🧵What’s layer strain, and what does it mean? With speckle tracking, the ROI can be divided into layers, and strain measured selectively in each layer, both longitudinal strain in apical views, and circumferential strain in short axis views. But what is this actually?
Strains differ between layers, but the difference is NOT due to differences in fibre function in the different layers, it is again a function of geometry.
1/ 1/ starting with circumferential strain, which is conceptually easiest, in the HUNT study, with linear strains, we found outer Sc ca 13%, midwall Sc ca 23% and endocardial Sc 36%, so there is a clear gradient of Sc across the wall. pubmed.ncbi.nlm.nih.gov/31673384/
2/ In the previous thread on strain in three dimensionshttps://twitter.com/strain_rate/status/1459845380414353415?s=20, I showed Sc to mainly be a function of wall thickening, except the outer Sc, which is circumferential fibre shortening.
3/ let's look at that in more detail: Outer Sc pushes the myocardium inwards, where cross sectional area is smaller. Thus the wall will thicken a bit as the circumference decreases . And this wall thickening will push the endocardium more inwards that the outer.
4/ In addition to that, of course there is wall thickening due to the longitudinal shortening, as explained in the previous thread .
This will push the endocardium even further inwards.
5/ Consider the wall as two layers, separated by the midwall circumference. Outer layer expands due to being pushed inwards from circumferential shortening and thickens from longitudinal shortening. Thus midwall circumference, is pushed further inwards, and thus, shortens more.
6/ The outer layer will push the inner layer into an even smaller space, so the inner layer has to thicken even more, in addition to also thickening from longitudinal shortening, so it thickens more than the outer, expanding in a smaller space
7/ So there is a gradient of Sc across the wall but due to geometry, not differential fibre function. In the previous thread, I showed that Sc = relative diameter shortening.
8/ Midwall Sc is closest to mean wall Sc as measured by speckle tracking. But as it can be estimated by diameter shortening, In M-mode midwall diameter shortening will be: Sc = (((IVSd + LVPWd)/2 + LVIDd) - ((IVSs + LVPWs)/2 + LVIDs))/ ((IVSd + LVPWd)/2 + LVIDd)
9/ the gradient of Sc across the wall, will simply be the ratio of endocardial Cs / Outer Cs: Outer Sc = ((IVSd + LVPWd + LVIDd) - (IVSs + LVPWs + LVIDs))/ (IVSd + LVPWd + LVIDd), endocardial Sc = (LVIDd - LVIDs) / LVIDd.
10/ The gradient may give additional information, as a function of both longitudinal shortening, circumferential fibre shortening, wall thickness and LV diameter, but the concept "layer strain" is erroneous, as the gradient is continuous.
Now let’s look at longitudinal layer strain, which has also been reported with a gradient from outer to inner. As stated in a previous thread on GLS, , ST based LS, do not only track in the longitudinal direction, but also in the inward direction
This inward tracking means that the longitudinal shortening adds a shortening due to inwards motion as well, so ST based GLS overestimates the true shortening. In fact, there would have been apparent shortening even without shortening of the LV
12/ This effect is not due to curvature, but as the lines move inwards in a cone, they become shorter.
13/ As the wall thickens, the midwall line moves more inwards than the outer, and the endocardial line moves more inwards than the midwall. Thus the ST based GLS incorporates more of this artefact towards the endocardium.
14/ Just consider the absurdity if there had been more longitudinal shortening in the endocardium, the mitral ring would have torsion. And as the mitral ring is a part of the fibrous AV-plane this would make total havoc with the structure of the heart!

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More from @strain_rate

14 Nov
🧵Strain is defined in three dimensions; longitudinal, circumferential and transmural (radial). Each strain component defines deformation in one dimension. It is, however, absurd to consider the three components independently, or as reflection of shortening of specific fibres.
1/ Any three-dimensional object is defined by a three dimensional coordinate system. The simplest is the cartesian system of xyz. In the LV myocardium, being more of a a hollow ellipsoid, the longitudinal, circumferential and transmural directions are more convenient.
2/ Thus, systolic deformation of a 3D object occurs along the three axes, simultaneously. With some incompressibility (not necessarily total), deformation in one direction must relate to deformation in the two other, expansion in one usually follows shrinking in the two others.
Read 17 tweets
12 Nov
🧵GLS is higher (absolute values) in women,shown in the HUNT study by proprietary software pubmed.ncbi.nlm.nih.gov/19946115/, in meta analyses , lately in the Copenhagen heart study by ST (GE software) pubmed.ncbi.nlm.nih.gov/33624014/
and even MR pubmed.ncbi.nlm.nih.gov/25890093/
So, it seems pretty general
However, in the HUNT study, we found no significant sex differences in MAPSE (although a trend, p=0.1), but in a large study of 1266 subjects, the difference was small < 0.05mm - far below measurement limit). pubmed.ncbi.nlm.nih.gov/29399886/ Why, when both are long axis function?
1/ In our study, we compared GLS derived from segmental values by our software, with MAPSE normalised for the corresponding end diastolic wall length (straight line) and non-normalised MAPSE pubmed.ncbi.nlm.nih.gov/29399886/
Read 12 tweets
10 Nov
🧵What is GLS?
1/ It is evident that it is some measure of the systolic LV longitudinal shortening, normalised for the diastolic LV length, after the basic Lagrangian formula S = (L-L0)/L0
But how do we chose the numerator and denominator?
2/ The simplest measure would be LV systolic shortening / LV end diastolic length. In the HUNT 3 study, strain by this method was -17.1%. pubmed.ncbi.nlm.nih.gov/32978265/
LV shortening can be approximated by MAPSE, so GLS is similar to MAPSE normalised for LV diastolic length. Average MAPSE of sep-lat was similar to average of sep-ant-lat-inf within the measurement accuracy in the HUNT3 study. pubmed.ncbi.nlm.nih.gov/29399886/
Read 20 tweets
21 Oct
And the final short 🧵 from pubmed.ncbi.nlm.nih.gov/34620522/ about the findings in the ejection phase, continuing 🧵🧵
and
dealing with ejection.
1/ During pre ejection, the vortex is seen to persist after MVC, and the septal part aligns with left ventricular outflow. This adds momentum and kinetic energy to the ejection flow.
2/ During ejection, however, the vortex seems to disappear, outflow more or less filling the whole apex, as flow in the lateral part is recruited by the rapid flow into the LVOT.
Read 6 tweets
20 Oct
🧵Continuing the tweet the paper pubmed.ncbi.nlm.nih.gov/34620522/ into the diastasis: At end of early filling, the vortex fills most of the ventricle.
1/ The intraventricular vortex fills the ventricle, and the downwards flow in the septal part, will close the anterior MV leaflet. This also isolates the vortex in the ventricle, which may conserve the kinetic energy in the vortex
2/ At the end of diastasis, the lateral part of the vortex, with apical flow, is aligned with the incoming inflow in atrial systole, adding momentum and kinetic energy to the inflow during atrial systole.
Read 13 tweets
17 Oct
🧵In our paper Intraventricular Vector Flow Imaging with Blood Speckle Tracking in Adults: Feasibility, Normal Physiology and Mech… we use a new method, not only BST, and can be applied on adult probes. pubmed.ncbi.nlm.nih.gov/34620522/
The main aim was to investigate the normal adult, intraventricular blood flow throughout the whole cardiac cycle, to compare with pw and colour Doppler M-mode and wall mechanics. (2D images courtesy of AS Daae).
As tweeted before, during IVR, there is simultaneous shortening of the base and elongation of the apex, inducing a volume shift with intraventricular apical flow, imparting a momentum and kinetic energy towards apex before start of early filling. This is thus *not* "wasted work"
Read 11 tweets

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