Det medisinske fakultet

Regional functional imaging

This is what strain rate imaging is really about.


Asbj°rn St°ylen, Professor, Dr. med.

Department of Circulation and Medical Imaging,
Faculty of Medicine,
NTNU Norwegian University of Science and Technology

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This section:

This is what strain rate imaging is really about. This section is mainly about the pathophysiology responsible for the changes seen in regional dysfunction, explaining the various patterns in terms of segment interaction.

  References for all sections

Regional systolic function

The regional systolic function is traditionally shown as wall motion score:
  1. Normal
  2. hypokinetic
  3. Akinetic
  4. Dyskinetic
Wall motion score index (WMSI), being the  average of wall motion score  of all evaluable segments becomes a measure of  global function, and has been shown to correlate with EF in infarcted ventricles (40). However, the index is useless unless there is regional differences. Any dilated cardiomyopathy will show hypokinesia in all segments, giving a WMSI of 2, regardless of EF. Thus, wall motion score is useful only in regional dysfunction. 

Segmental division of the left ventricle. The segments are related to different vascular territories, as shown by the colours. After Lang et al (146).  However, in the figure given in that paper, the apicolateral segment is given as Cx or LAD, while the apical inferolateral is not, despite the model is only giving four segments in the apex.  Thus, there is a slight inconsistency.

This segmental model gives a longitudinal resolution of the model of about 3 cm, and a circumferential of 60░, which may be considered low. However, in relation to vascular territories, it seems sufficient, and deformation rate measurements with higher resolutions (which are possible with both speckle tracking and tissue Doppler) have not so far demonstrated added clinical value.

16, 17 or 18 segments?

It has been an issue of discussion how many segments the left ventricle should be divided into. As there are different recommendation, and the reasons for the recommendations are partly historical, they are reviewed. The original ASE recommendation was six segments in the base and midwall, but only four in the apex (239). The reason for this was that the three standard planes were visualised as the apical four- and two-chamber planes, but the parasternal long axis. AS apical segments were not seen in most parasternal windows, there was only four segments, and the lateral and inferolateral and likewise the septal and anteroseptal segments were considered the same.

In an attempt to harmonise nuclear and echo imaging terminology (240), an apical "cap" segment was added, giving a total of 17. This, however is due to the thickness that is vuisualised in nuclear myocardial images, while the wall in the apex in reality is very thin, and is in fact only useful in perfusion studies.

In the present ASE/EAE consensus recommendation (146), this is commented on, and there is no direct recommendation on using 17 segments. On the contrary, it says explicitly: "When using this 17-segment model to assess wall motion or regional strain, the 17th segment (the apical cap) should not be included. A 16 segment model can be used, without the apical cap, as described in an ASE 1989 document."

The present standards paper for deformation imaging (287), specifically states that 17 segments, (including an apical cap) "is not recommended for functional imaging as the apical cap does not contract".

At present, using three standard apical planes, the approach will result in 18 segments. For segmental analysis, this doesn't matter, and we have used that approach in the HUNT study (153), giving normal values for each wall and level. However, for global function calculated as an average of segmental values, 18 segments is incorrect (146). the amount of myocardium in the apical level is less, and should be weighted less, as the 16 segment model will do automatically. For this we have reduced the number of segments by averaging the the lateral and inferolateral segmental values and likewise the septal and anteroseptal segmental values before calculating the global average of 16 (153, 223).

It is regional systolic dysfunction the deformation imaging has it's main use, as it makes it possible to differentiate between passive motion due to tethering and active contraction. Longitudinal strain can give the wall motion score by parametric imaging . It has been shown to give about the same infrmatin as wall thickening by B-mode (6, 7).

Segment interaction

To fully appreciate the deformation patterns in regional dysfunction, the concept of segment interaction (meaning that segments pull on each other) must be considered.

The segment interaction is important to understand all kinds of deformation patterns showing, not only in ischemia, but also in other kinds of asynchronia as well.

Thus Segment interaction within the AV-plane leads to the specific patterns of regional dysfunction. This includes both delayed onset of shortening/intitial stretch, systolic hypo-/a-/dyskinesia, and post systolic shortening, which all are part of the same mechanism. This also shows that which has be shown in studies, mitral annulus motion will not give information about regional function. Post systolic shortening is thus not an isolated event, but part of the total pattern in ischemia, but on the other hand is not limited to ischemia, being seen both in left bundle banch block and hypertrophy.

1: Segments interact within the framework of the AVplane.

The mitral ring is stiff, each segment does not move independently.Not only are the segments around the mitral ring closely bound together, thus excluding the possibility of each segment moving independently, but the mitral ring itself is part of the whole AV plane, consisting of the connected rings of the pulmonary artery,  the aorta, the mitral and the tricuspid valves. There is no isolated mitral ring, the ring is simply part of the much bigger fibrous AV plane, and thus even  the possibility of the ring tilting as each wall functions differently, is severely restricted. :

The AV plane. It consists of a fibrous plane connecting the rings of the pulmonary artery (PA),  the aorta (Ao), the Mitral (MV) and the tricuspid (TV) valves, and surrounded by the muscular base of the heart. The sections of the mitral ring cannot be seen as indepndently moving structures. Thus, segments will interact within this framework. And both ventricles move the AV plane. (It might seem to be slightly flexible, as the motion of the tricuspid corner (tapse) is higher than the mitral motion, but still the palne will move as a whole, even if there is some deformation. The velocities of the lateral left wall are higher than the septum, but this is due to the longer wall. The overall systolic strain rate is not so different.

From the understanding that the AV plane is a rigid frame, the segment-segment interaction is necessary to understand the effects of regional function measured by deformation imaging.

2: Load is more than pressure, segment interation forces is part of segmental load.

Looking at longitudinal function, the concept of load is not limited to the simple model of Laplace, as it should include the effect of segment interaction (forces).

Diagram of longitudinal segment interaction. the longitudinal shortening of one segment results in shortening of the segment itself (orange arrows), but also in motion (red arrows) of the segments basally to it. (In this illustration, the red arrows show the motion of the middle of the segment, meaning that it also included the effect of the shortening of the apical half of the segment itself.)and the motion of each segment is equal to the summation of the shortening of the segments apically.  However, the primary effect is force generation. And this means that contraction in one segment results in a force applied to the neighboring segments. This force has different effects, as the apex is considered anchored (by the recoil force from ejected blood), while the midwall segment has force applied from both sides, and the basal segment is freely movable.  The main point is that the force from neighboring segments may be considered part of the load of each segment, and that motion is secondary to deformation, but deformation is secondary to force and load.

