🧵While it is doubtful that GLS adds anything to MAPSE in global function, strain (and strain rate) are useful to assess differences in regional function, both in CHD and dyssynchrony. Regional myocardial work, however, doesn't seem to add information.
1/ The typical finding in CHD is delayed onset and reduced magnitude of systolic shortening, and post systolic shortening in affected segments as seen here in the apex (white curve - compare normal magenta curve).
2/ In segmental length-pressure loops, using a reconstructed pressure curve, the width of the loop at AVC, corresponds to the strain at AVC. But any regional difference in the loops, must be a function of the difference in strain, as all segments relate to the same pressure curve
In LBBB, the pattern arise from timing differences in the shortening-lengthening cycle betweeseptum and lateral wall, giving shortening of one wall stretching the other, in a complex pattern as seen here.
4/ The "wasted work" arises when one wall shortens, and the other in a passive state is stretched by this shortening, and can be identified by comparing strain from different walls. pubmed.ncbi.nlm.nih.gov/22520537/
5/ Again, the pressure curve is the same for both walls, and the difference in pressure-strain loops must be due only to differences in strain. In this image, the strain curves (below) are plotted against the pressure curve (white) to generate corresponding pressure -strain loops
6/ the "wasted work" seen by clockwise rotations the septal loop, arises from the stretching of the septum simultaneous with pressure rise, but is easily seen by divergence of the primary strain curves. There is no new information.
7/ using the same reconstructed pressure curve, but substituting regional strain with global strain, you get a measure related to global myocardial work. As longitudinal strain is responsible for about 60 - 70% of SV, strain based GMW should be less than SV based GMW.
8/ The area of the PV-loop is the true GMW. The height of the PV-loop is the SBP-LVDBP difference, the width is the SV. Mean SBP and mean LVDBP ((blue dotted rectangle), shows the relation in an easy way. GMW is SV x (mean SBP - mean LVDBP).
9/ As the reconstructed pressure curve onlu assumes diastolic LV pressure, and SV is available by Doppler or B-mode, I'm uncertain what GLS based GMW adds compared to a simple estimator of SV x SBP.
10/ Being the the product of SV and BP, it's a measure of myocardial work (i.e. = energy expenditure), and definitely load dependent, as preload increases SV, while BP is a measure of afterload, this was shown already by Sonnenblick. pubmed.ncbi.nlm.nih.gov/13978233/
11/ Unlike SV, EF, MAPSE or GLS, which ⬆️ with contractility and preload and ⬇️ with afterload, GMW ⬆️ with contractility, preload AND afterload. This means ⬇️ GMW is bad in HF, while ⬆️ GMW is bad in afterload states as HT or AS. So the clinical impact is uncertain.
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🧵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/
🧵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.
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.