The page is part of the website on Strain rate imaging

Contact address: asbjorn.stoylen@ntnu.no

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.

Albert Engström 1869 - 1940

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.

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 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 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.

The challenge. Musk oxen, Grønnedal, 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.

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.

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:

Stress echocardiography

Stress echo can be done with:

• Exercise
• Upright bicycle, which probably results in the worst image quality
  
• Supine bicycle, resulting in better image quality, but with a large proportion of patients unable to reach an adequate heart rate, as muscular endurance is often limiting, and thus the stress protocoll has lower feasibility not related to image quality.
  
• Threadmill pre - post, which means that recordings has to be made before 1 minute after, to be sure to capture ischemic stunning. Negative test at a later time has lower negative predictive value. Thus, the local experience with the method seems to be the limiting factor.
  
• Dobutamine, which probably gives the best images, but which also vasodilates, resulting in afterload reduction that may mask ischemia.
• Adenosine (or indirectly, adenosine by dipyridamole), only results in increased flow, to asses absolute or relative coronary flow reserve, which is suitable for perfusion studies, but very rarely causes coronary steal leading to real myocardial ischemia. Thus, it is not suitable for stress echo using regional myocardial function to asses ischemia.
  

In general, the image quality deteriorates with increasing stress.

• The main point of stress echo is that during stress the heart rate is increased. This means shorter and more abrupt movements of the heart.
• In addition, the ratio between filling and ejection is changed, filling being abbreviated more, and very often there is fusion of E and A phases.
• Exercise will increase motion of upper body, as well as breathing.
• Dobutamine increases heart rate without increasing venous return, leading to decreasing end diastolic volume, and thus smaller acoustic window.

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.

• Tissue Doppler derived strain rate (but not strain) is noisy, and random noise increases with increased contraction rate (by both increased EF and heart rate)
  
• Tissue Doppler derived strain rate and strain is especially susceptible to clutter noise, which will increase with reduced image quality.

Still it has proved to give additional information (113, 114, 128, 133).

• Speckle tracking is susceptible to increased heart rate, as increased heart rate, (causing a greater change from frame to frame - in reality a decreased frame rate per heart cycle) will lead to decorrelation in speckle tracking.
• Also possibly smoothing, may lead to reduced sensitivity.

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:

• Contrast in the myocardium leads to de-correlation as the bubbles burst on ultrasound impact, thus the auto-correlation algorithm doesn't work (303).
• Low mechanical index leads to low myocardial intensity, and few speckles to track. Probably most applications would track blood flow, if anything at all.
  

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:



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:




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.

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.


This is confirmed in the CAMM:

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.

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.

• Not all patients with LBBB have mechanical asynchrony, it depends on which parts of the left bundle that are affected, and to what degree.
• Even if there is mechanical asynchrony, that does not mean there is mechanical inefficiency, at least not to a great degree.
• If there is mechanical inefficiency, it might be distributed differently, it may not be sufficient to compare walls.
  
• It may be that the degree of mechanical inefficiency is dependent on development of a vicious circle, where a failing ventricle leads to more mechanical inefficiency
• The width of the QRS, 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.

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.

• Some patients display an apparent normal activation pattern
• Some patients display normal pattern at rest, but shows mechanical asynchrony at higher heart rate, due to the relative conduction delay that may manifest with increasing HR.
• Some patients display mechanical asynchrony at rest.

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 evoídent 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.



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:

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.

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: