1/ #GLS is not an objective measure, it's totally method dependent, and therefore with no gold standard, and no possibility of validating measurements. Why is this?
2/ Let's go into the definition of strain. The Lagrangian definition is S = (L-L0)/L0, change in length divided by original length. For GLS, that means (roughly) longitudinal shortening / end diastolic length.
3/ Since longitudinal shortening can be measured by longitudinal M-mode as MAPSE, this means GLS can be measured as MAPSE / end diastolic length.
4/ In the HUNT study, Mean MAPSE was 1.58 cm, with less than 1 mm Difference between mean of 2, 4 or six walls. pubmed.ncbi.nlm.nih.gov/29399886/ Mean end diastolic mid LV length was 9.24 cm (unpublished), giving a mean GLS of -17.1%
5/But this measure is only related to this specific choice of reference length (denominator). We previously chose the straight line from apex to the mitral points, calculating strain per wall and mean. pubmed.ncbi.nlm.nih.gov/29399886/
6/ This was more robust, the straight lines were closer to wall length, giving a measure closer to wall strain. But it's evident that this mean WL is a little longer than LVL,
9,47cm, and mean GLS by this denominator was -16.3%, lower absolute, because of the higher denominator
7/ Following the curved wall, would give even longer WL, and lower GLS, evident from the fig. We didn't do this exercise, as manual drawing would be to variable, and HUNT3 is vivid7 data. It could be done now, by automated methods in HUNT4, with better data, (If interesting).
8/ So even with these straightforward methods, the choices of denominator influences strain values, and there is no ground truth. Speckle tracking opens a new can of worms, as the algorithms are "black boxes", proprietary to vendors, and subject to change w/software versions
9/ There are, however some general priciples. In general, ST GLS tends to give higher absolute values, around -19 - -20%. Thus, even having curved ROIs following the walls ST draws in the opposite direction from the method outlined in tweet 7/. Why is this?
10/ Speckle tracking in general not only have curved ROIs, but also tracks crosswise motion of the speckles. As the wall thickens, this means that speckles move inwards in the cavity, in this example it's the endocardial boundary
11/ This is most pronounced at the endocardial border, leads so, but still present in the midway, and least at the external LV border. Most applications use either endocardial border, or a thick ROI, where mean motion most closely corresponds to the midwall
12/ But what happens when tracking a curved boundary that moves inward toward the curvature centre? Exactly, it becomes shorter. This effect is there, even when there is no longitudinal shortening, best illustrated with circumferential shortening.
13/ Circumferential strain is negative (shortening), but as seen by the unmoving diameter, this is *only* due to inward motion, which is a function of external circumferential shortening *and* wall thickening. pubmed.ncbi.nlm.nih.gov/31673384/
14/ But this means that tracking derived GLS actually over estimates the longitudinal shortening, by incorporating some curvature shortening, which again is mainly wall thickening. In my opinion, this is another systematic error in ST derived GLS.
15/ And as this inward motion due to wall thickening is most pronounced at the endocardium (due to full wall thickening, as opposed to midwall, which only relates to outer half thickening), this is probably some of the basis for the unsound notion of "layer strain".
16/ In addition, the black box ST applications all have complex algorithms with different choices for
-Assumptions of LV shape and ROI width
-Number, size and stability of speckles
-Spline smoothing along the ROI and weighting of the AV -plane motion
17/ Interestingly, we developed an in-house application for strain, tracking kernels longitudinally by TDI and transversely by ST, calculating segmental and global strain. It gave nearly the same GLS as the linear method in 5/.
18/ I would expect it to be subject to the same error by inward tracking as ST, but as this used TDI data with a low underlying B-mode FR and lateral resolution, the lateral tracking may have been so poor, the technical shortcoming offset the systematic error.🤯
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More from @strain_rate

15 Sep
1/ I could go into the specifics of GLS (and perhaps I will later),but this pertains to imaging in general, not only GLS. Very few #echofirst measures have been evaluated as part of a treatment strategy, newer technology mainly in observational prognostic studies.
2/ But when treatment strategy is evaluated, we turn to the oldest measures, because that's where we have basic prognostic data. In valvular disease, we have pressures and stenosis areas, where intervention cut offs have been transferred from invasive to Doppler data
3/ But for ventricular function, even newer studies return to EF!! So EF have been evaluated as treatment guide for CABG, CRT, ACEI. And even in the present days, EF is the inclusion criterion for an ongoing post MI study of beta blocker treatment (EF>40).
Read 4 tweets
9 Jun
#Cardiotwitter @fpmorcerf Thread. The end ejection is also a complex series of events, with interaction between the aortic and mitral valves that is reflected in the septal and ring motions.
1/ The determining AVC by Tissue Doppler has been subject to confusion. In the septum, just after the ejection, there is a short negative spike. This was assumed to be IVR, among other things based on the proximity to peak negative dP/dt, which, however only is a proxy for AVC. Image
2/ This negative velocity is seen in both septal M-mode, spectral Tissue Doppler, colour TDI, and even as a septal elongation in strain rate. It was visual even in colour TDI of the mitral valve. Thus, AVC was assumed to be at the start of this event. Image
Read 12 tweets
12 May
#Cardiotwitter: Continuing with timing. Timing can easiest be determined by Doppler, by the start of flows and the closing clicks of valves. The timing by Tissue Doppler is less obvious, but can be done, when the correct events are understood.
1/ IVC duration is shortened by rate of force development, which again is a function of preload and contractility, however also increased HR, by force-frequency relationship. Time to AVC depends on the SBP, I.e. afterload, so IVC is both preload, afterload and HR dependent.
2/ LVET is related to SV. Thus, just as IVC, it increase with preload and contractility. But on the contrary, LVET decreases with afterload (⬇️ SV). And finally, it decreases with HR. Thus, for LVET to be useful, HR correction must be applied (LVETc).
Read 10 tweets
9 May
#Cardiotwitter, thread no IV on mitral annular dynamics, still in the ejection phase, going rom early to late ejection (which was defined already by Wiggers). Image
1/ Early ejection measures;, peak flow velocity, peak annular velocity and peak global SR are all afterload dependent, by the peak determined by the early termination by the rise in afterload. Thus, peak velocities (or acceleration) are not measures of peak force. Image
2/Peak strain rate is velocity normalised for length apical velocity is near zero, they are equivalent in terms of contractility and load. Image
Read 10 tweets
6 May
#Cardiotwitter. Continuing the series on time intervals, I’ll now use some time on the ejection period. It’s not as simple as it may seem at first glance, and there is a lot going on. Image
1/ Comparing a tension length diagram of an isotonic/isometric twitch, and a pressure/volume (Wiggers)diagram. I've added the division of pre ejection into protosystole and IVC from previous threads. Image
2/ The ejection period is not isotonic, as pressure increases and then decreases, and the myocardial tension must follow a similar course. Thus the tension increase is only during the first part of ejection, and then tension decline so last part of ejection is relaxation
Read 14 tweets
30 Apr
#Cardiotwitter. Seems that the interest in the #mitral_annular_dynamics during pre ejection would justify a continuation.
1/ Firstly, I’ll return to the protosystolic peak velocity, it’s occurring before MVC. Thus there is no such animal as peak isovolumetric velocity or acceleration. But does it matter, what we call it, and what does the peak protosystolic velocity mean physiologically? Image
2/ It is the peak velocity of longitudinal shortening before MVC. At this point, the load is low (= LA pressure), so it is related to the velocity of unloaded shortening. But this occurs before peak rate of force development, and is not a contractility measure. Image
Read 9 tweets

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