Bj÷rk Ingul).

How do speckle tracking and TVI derived deformation imaging compare?

The challenge. Musk oxen, Gr°nnedal, Greenland.

Case 1: Strain rate curved M-modes from tissue Doppler (left) and Speckle tracking (right). The speckle tracking image is much more smoothed, in time due to lower frame rate of B-mode compared to tissue Doppler. IN depth due to the spline smoothing of the 2D strain application. However, in this case, the resolution is sufficient to show intial stretch, apical hypokinesia and post systolic shortening also by 2D strain.

This can also be seen in strain rate curves, the magenta curve in the left panel and the cyan curve in the right panel are from the middle septal segment. The scales on the TVI and speckle tracking are not equal.

And in this case, the strain values do show the infarct, both  as curves, peak values and on the bull's eye map.

In this case, the infarct was rather large, and no method had any trouble in diagnosing it (nor has B-mode).

Case 2 had a small apical infarct.

Again, the SRI CAMM from speckle tracking has much less resolution both in time (due to lower frame rate) and space (due to smoothing). The apical hypokinesia cannot be seen, but the presence of initial stretch as well as post systolic shortening in the apex might be considered (but is far less evident than in TDI). Also in this case, the time course seems to give most information.

Here, the peak systolic strain in the apex of -14 and -15 is near normal, and the Bull's eye of peak values is not convincing either. There might be a slight discernible PSS in the two apical curves (green and cyan), but this is also within normal range. Time course in SR CAMM seems to be the best indicator.
TDI strain shows a peak systolic strain of -6, and evident PSS.

In this case both smoothing and curvature dependency might contribute to hide the apical dysfunction.

In case 6, the peak strain in the inferobasal segment is reduced, but might be interpreted as inaccurate processing when seen in the bull's eye view. The best clue to the infarct is the curve from the basal segment (yellow) showing reduced systolic strain and post systolic shortening, i.e. the time course, but in this case the hypokinesia is evident. And in this case both curves and values correspond with the two methods

In this case, the inferior infarct is visible. In another, nearly similar case, however, the infarct was not very visible in speckle tracking:

Strain by tissue Doppler, showing systolic akinesia in the basal segment (cyan curve) - mark how the ROI is placed to avoid the lower part of the segment where there is angle discrepancy), and normal strain in the apical segment (yellow) and the anterior wall (red). Strain by 2D strain, showing borderline reduced strain of -12% in the basal segment. In this case, the strain  is due to the inward motion (by tethering) which reduces the length of the curved segment. In addition, the ROI, being the same all the way around, overestimates the wall thickness in the infarct. In this case, the effect is due to the curvature, not smoothing.

Finally where there are drop outs, the spline smoothing may distribute the motion over fewer segments, thus masking the infarct totally:

Stiff inferior wall due to an infarct, but fair annulus motion due to normal, or even hyperkinetic apical segments.

-  which results in the normal annulus motion being splined over only three segments, instead of six, as there is a drop out of the whole anterior wall, and the segments are excluded, as opposed to TDI where analysis is only local.

Ladies and gentlemen of the jury, what's your verdict?

Stress echocardiography

May ways of stressing. Hiking to top of Ytre Norsk°ya, Spitsbergen
Cross country skiing in Lesjaskog, Norway

Stress echo can be done with:

In general, the image quality deteriorates with increasing stress.
Early studies did show low feasibility of Tissue Doppler derived SRI in upright bicycle echo (111). However, threadmill (pre- post), or dobutamine is feasible.

Thus, there will be severe limitations to the utility of deformation imaging in stress echo. In addition, the two imaging methods have limitations that becomes more pronounced during stress.

Still it has proved to give additional information (113, 114, 128, 133). Thus, the results by speckle tracking are very modest (302).

Tissue Doppler with higher frame rate seems to be the best option for deformation imaging so far. However, it may change with increasing B-mode frame rate.

Thus, feasibility of deformation imaging in stress echo, should be expected to be lower than in myocardial infarction.

A cooperative study of dobutamine stress from Trondheim and Brisbane (128), showed that the feasibility of analysis was 65 - 85% of segments at peak stress, depending on method, but significantly lower than WMS by B-mode, which was 98%. Still, analysis was feasible in all patients. Other studies consistenly have reported higher feasibility in terms of swgments. In my opinion that must mean either that patients are highly selected, or that they

B-mode analysis can be enhanced with contrast. However, contrast precludes the use of deformation imaging:
Thus, at the start of a stress echo, one is forced to make a choice between contrast or deformation imaging, based on resting image quality. 

If image quality is good, strain rate imaging will resolve details that arre not visible by B-mode, as seen here. The following example has good image quality, and shows details in the development of contraction changes:

Stress echo from a patient devolving apical ischemia. From a fairly normal pattern at baseline, there is increasing contraction at 10 ug/kg/min, but mainly in the base, some apical hypokinesia at 20 ug, and the protocol was terminated at 30 ug because of pronounced apical akinesia. SPECT showing reduced uptake in the anteroapexapex at rest, but worsening during stress, due to the distortion of the polar ("bulls eye") projection, the apical area is underrepresented. It seems that the SPECT is able top detect a hypoperfusion at rest that is not very evident in B-mode echo. 

Baseline shows slightly reduced strain rate and post systolic shortening in the apicolateral segment (cyan) already at rest. Thus there is additional information that is similar to that obtained by SPECT.
At 10 ug/kg/min, there is initial stretch in the apicolateral segment, reduced systolic strain rate and strain, as well as post systolic shortening.
At 20 ug/kg/min there is prolonged initial stretch, near zero systolic strainrate and strain and extensive post systolic shortening in the apicolateral segment. In addition there is reduction in systolic strain from 10 ug, and initial post systolic shortening in the apicoseptal segment (yellow).
At peak stress (30 ug/kg/min) there is holosystolic stretch in the apicolateral segment,but with some post systolic shortening indicating that the segment is not completely passive. There is also extensive hypokinesia with post systolic shortening in the apicoseptal segment.

However, timing can also be evaluated in strain rate colour CAMMs from the different stages, drawn from the septal base (top), through the apex, (middle) to the lateral base (bottom). Strain rate is most sensitive for changes of short duration, as strain is the cumulated deformation from the start of the heart cycle.The same phenomena as described above, can be seen marked with white ellipses in the curve M-modes below, while the white rectangle is the apical area of distortion.

Slight apical hypokinesia and PSS apicolaterally Development of initial stretch Apicolateral hypokiesia and apicolateral and apicoseptal PSS
 Apicolateral systolic a- to dyskinesia and post systolic shortening, apicoseptal hypo- to dyskinesia and PSS.

And the angiography showed:

Angiography findings, showing three vessel disease. The most seriously affected area probably the LAD, due to the retrograde filling from a severely stenosed vessel.

In this case, the ischemia is evident without recourse to deformation imaging, but with additional information about severity and extent. The development of ischemia is very evident. One of the main things seen in this example is that a lot of the information about ischemia is in the development of timing changes, especially initial a- or dyskinesia (46, 304, 305). This is equivalent to the tardokinesia seen in B-mode stress echocardiography (306), and in addition  post systolic shortening (100, 114, 299), although it is uncertain whether post systolic shortening imparts better sensitivity than peak strain rate (128).

Thus, the curved M-mode will give several advantages, both having better spatial resolution, and the most important being much more robust against noise. This will increase feasibility in patient with, or who develops poor image quality:

Stress echo at peak stress showing fairly poor image quality in B-mode.
CAMM at peak stress, showing a lot of clutter noise (seen by the alterations between intense red and blue bads), as well as random noise (seen by the red and blue speckled pattern, which is due to peaks and troughs of noise). Still, there is no evidence of delayed contraction onset in this image.

With stress echo, it is possible to do wall motion scoring semi- quantitatively, but timing can be both assessed and measured:

In WMS = 2, there is both hypokinesia and tardokinesia as well as PSS, in WMS 3 there is PSS and in WMS=4, there is dyskinesia and PSS in the apical segment, but also PSS inthe midwall segment indicating a more extensive partial ischemia.

The combination of hypokinesia and PSS may give an asynchrony between walls, where almost all of the wall may be out of phase, even if there are gradients of ischemia as shown below.

Stress echocardiography with development of ischemia in the inferolateral wall. At peak stress, the whole ventricle can be seen to rock. In this case, however, the rocking motion is biphasic, first toward the inferolateral wall, and then back toward the anteroseptum. This would be more visible if the loop could be stopped and scrolled (which it can on a workstation.
The velocity (motion) confirms the visual impression, the whole inferolateral wall moves downwards in systole, and upwards at end systole (Yellow and green curves), while the septum shows normal apically directed velocities n systole, and downwards in diastole. Thus the rocking can be very easily confirmed by tissue velocities.
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.