Thus segments can be seen pulling at each other, and the relative shortening (sgtrain) is dependent on the relative strength.

When doing imaging, the parameter is always shortening, and shortening is the result of both contractility and load:

In contraction, the muscle will increase tension, but resulting in no shortening as long as the tension is below the total load (isometric contraction). When tension equals load, further contraction will result in shortening at constant tension (isotonic contraction). This is what we see in imaging.
However an increasing  load will both delay onset of shortening, as the development of higher tension takes longer time, but will also result in less shortening, as well as a lower initial rate of shortening.  In these diagrams, the effect of load in slowing relaxation(224) is not shown. This effect would show up in prolanged duration of the downslope in the tension diagram. However, the lengthening phase would still be shortened by the load.
Reduced contracility will give a slower tension development and lower peak tension. However, this has the same effect as increased load on shortening, resulting in delay in onset of shortening, lower rate of initial shortening and less total shortening. Thus, reduced contractility would also have effect on relaxation (224), seen in the tensin curves, but this is not shown here.

Thus, differences in contractility will affect both normal and pathological segments, but differently:

Symmetrical forces in all segments, will result in symmetrical shortening. Thus, all segments shorten equally (orange colour), which means that the base moves most (the sum of shortening of all segments), as the apex is stationary.
Loss of contractility in a basal segment (smaller black arrows in the left basal segment), results in less shortening in the affected segment. However, this means that the load on the more apical segment is reduced, and thus, this segment will shorten more Red colur9 , not due to hypercontractility, but to less load. Also, the total force acting on the base is reduced, resulting in reduced total shortening (smaller red arrows in the base).
Even more reduced tension in a basal segment will result in the segment actually stretching, while the apical segment shortens even more in response to the basal segment stretches. This will not result in reduced motion of the regional mitral ring point, mainly a shift in the distribution of shorteningbetween segments, and a reduced global shortening.
Reduced tension and stretch of an apical segment may result in increased shortening of the opposing wall, as well as the basal segment, but this may result in a rocking of the apex toward the healthy wall. 
Symmetrical weakening of the apical segments, may result in increased shortening of the basal segments, but as the apex stretches, the motion of the AV-plane is more reduced.

3: Thus, annular measures do not give regional information.

As strain and strain rate are noisy methods, it is an attractive thought thay annular measures (annular systolic displacement or velocity) will give some regional information, in that points on the mitral ring close to a hypo- or akinetic area will show reduced motion, while remote points will not.

 However, this is definitely not the case, as we showed already in 2003 (40).

In a study of 19 infarct patients versus 19 control subjects, we found that while global function was reduced in patients, the variability between the difference between annular points was not:


S' (cm/s pwTDI) S' (cm/s cTDI) Segmental SRs (s-1)
Patients: 41
Controls: 55*

Mean intra subject variation (max - min)



Thus, no ring measures showed increased variability in infarct patients who had regional dysfunction. Only the segmental measure of strain rate did show that, despite having the highest variability. Moreover, in the patients; there were no differences between the magnitude of ring measures close to the infarct, compared to the measures remote from the infarct:

MAE(mm) S' (cm/s pwTDI) S' (cm/s cTDI) Segmental SRs (s-1) Mean SRs (s-1) per wall

The mitral ring motion were reduced in infarct patients compared to controls, and more reduced in anterior than in inferior infarcts due to the difference in infarct size.Thus, it can not be inferred that the point on the ring close to the infarct can identify the affected wall.Oonly the segmental measure did show difference between close and remote points, while the ring measures did not. And finally, averaging all three segments in a wall, resulting in a wall measure equivalent to the ring measures, made this difference disappear. This means that ring measures all are global measures, local reduction of contractility will affect segmental shortening, but not local ring motion. The global systolic motion of the ring is a measure of the infarct size (32), being reduced in proportion to the total amount of longitudinal fibre loss (210). Segmental reduced function will not cause the ring to lag in part of the circumference, however, the total ring motion will be reduced as a function of the reduced total shortening force. This may explain why the global strain is just as useful as regional strain in assessing the infarct size (205).

This has recently been confirmed in a newer MR study (436).

Motion is global function, only deformation can be regional.

As shown above, motion parameters will thus always reflect global function, only deformation parameters can show regional function.

In studies of the course of infarcts (92, 188), it has been shown that as there is initial hypo- to akinesia in infarcted segments, there is corresponding hyperkinesia in neighbouring non infartcted segments. As contractility in infarct segments improve due to recovery of the stunning part of the injury, the resiproke hyperkinesia will regress as illustrated below.

Strain rate (A, B) and strain (D, E), of an inferior infarct at day 1 (A, D) and Day 7 after successful acute PCI (B, E). There is akinesia in the basal segment (yellow curve) and hyperkinesia in the apex (cyan curve). The hyperkiesia can be explained by the load reduction due to the lack of force from the infarcted segment. 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. After 92

Another patient shows the same segmental interaction, and with no effect on the regional mitral ring motion:

Day 1:

Patient with a small apical infarct at admission, showing reduced strain rate of - 0.25
s-1, and strain of  -2% in the apical segment (yellow), with slightly high strain ate and strain (-1.3s-1 and -25%, repectively) in the basal segments (cyan). Mitral ring motion is 16 mm, both by tissue tracking (integrated velocity, and by annular M-mode.

Day 7:

Same patient after sucessful PCI of the LAD. There is moderate recovery of contractility in the apical segment (to peak strain rate - 0.5
s-1 and peak strain - 7%). There is decrease in basal strain to 20%. Peak strain rate do not seem to have decreased, but as strain rate is instantaneous, we see that strain rate in the base at the time of peak strain rate in the apex has decreased to - 1s-1. The reciprocal changes in strain in the two segments results in no change in the regional annulus motion which still is 16 mm by both methods.

The hypothesis of the regional effects on the mitral ring is thus disproved by anatomy, by the load dependency of regional deformation and by studies (40, 92, 188)

There is no regional reduction of mitral motion in regional dysfunction.
Only global reduction of mitral motion, and segmental hypokiesia with resiprocal hyperkinesia.

The myocardium moves within the stiff framework of the annular plane and the "eggshell", but within this, there are differences in deformation, both in amount and timing, which will lead to segments deforming differentially.

Thus, as deformation is a result of tension, or rather tension versus load, strain does not measure function directly. But the effect of the force from neighbouring segments is part of load. Taking regional function into the concept of load, deformation imaging can be used to infer force, or at least inequalities in force developmen. This means that regional deformation is closer to contractility than global measures, which are dependent on absolute load. And that is the main point in regional diagnosis.

4: Regional circumferential and transmural strain

Regional circumferential and transmural strain may be sensitive indicators of infarct, but as discussed earlier, they will to a great degree be affected by geometry, not only layer function.

As discussed earlier, the circumferential strain is a function of wall thickening, causing the midwall line to shift inwards and thus shorten, not a measure of circumferential fibre function. At least in ischemia, if there is differential myocardial function, the reduction will always be most severe in the endocardial layer. However, in the case of reduced endocardial function, there will mainly be reduced transmural and circumferential strain due to reduced thickening (and hence, reduced circumferential shortening because of reduced inward circumferential shift, and not to the same degree due to reduced circumferential force. In that case reduced endocardial circumferential strain is a function of geometry. If there is reduced circumferential strength as well, as in more transmural ischemia which will affect the midwall circumferential fibres, resulting an an imbalance of forces equivalent to what is seen in the longitudinal direction. Thus there will be decreased load on the normal segments which may shorten more, stretching the affected segment, depending on the degree of stiffness. This is illustrated below:

Circumferential strain in a symmetrical ventricle model. For simplicity, the wall is divided into two layers. As the wall thickens, there is thickening and inward shift of the midwall line of both layers, but the innermost layer is in addition shifted inwards, cusing both a greater wall thickening (due to lack of room), and a greater midwall circumferential strain, both due to this, and due to the inward displacement of the innermost layer due to thickening of the outer layer. Akinesia of the inner (sub endocardial) layer. In this case there will be normal wall thickening and cicumferential shortening of the outer layer, and almost no thickening of the inner layer. Still, there will be inward shift of the inner layer due to thickening of the outer, this will reduce the space and may cause some thickening even without function. Mainly due to inward shift, there will still be midwall circumferential shortening of the inner layer. Reduced circumferential strength in a segment, will result in the normal segments contracing more (due to reduced regional circumferential load, and the affected segment may stretch. In that case this will also result in thinning, as the segmental volume stretches.

Thus circumferential and transmural strain will be much more profoundly affected by the transmurality of the infarct, as shown in an observational study (262), as in this case the circumferential tension is recuced. Some authors have found a higher sensitivity for transmurality by circumferential than longitudinal strain (221), which may be in accordance with this model. The interesting thing is that for identifying non-transmural infarction, the accuracy was highest for endocardial circumferential strain, and lowest for epicardial strain, with total wall thickness circumferential strain was in between (263). For identification of transmural infarcts, epicardial circumferential strain was more accurate, while accuracy of endocadial and total wall circumferential strain was lower and similar (263). This is in accordance with the model, but also confirms that circumferential strain analysis seems to be  feasible in clinical analysis. Whether layer strain will increase over all accuracy, compared to over all strain, needs to be confirmed by more studies.

5: Differences in segmental function changes segmental interaction and timing of segmental deformation

This results in specific patterns seen in ischemia.
There are fundamental anatomical and physiological reasons for this

The load dependency of deformation parameters, as well as the understanding of load as partly the global load (determined by the radius of curvature and the intracavitary pressure), and the regional load, being dependent on the force from neighbouring segements, is the basis for the differences in systolic deformation. Thus the main point is that deformation parameters are load dependent. But this means that if the contractility in one segment is reduced, the part of the load of neighbour segments that is caused by the contraction from that segment, is reduced.  This lead to increased deformation of neighbouring segments, due to reduced load - without any increase in contractility, and, concomitantly, the affected segment will show reduced deformation.  The global loss of contractility by a regional process (as ischemia or infarction) will reduce the global deformation, and within the ventricle the regional deformation will reflect the inequalities of force development (contractility). Thus, regional loss of contractility may be inferred from the reduced regional deformation.

This is extensively described in the basic physiology section.

As a segment becomes ischemic, there will be reduced energy (ATP) available, this will lead to:
  1. Slower tension buildup
  2. Lower total tension
  3. Slower tension devolution:
    1. The removal of calcium from the cytoplasm by the SERCA complex is necessary for releasing the actin myosin cross bridges, and this calcium removal is an energy demanding process, the release of the cross bridges, and hence, tension release is slowed (296). Thus, the tension remains longer in an ischemic segment. 
    2. Increase in load itself slows onset of relaxation (224). Weakening by ischemia may be considered a relative increase in load, and thus itself may be a contributing factor to reduced relacation rate.
But the deformation pattern of the ischemic segment is then a result of this process in interaction with non-ischemic segments. A mathematical model describing the segment interaction was published by the Leuven group (298). The focus on the segment interaction, to explain the deformation patterns is important, but the model is erroneous. The model errs in the timing of tension, as they confuse the time of active tension with the time of active buildup of tension, thus considering the period of tension devolution as a period without any muscular tension at all, which is wrong. During late systole and post systole, the model then is concentrating solely on the elasticity / active force interaction. And finally the model do not include the ischemic slowing down of relaxation (296).

In a totally passive segment, without any systolic shortening, the post systolic shortening may be simply passive recoil, as in the theoretical instance 5 above. However, even if there is holosystolic stretch, if the segment shortens more than it is stretched (instance 4), this is an indication of remaining tension, although too little to withstand the tension of healthy segments. This was demonstrated by Lyseggen et al (299).

An example of progressive ischemia during dobutamine stress echo can be seen below:

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.

Baseline shows slightly reduced strain rate and post systolic shortening in the apicolateral segment (cyan) already at rest.
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.

The same can be seen in strain rate colur CAMMs from the different stages:

Thus initial delay of shortening (tardokinesia) has been seen as a component of ischemia from early experiments (46) as well as in late experimental (304) and semi-clinical (305) work. It is commonly used as a method for assessing B-mode WMS i stress echo (tardokinesia - 306)

Post systolic shortening in ischemia

1: PSS is not only seen in ischemia.

It is important to realise that post systolic shortening is not only a phenomenon of ischemia, it can be seen both in left bundle branch block and hypertrophy. The mechanism is also in those cases asynchronous interaction between segments, but with different causes of asynchrony. While ischemia results in prolonged relaxation, LBBB results in delay of the whole activation relaxation sequence, and, surprisingly, PSS in not in the delayed wall, as the final mechanism for PSS is stretch - recoil, it occurs in the earliest wall (septum). Thus, the mechanics are different.

2: PSS in ischemia is only a part of a set of specific deformation changes in ischemia.

As seen above, PSS is part of a complex change in deformation pattern, which is the delayed evolution of tension, reduced absolute tension and delayed relaxation in acute ischemic segments interacting with normal segments that causes the pattern of initial stretch, systolic hypo-, a-, or dys kinesia, with post systolic shortening. 

