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).
And even in observational prospective studies, news methods aren't even compared to each other, only to EF!!!
So I don't think you can put the blame entirely on the method, the research community has to take some responsibility.

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More from @strain_rate

20 Sep
1/ Tweetorial. Prompted by a question of "layer strain", I'd like to go into that, as the concept is based on a completely erroneous perception of strain components somehow related to the directional fibre shortening. This is not the case.
2/ The three normal strains are longitudinal, circumferential and transmural (or radial). The relations between all three major strains are explored in the HUNT study: openheart.bmj.com/content/openhr…
3/ Transmural (radial) strain is simply wall thickening, while circumferential strain is fractional circumferential shortening, which, as the circumference is 3.14*diameter, equals fractional diameter shortening.
Read 18 tweets
16 Sep
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.
Read 19 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

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