🧵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.
3/ Longitudinal strain has been the subject of a recent thread. Even if there is no basic definition, all instances are longitudinal shortening, which means negative strain as the wall becomes shorter: Sl = (L -L0)/L0 = (Ls - Ld) / Ld
4/ Given any degree of incompressibility, if the wall shortens, it has to thicken. Wall thickening is in the transmural direction, transmural strain is simply relative wall thickening. Wall thickening is thus largely a function of wall shortening.
Wall thickening occurs in the transmural direction, so transmural strain is nothing more than relative wall thickening: St = (WTs - WTd) / WTd, which is positive as the wall becomes thicker in systole. It can be estimated by M-mode:
6/ Thus, transmural strain should be on the order of 50%, as known from M-mode studies. Using speckle tracking the tracking is vulnerable to reduced lateral resolution. As lateral resolution decreases with depth, transmural strain cannot be estimated from apical views
7/ In transverse views, lateral tracking is poorer than vertical, in addition the values are smoothed, giving low values all over as in this example.
7/Firstly, there are no transmural fibres, and secondly if there had been, shortening would not result in wall thickening. Wall thickening is mainly a function of wall shortening and myocardial volume conservation (partial or total incompressibility).
8/ so what about circumferential strain? In systole, the outer diameter, and hence, circumference decreases somewhat, about 12 - 13%, we found in he HUNT study pubmed.ncbi.nlm.nih.gov/31673384/ This must be a measure of circumferential fibre shortening, geometric change cannot explain that
9/But as the wall thickens, midwall and inner lines move inwards, inner more than midwall. There would have been circumferential strain due to thickening of longitudinal fibres, even without circumferential fibres if there was pericardial restraint.
There is a gradient of strain from the outer to the inner circumference, as we did show pubmed.ncbi.nlm.nih.gov/31673384/
The gradients of strain will be subject of another thread.
11/ So circumferential strain is shortening, i.e. negative. But as circumference is Pi x D, so circumferential strain is equal to the shortening of the corresponding diameter, and circumferential strain is the negative value of fractional shortening.
12/ But this means that fractional shortening actually is circumferential, not transverse (radial) deformation, the true radial deformation is wall thickening. This is shown here: thicker wall will give reduced wall thickening (radial function), but increased FS.
13/ And the take home message: The three strain components have nothing to do with *selective* fibre function. They are the three spatial coordinates of ONE deformation of ONE object, the LV myocardium, and the summed function of ALL fibre shortenings.
14 / As there is very little myocardial compressibility, pubmed.ncbi.nlm.nih.gov/32978265/, the three strain components are very inter related, and longitudinal strain (if any) should be sufficient for global function
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/
🧵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/
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.
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.
🧵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"