3: Without normal segments there will be no PSS

Without any normal segments to interact with, there will in fact be no PSS, as shown by the following example where there is total ischemia, and hence, no normal segments and (almost) no PSS in the ischemic segments:

Severe ischemia in all walls in a patient with severe three vessel disease (among other things stenosis left main, occluded LAD filled from RDP, even with occluded RCA filled from collaterals) .  Visually, the most striking finding is fall in EF with increasing stress.

Strain rate colour M-mode.  No significant PSS can be seen (Except possibly apicolaterally). Thus at first glance, the M-mode looks normal, at least concerning synchronicity.
Strain rate  curves (top) and strain (botom) of the ventricle at peak stress. Again, no significant PSS can be seen (Except possibly apicolaterally), demonstrating clearly that there are little PSS  when there are no segments with normal contraction-relaxation cycles.  The AVC is evident from the phono traces. The strain curves show delayed and prolonged shortening, but more or less in all segments. This is equivalent to the balanced ischemia of scintigraphy.

Post systolic shortening (PSS) means that the segment continues shortening after the aortic valve closure, often after a short relaxation giving one or two peaks a systolic and a post systolic, or a single peak after AVC as shown in the figure below, left. The definition of shortening as post systolic is dependent on the location of AVC, which can be done by TDI as described above. This holds even in the presence of iskemia (with PSS) and in high HR (170).

Normal strain rate curves. Note that there is a little shortening of the lateral wall (cyan curve) after AVC (green vertical line). This is normal, and related to the shape change in IVR. Initial systolic stretch, reduced systolic shortening and presence of post systolic shortening in the apical segment (cyan curve), with normal systolic shortening and no post systolic shortening in the basal segment (yellow curve). Two different instances of post systolic shortening. Apicolaterally, there is stretching and then recoil after AVC (cyan curve), with possibly a little overshoot as indication of a remnant of tactive tension.  Apicoseptally there is systolic shortening and then further post systolic shortening (yellow curve), which thus has to be active. It also shows the mechanism for PSS to be different than recoil.  

The phenomenon of post systolic shortening in acute ischemia was demonstrated already by Tennant and Wiggers in 1935 (46), although it was not discussed explicitely in the paper. Already in the eighties, however, it was recognised that post systolic thickening and post systolic shortening was the same thing, due to the incompressibility as discussed above, and that the PSS in acute ischemia was a marker of active tension, and thus a possible predictor of functional recovery (297). 

Inferior infarct (yellow), showing both reduced strain rate and strain, with shortening after the normal shortening of the healthy segments (post systolic shortening). In this case, there is both systolic (although reduced) and post systolic shortening, thus the PSS has to be due to active tension, as in instance 2 above.

The presence of PSS in acute ischemia in the clinic was shown with M-mode by Henein (300), and later with strain rate by Jamal in 1999 (185) and Kukulski (99, 100).

Post systolic shortening has been proposed to an additional diagnostic criterion for ischemia in stress echo (113), but other studies has not shown additional diagnostic value of this (128).

As seen by the colour M-mode below, the presence of post systolic shortening in a segment, leads to a delay in the onset of segmental lengthening compared to the normal segments, so the finding is equivalent to the delayed compression/expansion crossover described by some authors (186).

Apical myocardial infarct in the inferolateral wall. Inward motion after systole can be seen in the apex.
In this case we see systolic stretch in the apex, and with PSS as in instance 4 above, midwall initial stratch and then systolic shortening with further PSS as in instances 2 and 3 above, and then normal shortening and relaxation in the base. That post systolic shortening in the infarct area is simultaneous with elongation (relaxation) in the normal basal part, is very evident from the colour M-mode.

Looking at tissue Doppler, there is post systolic motion of the borders of the midwall segment (lilac and orange curves), but very little in the apex (green) or the mitral annulus (white).
But this of course means that post systolic deformation happens in the apical segment (yellow coloured interval between green and orange curve).

The post systolic shortening is thus in the infarcted apical segment (yellow cirve, negative deflection) as seen from the strain rate .....
.... and strain curves.
Also, comparing strain and strain rate curves, with the velocities, it can be seen that post systolic shortening only reslts in relative motion, without much over all effect on the motion of the mitral ring.

Post systolic shortening can also be seen to affect flow directly, actually no surprise, but this was described early in an observational study (365) before the concept of PSS was fully described.

The post systolic shortening of the apex can in this instance be seen to cause an ejection of blood from the apex towards the base after normal ejection.
This is evident in the still frame from early diastole (top), and from the colour M-mode where the duration and extent of the jet cab be seen (arrows) just before onset of early filling.

As in the example above, the area of a- to dyskinesia is the area most affected by ischemia (instance 4 -5 above), while the surrounding area will have systolic and post systolic shortening as in instance 2 - 3 above showing a lesser degree of ischemia. 3D starin rate mapping will show this, the area of dyskinesia being smaller than the area of PSS:

Strain rate bull's eye and three dimensional reconstructions of a ventricle in systole (top), showing an area of dyskinesia (blue) in the apex, and diastole (bottom), showing a larger area of post systolic shortening (yellow). Strain rate bulls eye from systole and early diastole (top, left) , below 3D reconstruction (bottom, left) in systole and M-modes from all six walls (right), showing an inferior infarct with slight dyskinesia and more extensive akinesia in systole and post systolic shortening in a larger area also around the infarcted wall.

Duration of post systolic shortening after infarct

In acute ischemia, the prolonged tension / delayed relaxation is due to a reduced rate of removal of cytoplasmic calcium due to energy depletion. As shown in experimental ischemia, as well as in PCI studies, this reverses quickly with normalisation of flow ( 99, 100, 299, 300). However, longer duration of ischemia, or repeated ischemia will lead to a prolonger stunning of the myocardium, affecting both contraction and relaxation (301). Normalisation of systolic function would be expected to be paralleled by a reduction of PSS, as seen below:

Strain rate of an inferior infarct at day 1, showing akinesia in the basal segment (yellow curve), but with pronounced PSS during systolic relaxation. (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 PSS is correspondingly reduced.  (Image courtesy of Charlotte Bj÷rk Ingul).

Thus, PSS as well as systolic dysfunction is expected to be present for some time during the acute phase of infarction (92, 174, 188). Those studies showed that systoic function in affected segments normalised mainly within the first two days, with little improbvement during later obervation, thus reduced systolic function seen later would be permanent (loss of myocytes / scarring). PSS decreased concomitant with increase in systolic function. The post systolic shortening was about the same in border zone segments and infarct segments, despite infarct segments having lower absolute value of peak systolic strain rate. The PSS diappeared in the border zone segments in a week, but continued to decrease somewhat in the infarcted segments during a longer observation period (92), indicating that the diastolic stunning might last somewhat longer. However, some PSS remained also after 3 months.