In this case the development of asynchronia during stress is evident from B-mode. Tissue velocities confirms this. However, this will not give a more detailed localisation of ischemia. The explanation is that there is reduced contraction in the inferolateral wall in systole due to ischemia, and then a late systolic shortening in the same wall.

Comparing walls with tissue Doppler and strain rate:

As seen above, tissue velocities at peak stress show initial systolic downward motion of the whole inferolateral wall (yellow, red, cyan), compared with the normal motion of the septum (green). The downward motion (apparent dyskinesia) is greatest in the apex, being a little difficult to interpret in terms of contraction, but using the comparison described above , there is actually a positive difference from apex to midwall (yellow to cyan, negative velocities are greatest in the apex), denoting a positive strain rate (stretch), while there is negative difference between midwall and base (cyan to red), denoting shortening.
This is much more readily seen in strain rate, there is initial stretch and late systolic shortening in the inferolateral base, not in the apex. Thus the ischemia seems to be located in the inferolateral base, indicating Cx ischemia. In addition, there is hyperkinesia in the inferoapical half, due to reduced load from the ischemic neighbour segment as explained here. This is what actually causes the rocking towards the ischemic wall, which seems a little counter intuitive at first.

Also, there is late systolic, not post systolic shortening of the ischemic part, It is concomitant with the early relaxation of the hyperkinetic inferoapex.

Strain rate colur M-mode shows the same,with better spatial resolution it is possible to see that both basal and midwall inferolateral segments are ischemic, showing initial systolic stretch. In addition there is late systolic, instead of post systolic shortening, but this is simultaneous with the premature stretch of the apical segment, as compared with the septum. Thus the diagnosis of Cx ischemia is very probable.
And this was confirmed angiographically, with no other significant stenoses.

The next case also shows asynchrony as the initial visual effect of ischemia.

2-chamber view. At peak stress there is an obvious rocking towards the anterior wall. There is no frequency induced LBBB, as the QRS doesn't change shape.

This visual impression of rocking again can be confirmed by tissue velocity:

Fairly synchronous motion at baseline (especially looking at onset of anterior motion, although peak velocity is later in the anterior wall (red and green). During peak stress, there is evident rocking, with basal  motion of the anterior wall (red and green), simultaneous with apical motion of the inferior wall (yellow and cyan), and then opposite rocking at end systole. The lack of deformation in the anterior wall is also evident, seen by the close proximity of the red and blue curves.

This is confirmed in the CAMM:

- showing systolic hypokinesia at peak stress in the anterior wall - evident by the spotty pattern, changing between blue /cyan and red / orange in about equal amounts, although the colours are more intense at start systole. Even more evident is the post systolic shortening in the anterior wall, and in this case the whole of the wall, so the comparison with the inferior wall by drawing the curve trough both walls facilitates recognition.

And the same is visible in the curves.

Again, the mechanics seem a little counter intuitive, the heart rocks toward the ischemic wall. In this case, the influence is probably from the right ventricle, which was not included in the stress acquisition protocol.

- and the patient had an LAD stenosis (which is actually curious, the stenosis is distal to the diagonal, and there is no echocardiographic evidence of ischemia in the apex.

Left bundle branch block

Differential diagnosis:

Before looking at an asynchronous ventricle, it's of course important to understand that there is other causes of both apparent and real asynchronia, for instance ischemic post systolic shortening, or translational effects from rocking of the whole heart. Deformation analysis will help in differentiating this. :

1: Ischemia

This is evident in the first case from above:

In this case there is evident rocking of the heart, there is an acute, large apical infarct, with reduced global function.
However, with strain rate imaging, there are more details, showing initial stretch in the septal apical and midwall segments(1), hypokinesia (2) and post systolic shortening (3) in the apical half.

There is rocking motion, and asynchronous shortening and lengthening, but in this case due to ischemia. Other examples can be seen here, where ischemic  post systolic shortening gives the impression of asynchrony of whole walls.

2: Translation effects (Whole heart rocking)

Translation effects may also mimic asynchrony, but in this case deformation will show that there is no asynchrony in myocardial mechanics:
motion of the whole ventricle, may also result in apparent asynchrony as shown in the example above (main images repeated below for repetition):

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 synchronous.

Tissue 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.

In this case, the motion (velocity imaging) is mis informing, giving the appearance of dyssynchronous function of the left ventricle, while deformation shows this to be untrue.

