🧵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
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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!
🧵Atrial strain 1/ In Norway, we have an idiom: “The north wind is just as cold, from wherever it blows”, meaning the basic properties of something doesn’t change with the perspective you apply.
2/ AV-plane motion exerts opposite effects on the ventricles and atria: LV shortening vs Atrial elongation in systole, LV elongation and atrial expansion during early and late LV diastole. Thus, both LV and LA strain are inseparable from AV-plane motion.
3/ Global left ventricular systolic strain (GLS) is the relative shortening of the LV (wall) by the longitudinal contraction of the LV, the physiological interpretation is as a measure of myocardial systolic function.
🧵On the Wiggers diagram. It is an illustration of temporal relations of atrial, ventricular and aortic pressures with ventricular volumes, in a simplified, schematic illustration of the main relations, for basic teaching purposes, but is not the full truth about physiology.
The full picture is far more complex, the typical version of the Wiggers diagram as shown here, do not show the effects of inertia of blood, the knowledge from newer physiological studies with high-fidelity catheters, nor from Doppler and TDI. Let’s look at what’s missing.
🧵on ventricular ejection. Does blood always flow downwards a pressure gradient? Certainly not. A pressure gradient accelerates stagnant blood to flow down the gradient, but blood in motion may flow against the pressure gradient (by inertia), being decelerated.
2/ It was shown in the early 60ies that the pressure gradient from LV to Aorta was positive only during early ejection, and then negative during most of ejection. Pressure crossover occurred earlier than peak pressure. pubmed.ncbi.nlm.nih.gov/13915694/
3/ The negative gradient after pressure crossover would then decelerate LV outflow, so peak flow must be at pressure crossover. As flow = rate of LV volume decrease, peak rate of volume decrease mus also be: - later that AVO (due to the acceleration) - before peak pressure
Old misconceptions become as new. A 🧵 A recent paper focusses on pre ejection velocities as a contractility measure. In addition, the authors maintain that these velocities are isovolumic contraction, which they also maintain, is load independent. pubmed.ncbi.nlm.nih.gov/37816446/
All three concepts are wrong. True, the peak contraction velocity (peak rate of force development) occurs before AVO, and thus is afterload independent. But it's not preload independent and thus not a true contractility measure. pubmed.ncbi.nlm.nih.gov/13915199/
🧵 on atrial systole. 1/ Already in 2001, did we show that both the early and late filling phase was sequential deformation propagating from the base to the apex. pubmed.ncbi.nlm.nih.gov/11287889/
2/ This means, both phases consist of a wall elongation wave, generating an AV-plane motion away from the apex. So what are the differences?
3/ Only e’ correlates with MAPSE, so the elastic recoil is finished in early systole, while a’ do not, so atrial systole is a new event, caused by the next atrial contraction. pubmed.ncbi.nlm.nih.gov/37395325/
🧵1/ Sorry, I accidentally deleted the first tweet in this thread, here is a new and slightly improved version. Looking at the physiology of AVC propagation velocity, there are confounders galore, so taking it as a marker of fibrosis, is premature, to put it mildly.
2/ Firstly, The AVC is an event of onset of IVR, i.e at a part of heart cycle with relatively high cavitary and myocardial pressure. This may contribute to wall stiffness, which again may affect (probably increase) wave propagation velocity.
3/ Secondly, This may affect AS patients; who may have a higher wall/cavity pressure at end systole than controls, and thus higher pressure related stiffness.