Small acute apical infarct showing delayed onset of shortening, hypokinesia and post systolic shortening in the apicoseptal segment.
Same infarct 1 month after successful revascularisation of LAD, showing still some hypokinesia and post systolic shortening, although the PSS have decreased in amplitude.

In a cross sectional study (47) Voigt et al found PSS to be present in normals as well as infarcted hearts, in normals it was present in up to about 30% of segments, but then associated with normal systolic strain, and being both less in magnitude and earlier in the peak than in infarcted segments. It was present both in acute infarctions and in chronic infarcts. In acute infarcts, it was seen in 78% of ischemic segments, in older infarcts in 79% of scarred segments (which may presumably be fewer than in acute ischemia as seen above). Thus, the ischemic relaxation dysfunction is not the only explanation for PSS.

Loss of longitudinal fibres in myocardial infarction (210) will lead to loss of contractile force in the longitudinal direction. This is equivalent to a local increase in the load/contractility relation. Thus, reduced muscle mass will result in increased relative load from healthy segments, and this alone may be a mechanism for delayed relacation in affected segments (224), although without the additional delay from hypoxia. So, the PSS in infarcts would be expected to decrease in magnitude with time as shown (92).

Large apical infarct in the acute phase. Initial stretch (1), pronounced apical hypokinesia (2) and pronounced PSS (3).
Same infarct after 3 months, evidently some recovery of stunning, less tardokinesia, less hypokinesia, and the PSS is far less in magnitude.

Thus, post systolic shortening can be expected to decrease with the normalisation of ischemic stunning, but may partly remain where there is noticeable loss of fibres leading to reduced regional contractility.

Post systolic shortening and diastolic filling will interfere, as we see a delay in mitral annulus e' wave in walls with PSS:

Asyncronous motion.
Showing initial stretch, systolic hypokinesia and post systolic shortening in the apical half, PSS can be seen to be simultaneous with lengthening in the base, thus interfereing with the filling phase. THese effects may be real, as seen above, PSS can actually affect flow. 
Looking at annular velocities and comparing with mitral flow, onset of mitral flow in this case can be seen to be earlier than onset of annular elongation (e'), even in the lateral wall, but especially in the septum. This might indicate increased atrial pressure.

Diastolic effects of PSS are discussed further below under diastolic function. However, some authors have suggested that PSS is actually the cause of diastolic dysfunction. This is really putting the cart before the horse, to say it mildly. From the discussion above, it is really the other way around, delayed relaxation in ischemia that is the cause of ischemic PSS.

It must be emphasized that the presence of PSS is mainly a measure of inhomogeneity of force development, due to differences in activation, load or contractility, and not as specific marker of ischemia. While ischemia results in prolonged relaxation, LBBB results in delay of the whole activation relaxation sequence, and, surprisingly, PSS in not in the delayed wall, as the final mechanism for PSS is stretch - recoil, it occurs in the earliest wall (septum). Thus, the mechanics are different.


Asynchrony may arise from various mechanisms.

Left bundle branch block

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

left bundle branch block may have  very different mechanical effects. This is due to the very large variability in how much, and which parts of the left bundle that are affected, and to what degree.

Basically, left bundle branch block means a reduced conduction velocity in the left bundle, below that of the right bundle, causing the septum activation direction to shift from left-right to right-left, but also meaning that parts of the left ventricle are activated later than the right, and later than normal, causing a widening of the QRS. The mechanical effects of the LBBB may be quite various, however:

  • The Left bundle fans out in a mesh of fibres, and the conduction velocity may vary in different parts. (Most typical left anterior vs. left posterior hemi block)
  • The width of the QRS reflects the delay to the latest activation area. However, this may not be the mechanically most important parts. Thus, the width of the QRS have some bearing but not closely to the mechanical delay.

Thus, the mechanical manifestations are various:
  • 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.

The bundle branch block may cause
  • Inter ventricular asynchrony, with LV activation after RV activation. However, the onset of ejection is a poor marker of this, as ejection onset comes after IVC, and IVC is dependent on the load of the actual ventricle, as well as the contractility. Thus, a poor LV, will have a longer IVC, and ejection starts later, if the RV is more normal, this will cause delay in onset of LV conduction. If ejection should be used as a marker, it should use MVC compared to TVC.
  • Selective AV block to the left ventricle, causing shortening of the LV filling time
  • Intraventricular asynchrony in the left ventricle, due to the delay in lateral wall activation compared to the septum (even if the septum is activated right-left, this doesn't affect the time to activation of the septum to any noticeable degree.

Mechanics of asynchrony in left bundle branch block

The pattern of deformation in left bundle branch block is also due to interaqction between walls, as they interact differently when the activation sequence interact.

If there is intraventricular asynchrony, this is usually very evident, and the most typical marker is the "septal flash".

Septal flash

The most typical pattern, originally called "septal beaking"(as it was origially described in M-mode), was described early (251). Later, it has been termed "septal flash" (252).

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" is evident in both parasternal long axis and short axis. Images from patient with normal systolic function.
The same phenomenon is seen as "septal beaking" in M-mode of the same patient, a short inward motion starting at the peak of QRS, and peaking at the same time as the onset of inward motion of the inferolateral wall. The contraction of the lateral wall is the force terminating the septal flash, so the time from onset of septal flash to onset of inferolateral wall thickening is the true mechanical delay between the walls.
The isolated contraction of the septum probably will not generate pressure increase, but rather stretching of the lateral wall as seen by strain rate and apical rocking. During septal tension, the start of lateral wall contraction will generate pressure increase, which can be seen by the trasverse outward motion after the inward peak.

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 septal flash can be seen early, then the ejection, then late systolic stretch of the septum, which is due to the continuing tension in the lateral wall (being delayed), and then post systolic shortening of the septum due to recoil from the previous stretch, simultaneous with the relaxation of the lateral wall..
The M-mode shows the same. (Another patient, but the pattern is similar). The septal inward motion starts early during QRS (first vertical line). The peak is when the lateral wall thickening starts (second yellow line). During lateral wall thickening there is much less thickening of the septum, which actually seem to move outwards. Then at peak lateral wall thickness (i.e. when lateral wall starts thinning), inward motion and thickening of the septum starts again (third yellow line - post systolic thickening) and then peak septal thickening is simultaneous with the end of the steepest part of lateral wall thinning. 