This chapter is mainly a slightly abbreviated version of the chapter on LBBB in the main section, here the mechanical explanations are omitted, in order to focus on the clinical interpretaion of the deformation in the four examples.

When looking at left bundle branch block, the main principles apply: A comprehensive evaluation based on deformation imaging again should be based on using the principles in the pfirst part:
  1. Assess image quality
  2. Use velocity curves
  3. Use Curved strain rate colur M-mode
  4. Take the entire time course of the deformation into account

In a failing ventricle, there is evidence that if LBBB induces mechanical asynchrony, this might lead to mechanical inefficiency and thus to worsening of heart failure. The mechanism has to be mechanical inefficiency, but still there is no very well documented selection of patients that will respond to resynchronization therapy, the responder rate still is only about 70% in most materials.

As only about 70% of CHF patients with LBBB respond to cardiac resynchronisation therapy (CRT), the need to elicit the effect on mechanics in order 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.

Some things are important to realise:

The first assessment is thus to assess whether LBBB induces mechanical asynchrony.

Mechanical asynchrony in left bundle branch block

If there is left bundle brach block this may have various effects.

So the first point is in assessing mechanical asynchrony:

Patient with left bundle branch block. Maybe not very evident septal flash, but some apical rocking, however, most evident is the late systolic rocking toward the lateral wall.
There is no apparent systolic asynchrony in the base (top panel, equal time to peak in septum and lateral mitral annulus, but some indication of post systolic shortening in the septum), but the apical rocking is very evident in the velocity traces from the apex. There is early rocking toward the septum, and late rocking toward the lateral wall.

Thus, in this specific instance, the apical rocking seems to be more sensitive than the "septal flash".

Identifying ejection period from Doppler
The whole set of tissue velocities from apex and base shows the rocking most obvious the lateral rocking at end ejection (green vs red curve)

Strain rate colur M-mode gives the whole picture, wirth an earlier onset of shortening in the septum, but no bacjkand forth motion as in the septal flash, because of earlier onset of activation of the lateral wall. However, at end ejection there is lateral shortening and septal stretch, and then post systolic shortening of the septum.
Strain rate from the walls compares with the tissue velocities, although there can be seen a slight shortening of the septum before onset of ejection, that do not correspont with shortening in the lateral wall. Most evoÝdent is end ejection stretch of the septum.

Thus, mechanical asynchrony can be demonstrated in this case, although with no symptoms and normal ventricular function, the finding has no consequences.

The next example shows the more typical septal flash.

"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 wall.
The   "septal flash" evident in both parasternal long axis and short axis.

The septal flash has also been called "rocking apex" (285), as the asynchrony induces a rocking motion of the apex as seen in the four chamber view. The rocking apex is equivalent with the septal flash, as it is the initial contraction of the septum without simultaneous contraction in the lateral wall that results in the rocking towards the septum. The rocking due to septal flash, is always toward the septum, while the rocking apexes shown above (not due to conduction anomalies), is more often towards the lateral wall. The rocking is also evident in the tissue Doppler images, although with a complex pattern:

The four chamber view shows both septal flash and rocking apex.
"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 the systole.
However, looking at the B-mode above, the motion is far more complex than this. The initial inwards motion of the septum is reversed, the rocking of the apex towards the septum, however is not reversed before the end of the systole, where the apex rocks back.

What we see is a pattern of septal flash, shortening during ejection, late systolic stretch and post systolic shortening.

Typical pattern of tissue velocity in the septal base, in a case where LBBB induces mechanical asynchrony.

The mechanics of this is discussed in another section.

This can be demonstrated by tissue Doppler:

The ejection period timed by Doppler flow from LVOT.
The phases are visible by tissue Doppler. This is the same image as above, but with two more sample volumes added in the base. (the differences in amplitude of the apical curves is due to autoscaling). Deformation is visible by the offset between the velocity curves; there is septal shortening when the red line lies above the yellow, and lengthening when yellow is above the red. Likewise in the lateral wall there is shortening with green above cyan, and lengthening with cyan above green. During QRS there is shortening of the septum (yellow to red), and stretching of the lateral wall (green to cyan). This is the septal flash. With onset of lateral shortening, the septal flash reverses, resulting in the peak of the septal flash (yellow vertical line), which also marks the MVC and onset of IVC. At start ejection, there is abrupt apical velocities of both basal points, marking shortening of the whole ventricle, as seen byt the velocity offset, there is shortening in both septum and lateral wall. before end ejection, however, the septum starts to stretch due to end of relaxation, as seen by the yellow/red crossover. This continues after end ejection, while the end of laterl shortening is marked by the cyan green crossover, also marking the onset of post systolic septal shortening.
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 actual amount of asynchrony.
The findings from tissue Doppler is confirmed by this curved M-mode, showing the phases of septal shortening and lateral stretch. The peak of septal flash is the shift from septal shortening to elongation, concomitant with the onset of lateral shortening, although in this case it is difficult to discern because of noise.
 The phase of simultaneous deformation during ejection is evident, as is the phase of continued shortening of the lateral wall together with stretching of the septum.