The complex motion pattern in the septum must be explained by the interaction between the walls:

The different timing of the two walls is evident in the tissue Doppler tracing from the base of the same patient with normal ventricle. The action of the two walls can be inferred from the ring motion, and the interaction as one wall or the other is active while the other is passive, explains the complex pattern seen in the tissue Doppler above. This raises the question, which is the septal e' wave? The late systolic septal stretch, is the septal relaxation, but firstly, is mainly introduced by lateral contraction, and secondly, do not occur during filling. The post systolic shortening, is closest to the early filling, but is actually an impediment to the filling itself.
The strain rate from the same pateient shows this more directly, illustrating the simultaneous stretching of one wall and shortening of the other. We also see differences in timing between base and apex both in septum and the lateral wall.


The problems of defining e' is evident, while the late stretch is the true relaxation of the septum, it is not due to only relaxation, being facilitated by the simultaneous lateral contraction, the post systolic shortening is closer to, and dependent on the relaxation of the lateral wall, but as the relaxation of the lateral wall is taken up by the septal recoil, it does not generate so much suction into the ventricle (amnd the post systolic shortening may be seen as opposing filling. Thus, mitral inflow is seen to start late, and showing a low E/A ratio.

Rocking apex

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 where the whole heart rock (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 stays in the new position for a period as seen by the two curves lying close together. the there is slow motion towards the lateral wall, and then an abrupt reverse rocking (negative cyan peak - downwards motion of the lateral apexand positive yellow peak - upwards motion of the septal apex). Finally, there is even another reverse of the rocking after end 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.

Delayed intraventricular conduction, will lead to delayed activation of the lateral wall.

Thus, the septum will contract for a longer time alone, with no balancing tension in the lateral wall, meaning that the septal contraction is free to stretch the initially passive lateral wall as seen by the rocking apex. This again means that the initial contraction of the septum actually results in shortening and thickening of the septum, and simultanelos stretch of the lateral wall, with no pressure increase (A).  Thus, there is septal deformation (shortening) earlier than in the normal ventricle.

At the time of initial lateral wall contraction, there will be tension of both walls, leading to pressure increase. Continuing tension in both walls will increase pressure (IVC). The increase in pressure will start to push the septum back (as seen on M-mode, but not longitudinal shortening), thus the peak of the septal beak is the start of the lateral contraction (B).

Then there will be shortening of both walls, but with uneven tension, as the septum will start tension decrease while lateral wall tension is increasing. There has to be some remaining tension in the septum, or else, with a totally passive septum, lateral contraction would simply stretch the septum, resulting in only rocking with no real ejection work . However, ejection will lead to volume decrease, and thus shortening of the left ventricle. Once ejection is under way, there will be shortening of the septum even if it is largely passive (C).

When the septum is relaxed, the delay in the apex will also affect the relaxation, thus there is still tension in the lateral wall. This will lead to stretching of the septum (D).

Post systolic shortening in LBBB

And finally, there will be relaxation of the lateral wall, when this is passive, there will be elastic tension in the septum, and it will recoil in a post systolic shortening  (E).

Septal activation alone. leading to septal shortening and thickening, with concomitant lateral stretch - the septal flash. No pressure increase.
Lateral wall activation, ending the septal flash which peaks) with remaining septal tension (or else there would be only rocking, no pumping). In this case there is pressure buildup, MVC, IVC and probably start ejection.
During most of the ejection there will be shortening, but part of this may be passive due to volume decrease, especially in the septum.
In the last end of the ejection there will be little or no remaining tension in the septum, which then will stretch, due to the remaining tension in the lateral wall (which have been activated later). Thus, there will be stretch og the septum and shortening of the lateral wall.
Finally, there is no tension in the lateral wall, which relaxes. In this phase there will be elastic tenbsion in the septum due to the previous stretch, which will shorten in post systolic shortening, whil the lateral wall stretches (both due to septal shosrtening, but also in the course of normal early filling).

All of this can be summed up by strain rate colour M-mode:

The phases wall interactions above, visualised in colur SRI.

The pattern from the septum can be seen in this SRI M-mode (this is another patient). But here the delay between walls, as well as the phases being result og interaction between the walls is mode visible.

Thus, while ischemia results in prolonged relaxation, LBBB results in delay of the whole activation relaxation sequence, and, surprisingly, PSS in not in the delayed wall, as the final mechanism for PSS is stretch - recoil, it occurs in the earliest wall (septum). Thus, the mechanics are different.

This can be further analysed in detail 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 netiher in the apex nor in the base, so time to peak velocity is not sufficient to diagnose 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 yellow marker have been carried over from the previous image with tissue Doppler curve.
 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.

Thus, mechanical asynchrony in LBBB can be diagnosed by the septal flash or the rocking apex, but NOT necessarily by time to peak systolic velocity. .

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

As CRT now has been a well established treatment modality for heart failure with Left Bundle Branch Block (291, 292, 293), much interest has been vested in eliciting how mechanical asnchrony may affect pumping efficiency. It seems that the mechanism may in many cases be through mechanical inefficiency, due to asynchronous work by the left ventricle. Resynchronization may result in improvement due to more efficient work.

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

Of course, simplistic approaches such as using dispersion of "time to peak systolic velocity" would be far too simple. Especially, as the peak systolic velocity in many cases is the effect of recoil, not of deformation per se, and may be differently directed in the two walls, this is not a function of only electrical activation. Time to peak strain rate (and especially strain) is dependent not only on the onset of contraction, but also on the rate of force development, which is a function of contractility. Uneven contractility would thus be expected to be a factor in timing of peak deformation rate.

Septal flash is a marker of mechanical asynchrony per se, but not necessarily of mechanical inefficiency.

The concept of "wasted work" describing mechanical inefficiency has been suggested (290) as a description of how the work of shortening in one segment leads to stretching in another, instead of resulting in ejection. The concept may be fruitful, as it indicates that much of the work in shortening parts of the ventricle do not contribute to ejection work, but instead stretches another part of the wall, and is thus " wasted".

Another 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.

Mechanical inefficiency may be more evident in the next case:

There is septal beaking in the M-mode, start of the septal beak 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 and finally onset of post systolic thickening at the peak of lateral wall thickness (onset of 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 at C, 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 wasrted 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 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, compered to ECG, as is IVC, and the ejection period is longer.
However, there is still E/A fusion, indicating an AV-block to the left ventricle, so the CRT may not be completely 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.

However, this could only be demonstrated, by a comprehensive analysis of mechanics and hemodynamics. Also, the cardiomyopathy may still be the cause, and the LBBB only the worsening factor, creating a viciuous circle. (That LBBB was truly a worsening factor, was actually demonstrated by the improvement after CRT.

It 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.

This, of course is bad news for large scale studies looking for simple echo criteria / indexes that may predict CRT response, in the words of the PROSPECT investigators: no single echocardiographic measure of dyssynchrony may be recommended to improve patient selection for CRT beyond current guidelines (286).

Multivariate analysis may still show factors positively associated by response, but a comprehensive hemodynamical analysis should be worked into a scoring system, if it is to be evaluated.

Pacing induced dyssynchrony

Pacing is commonly done by a transvenous lead into the right ventricle. For reasons of safet, it is often placed in the RV apex, to minimise the risk of lead displacement. This however, means that the initial activation may be in the right ventricle, also activating the septum before the lateral LV wall, analoguous with the LBBB. (In fact RV pacing is LBBB). But the lead placement may give differente effects, especially the efect in the apex vs. the base.

Looking at the apical septum (this is partly a 4-chamber view), there is initial inward motion, and then outward motion as the rest of the LV contracts. This is equivalent to the "septal flash", and is distinguished from ischemic dysfunction by the dyssynergic segment contracting first. It is also evident that in this case, with pacing from the RV apex, only the apex shows the normal flash, while the basal septum shows the same delay as the lateral apex.
Strain rate M-mode shows that only the apical septum shows early shortening (flash), while the basal septum as well as the lateral wall show delayed shortening, which induces apicoseptal stretch, and then recoil shortening as the delayed segments relaxes (elongates).

The strain curves show the same as strain rate. Here the initial shortening is followed by stretch, and it is seen that the segment remains stretched until the relaxation of the delayed segements.
The findings of the M-mode are shown here in strain rate curves. The low strain rate in the lateral apex is an artefact, as it incorporates apical thickening as well.

Also, asynchrony may also arise from mechanical causes.

Ischemia as cause of asynchrony

We have seen that activation asynchrony may result in post systolic shortening in some segments, due to recoil mechanisms.

However, PSS due to ischemia, may induce mechanical asynchrony as well.

Presence of ischemic PSS may give 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 of the wall can be seen to move paradoxically, moving inwards (and towards the apex) after end of septal contraction.  Again, in a clinical situation, the interpretation can be facilitated by stopping and scrolling.

The velocity (motion) confirms the visual impression, the whole inferolateral wall moves downwards in systole, and upwards after end systole (Yellow and green curves), while the septum shows normal apically directed velocities giving a total asynchrony between the two walls. This asynchrony is also evident by the curved M-mode, starting a the inferior base, going through the apex and ending at the septal base.This might be due to both apical and basal ischemia.

The strain curves below, separates the effects of the segments, showing systolic dyskinesia (lengthening)  with some net post systolic shortening in addition to the recoil in the base (yellow curve), and systolic hypokinesia in the apical segment (green curve) with post systolic shortening, compared to a fairly normal strain curve in the septum. Thus, deformation imaging showing most severe ischemic reaction in the basal part, giving highest probability of a Cx ischemia, which was confirmed angiographically.

In this case, the tissue velocities are sufficient to detect the presence of ischemia, but the deformation imaging shows the location and extent of the ischemia, while velocities shows asynchrony of the whole inferolateral wall. Thus, the basolateral ischemia might have been mis interpreted for lateral asynchronia.

The presence of regional systolic dysfunction in combination with post systolic shortening, may cause asynchronous motion of a whole wall, as shown above. This means that the presence of asynchrony in motion imaging is not specific. A further example, also from stress echo; i.e. ischemia, is shown below.

3D colour velocity images showing motion towards the apex in red,  away from apex in blue.  Left, systolic 3D reconstructed image, showing normal motion in the septum and inferior wall, and paradoxical motion in the inferolateral, lateral and anterior wall. Right, om top are bull's eye from systole, showing the same, as well as early diastole showing inverse motion during the e-phase, i. e motion of the whole wall towards the apex in diastole. Apparently, the whole anterolateral half of the ventricle is ischemic . 3D strain rate images from the same recording, left systole, right early diastole, showing that the ischemia is due to a smaller ischemic area in the inferolateral, lateral and anterior apex, where there is streching during systole (blue).  This stretching, results in the midwall and basal segments moving away from the apex, despite contracting normally. In early diastole there is recoil in the ischemic area (yellow), resulting in anterior diastolic motion in the whole of the wall.  In this case, the ischemia is obviously limited to a part of the apex, the rest of the motion abnormalities being due to tethering.

In both these cases, it is evident that asynchrony between walls, as seeen by motion imaging is not real asynchrony, but an effect of tethering to a smaller asynchronous (ischemic) area. Thus, simply showing asynchrony by motion imaging is insufficient in the diagnosis of conduction abnomalitiy induced asynchrony.


In this peak stress image, the tissue Doppler confirms the presence of initial asynchrony: The whole of the inferolateral wall seem to show dyskinesia (Yellow and cyan curve), with early motion (after IVC) away from apex. It seems to be most pronounced in the apical part.The septal base moves normally, toward apex (red curve). By placing the sample volume in the aortic ostium, the high velocities of the aortic closure is identified, giving the timing of end systole. This timing can then be transferred to the deformation images below.
Stress echo. In this case, the image is suspect of a delayed inward motion of the base of the wall at start systole at medium and peak dose.

Strain rate (left) and strain (right) showing that there is a slight reversal of shortening in the early diastole, but only in the base (cyan) .  The delay, however, is shown to be entirely within systole. The clinical meaning of this is uncertain, but it was not due to ischemia, as the coronary angiography was completely ("super"-) normal.

In this case, the deformation imaging helps in the timing confirms the delay,but shows it to be less pronounced, and not indicative of ischemia, and it also helps in showing the the extent, compared to tissue velocity. (The patient had completely normal coronaruy angiography):

Thus, a possible explanation may be a partial bundle branch block at higher heart rate, although the ECG configuration is not markedly different on the Echo registrations.

Translation effects mimicking asynchronia

However, translation effects with motion of the whole ventricle, may also result in apparent asynchrony as shown before (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.

Post systolic shortening has to balance somewhere!

In post systolic shortening, the shortening is always due to imbalance in forces. It is this imbalance that means tat some or more segments translate into shortening.