However, it is important to realise that the septal flash and indeed the rest of the mechanical asynchrony) can be seen in ventricles with good function as the above instance. The septal flash is thus a marker of asynchrony, but not necessarily to a degree leaading to heart failure. In the above case, there is evidence of some mechanical inefficiency, as there is end ejection shortening of the lateral wall and stretch of the septum, with stretch of the septum and some recoil (post systolic shortening) which may indicate "wasted work". However in this case, most of the rocking happens after end ejection, there seems to be little wasted work during ejection.

The asynchrony, may still be a marker of some degree of mechanical inefficiency, But this may not become important unless there is underlying myocardial disease with weakened myocardium from other causes as well. However, this may also be dependent on the degree of delay of the lateral wall.  It cannot, however be any doubt that the deleterious effect on mechanincs which may be improved by CRT, has to be through mechanical asynchrony.

The width of the QRS, however, even if being statistically associated with prognosis, may not be an individual marker of the degree of asynchrony. The QRS width is a marker of the amount of delay, but not where the delay is situated, and thus says less about mechanics.

Septal flash is a marker of mechanical asynchrony per se, but not necessarily of mechanical inefficiency. Thus mechanical asynchrony may be necessary, but not sufficient prerequisite for assuming that the patient suffers from mechanical inefficiency.

Mechanical inefficiency

It seems logical that for the LBBB to induce worsening of pumping function that can be corrected with CRT, has to be a mechanism where electrical asynchrony leads to mechanical asynchrony, which in turn leads to mechanical inefficiency. Still, the serch for echocardiographic markers of this, have only been moderately successful (286).

An approach looking at the shortening of one wall and simultaneous stretch of the opposing wall, called "simple regional strain analysis" seems to approach the same concept of wasted work, and is promising in being a marker of potential response to CRT (294).

 However, the approach by only looking at total strain may be too simplistic, and so may integrating it into a simple index.
  1. Firstly, shortening of a wall do not mean active shortening. As blood is ejected, the total ventricular volume will decrease, and even a passive wall will shorten. This is just as in healthy ventricles, where the last half of the shortening is passive due to continuing ejection and volume decrease during relaxation. Thus, a passive wall may still shorten during ejection phase.
  2. Secondly, inequalities of force may lead to one wall stretching as another contracts with more force, but the force used for stretching will depend on the tension in the wall being stretched. 
  3. In contrast, one wall may have sufficient remaining tension to resist stretching, but still not shorten, and thus not contribute to ejection, despite not being stretched.
  4. Fourthly; a wall being stretched, may still contribute to ejection if it recoils during ejection phase, but not if it does so after end ejection. Thus, timing of the interactions may be of importance
  5. Fifthly; using only strain, may mean that stretching in part of the ejection phase will not be detectable when looking at total systolic deformation
  6. And finally, there may be simultaneous stretch and shortening within walls, due to the complexity of the left bundle anatomy.
It still seems that echocardiography, especially deformation imaging, can go a long way in describing the mechanics in bundle branch block, and may also indicate if there is potential for CRT by describing "wasted work", but it seems that this needs a comprehensive evaluation of both mechanics and hemodynamics.  Simple indexes of mechanical asynchrony, such as time to peak velocity, time to peak strain, or even septal flash or rocking apex (as these may be present without very poor mechanical performance). Also, of course, intraventricular mechanics may not be the only factor in predicting CRT response.

Mechanical inefficiency may be more evident in the next case:

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 only 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.

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.

Looking 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 shortening.
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.

In this case, there is evidently more asynchrony, as well as indications of less energetical function more wasted work), as more of the systolic time seems to be used for stretching of opposite walls. The differences may be due to more delay in electrical activating the lateral wall. However, the QRS width is not a good indicator of this, as the factor for mechanical asynchrony here logically will be onset of lateral activation, not end.