  1. In ischemia, there is delayed relaxation due to energy depletion and deficient calcium transport, meaning that some segments maintain tension, longer than others. This tension inequality translates into post systolic shortening in some segments, normal elongation of others.
    1. If all segments are ischemic, there are no normal segments to interact with, and there will be no PSS despite ischemia and delyed relaxation.
    2. In chronic infarcts there is delayed relaxation due to relative overload where there has been loss of tissue, giving the same result, but to less extent
  2. In bundle branch block, there may be PSS due to inequalities of the end of tension. However, this PSS may be the result of interplay between tension and elasticity.
  3. In other cases, there may be interaction between tension and cavity pressure, and PSS may be global, without any segments stretching at all. However, not only cavity pressure, but also shape has to change.

Post systolic shortening in hypertrophy

In pathological myocardium this has also been demonstrated in hypertrophic cardiomyopathy, where the prolonged contraction persists into diastole, even causing ejection from the hypertrophied apex (87).

Recording from a patient with apical hypertrophic cardiomyopathy.  During systole there is virtual obliteration of the apical cavity.  Ejection can be seen in blue, and there is a delayed, separate ejection from the apex due to delayed relaxation. There is an ordinary mitral inflow (red), but no filling of the apex in the early phase (E-wave), while the late phase (A-wave) can be seen to fill the apex.  Left,  a combined image in HPRF and  colour M-mode.  The PRF is adjusted to place two samples at the mitral annulus and in the mid ventricle just at the outlet of the apex. The mitral filling  is shown by the green arrows,  and the late filling of the apex is marked by the blue arrow.  In addition, there is a dynamic mid ventricular gradient shown by the red arrow, with aliasing in the ejection signal in colour Doppler. The delayed ejection from the apex is marked by the yellow arrow (the case is described in (87).  
Strain rate from the same patient, showing PSS in the apical part of the septum, and nearly the whole of the lateral wall. (images were made in a very early software, but yellow is still shortening, blue lengthening.)
In this case, the prolonged tension is in the apex and the lateral , and the compensatory lengthening is in the basal septum.

Also in hypertensive cardiomyopathy is PSS a frequent finding (187). Sometimes they are detectable by tissue velocities, but not always.

Patient with hypertensive cardiomyopathy

There is no evidence for PSS, in annular velocities, neither with colour (left) nor pulsed (right) Doppler.

However, PSS is seen with strain rate imaging:

Looking at the strain rate, there is evidence of reduced strain rate in the midwall septum (a finding that was commonly believed to be associated with hypertrophic obstructive cardiomyopathy, but is now considered more doubtful (346)), and post systolic shortening in the hypokinetic part, a finding that is associated with reduced and prolonged tension, and thus the prolonged tension translates into shortening of the midwall segment (cyan curve) when more normal segments relax, as described above.

As the lengthening and shortening balances, there is no over all post systolic shortening, but still visible locally.

Post systolic shortening due to wall-cavity interaction, not segment-segment interaction

In another case, there is global post systolic shortening, i.e. not due to segment-segmentinteraction. How is that possible?

This patient has symmetric hypertrophy due to untreated hypertension.

Looking at the mitral ring, there is post systolic shortening both in the septal and lateral mitral ring.
Timing valve events by Doppler flow, they van be transferred to the analysis software
And the colour tissue Doppler confirms the presence of post systolic velocities both in the septal and lateral mitral ring, between aortic closure and mitral valve opening.

These post systolic velocities result in considerable post systolic apical displacement of the mitral annulus:

Reconstructed M-mode of the septal (right) and lteral (left) mitral annulus. Valve events are still transferred from Doppler flow recordings.
Displacement curves of the mitral ring obtained by integration of velocity curves above. Surprisingly they seem to give a slightly earlier maximum than the M-mode, although both are taken by the same software, and events are from the same Doppler cycles. (The red line is the apical displacement, which can be sen to be near zero.

But apical displacement of the mitral annulus must mean shortening of the whole ventricle, as the apex is nearly stationary. As this event is in the isovolumic phase, it has to mean a shape change of the whole ventricle, it has to become wider as it becomes shorter, as the blood within is incompressible.

Looking at strain rate, it can be seen that the post systolic shortening is present in all parts of both walls:

Looking at both walls they can be seen to shorten simultaneously during IVC, both by velocity curves (offset between apical (red and green) and basal (yellow and cyan), and by the strain rate curves.

Breaking the walls down to two segments each, both levels can be seen to have PSS in both walls.

As seen also by colour strain rate CAMM.
Now it seems to be a very paradoxical situation:
  1. There seem to be no segments stretching during the PSS, as all segments shorten simultaneously
  2. There is shortening of the whole ventricle in IVC, meaning that there has to be crosswise cavity expansion in order to conserve cavity volume
  3. There is wall shortening, meaning that there has to be wall thickening at the same time to conserve wall volume, and thus at the same time as the crosswise cavity expansion.
To answer the first question, it becomes necessary to look at flow:

Looking at colour flow, there is a delayed ejection of blood from the apex.
Looking at the colour flow reconstructed M-mode for timing, in systole there is ejection from the apex which stops, and then resumes during IVC, continuing even into early filling.

The finding is consistent with the fact that there is trapping of blood in the apex during ejection (as the ventricle becomes smaller, the wall becoming thicker), with pressure increase during the rest of the ejection period, and then release of the trapped volume during relaxation in the IVC.  Presumably, as the ventricle relaxes, the pressure in the trapped volume drops. AS this pressure drops, the continued (albeit decreasing) tension translates into shortening.

So in this case, there are no segments elongating to allow PSS in others. This is a case of tension-pressure interaction, i.e. wall-cavity.

By angling in, the trapped volume in the apex can be demonstrated, by ECH it is at end ejection if comparing with the colour M-mode above.
The shortening of the ventricle cavity can be seen in this image from the IVC, there is simultaneous flow out of the apec, and from the base of the ventricle towards the middle. This is not inflow, by the ECG it is during IVC by comparing to colour M.mode, and is simply the post systolic shortening lifting the blood by the motion of the base.
This can also be demonstrated by a properly aligned M.mode (although not as good for timing of the main flow events).

And finally comparing the longitudinal and transverse M-mode, both cavity expansion and wall thickening can be seen simultaneously during IVC:

Longitudinal M-mode from the septal mitral annulus, again showing PSS during IVC, reaching peak at MVO. The M-mode is generated by analysis software in order to keep event markers.
Transverse M.mode from a parasternal view, likewise generated by analysis software to keep event markers. The septum can be seen to thicken during IVC, reaching peak thickness at MVO. The septum and inferolateral wall can bee senn to diverge, indication crosswise cavity expansion as predicted. However, the pericardium om the inferolateral wall v┤can be seen to move more, indicating that also the inferolateral wall thickens.

This means that there is post systolic shortening, thickening and cavity expansion at the same time. In this case, it is the eggshell model that doesn't hold.

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