Ejection fraction is also lower in this case (The patient has had mitral annuloplasty, and preoperative dilatation due to MR), but it will be difficult to ascertain whether the function is reduced due to worse electrical asynchrony, or the mechanical asynchrony is worse due to a reduced ventricular function. However, in this case there may be potential for recruiting more contractility by CRT, and the patient may be candidate for CRT if developing manifest CHF.

The main consequences of this mechanics, is that the lateral wall does most of both pressure and ejection work, and thus less muscle is recruited for work. In the case of a weakened ventricle, at least, the reduced global force and wasted work force will tend to worsen the function.

The mechanics may be far more complex than this, as in the next case:

Apical rocking (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 during ejection.
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.

This is even more evident in the colour M-mode:

Vigorous systolic shortening in the basal part of the septum and apical part of the lateral wall, less so in the apical septum and lateral wall, systolic stretch being most evident apicoseptally.

This dissociation between the apical and basal parts may be the reason for the apparent dyssynchrony when assessed by the apical velocities (rocking apex), and the far less dyssynchrony evodent in the basal velocity curves.

However, in this case there is just as much asynchrony and wasted work (corresponding to one whole wall, but distributed between the two walls), not located in one wall only. However, with evidence of mechanical inefficiency, it is not surprising that the patient responded very well to CRT.

The response after 1 year shows reverse remodelling, increased EF, and abolished septal flash.
The same is evident from the apical view.

And synchronicity of shortening can be seen by strain rate.  

Finally, looking at an extreme example:

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 septum.

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 abbreviated.
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).

In this case, the unfavourable mechanics is even more evident, but to understand it fully, there has to be a comprehensive evaluation. As so much of the work seems to be wasted, there are indications that CRT might result in improvementby recruiting the septum for active pumping work.

This proved to be the case:

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 both walls.

Ejection is earlier, compared to ECG, as is IVC, and the ejection period is longer.
However, there is stil EA fusion, indicating the the CRT is not fully optimised.

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.

In this case, not only the mechanics due to the LBBB, but also the deleterious hemodynamic consequences of the asynchrony,  as well as the sucessful recruiting of the septum for pumping work,
was evident.

Tissue velocities on the other hand did not contribute to the understanding, neither before or after CRT:
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.

Left bundle branch block in diastole:

Looking at the diastolic measures, there is some evidence that the asynchrony in left bundle branch block affects diastole as well:

Looking at the spectral Doppler traces aligned by ECG (first vertical line)  there is post systolic motion (PSS) in the septal trace, which corresponds to a delayed e' wave. Laterally, there is no PSS, but there is corresponding delay in the peak e', the e' wave is seen slowly sloping towards the peak. The mitral flow is slightly affected as well, the peak E is similarly delayed. This leads to a partial fusion of E and A, as in 1st degree AV-block, as the next P and Awave comes early in relation to the delayed E wave. Thus, there may be potential for developing partial AV-block, despite normal PQ-time. In this case, however, there is similar dely of the septal e' wave, but the lateral peak e' is seen slightly earlier, abd the E wave corresponding to the lateral e'. It seems evident that in this case, the septal E/e' ratio is not strongly associated with filling pressure, as they are not simultaneous. In this case, the septal PSS is delaying the septal e' even more, but again with no delay in the lateral e'. And the mitral flow peak E is earlier than both. It seeems evident that in this case, meither E/e' ratio is not as strongly associated with filling pressure, as they are not simultaneous. And the fact that the flow E is earlier than the tissue e', might indicate that filling pressure actually is elevated.
Another case, but with lower S'in the septum, indicating a poorer septal function, again the e' in the septum can be sen to be delayed, and later that the mitral flow E, which in this case is more synchronous with the lateral e'. It is difficult to see that the E/e' ratio, at least the septal one expresses filling pressure, as the peaks are not simultaneous. In this case, the E/e' was 17.5 for the septal e', 7.7 for the lateral e' and 10.7 for the mean e' (however, the validity of taking the mean of non simultaneous peaks is dubious). As the lateral e' is simultneous with peak E, this should be a better measure of filling pressure????

However, in the last case, the Valsalva indicates an elevated atrial pressure:

During Valsalva, the E/A ratio drops from 0.78 to 0.33 and the flow pattern becomes that of typical delayed relaxation.

The main message is that E/e' is highly dubious as a measure of left atrial pressure in LBBB.

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Editor: Asbj°rn St°ylen Contact address:, Updated: 2016