🧵In our paper “Intraventricular Vector Flow Imaging with Blood Speckle Tracking in Adults: Feasibility, Normal Physiology and Mechanisms in Healthy Volunteers” pubmed.ncbi.nlm.nih.gov/34620522/ , findings were not only qualitative as described in previous threads, but also quantitative.
1/ Measures of kinetic energy (KE), vorticity (VO), energy loss (EL) and pressure gradients (PG) can be calculated. The figure from the paper shows the curves from all subjects in the study. What does these measures mean, and are they likely to add useful information?
2/ Starting with kinetic energy, this is the kinetic energy per volume, and can be integrated from the individual velocity vectors. As this was integrated over the 2D area only, the energy is given in J/m. The upper panel shows all subjects, the lower a curve from one subject.
3/ It's obvious that the peaks of KE is related to the in- and outflow phases where velocity peaks (and higher at the LV basis. This means that the pW velocities represent the resultant, and integrated KE represents mostly the same (squared).
4/ So chasing KE as a new measure, just because it's new, without establishing standards the method, and without any sound hypothesis that it gives added information seems unsound.😈 But what about Vorticity, which is a completely new measure?
5/ VO is the rotation of the blood in each point of the image, and is related to the complexity of the blood flow. It is calculated by the mean curl or momentum of the blood velocity field over the LV, and is given in Hz. However, still method dependent, with no gold standard.
6/ Which means
A: It can't be validated against other methods (like MR), B: Nor are values derived from different #echofirst methods comparable. However, qualitative information may be physiologically interesting, especially if they are consistent with other findings:
7/ VO peak seems to be somewhat more dispersed than KE, uncertain whether this difference in variability is methodological or biological. However, VO seems to peak close to, but slightly later than KE.
8/ This is consistent with qualitative findings that shows that the vortex is created by the interaction of inflow with the AV-plane motion subsequent to the inflow itself.
9/ Vorticity decreases in diastasis, but apparently less than KE, again consistent with the presence of a vortex through diastasis, where the septal flow closes the MV, and the lateral part conserves momentum for late filling.
10/ vorticity peaks again after peak KE of late filling, but this time extends into pre ejection, where the septal flow aligns the momentum with the ejection and closes the MV, while the lateral flow slowly fades, along with the whole vortex.
11/ vorticity decreasing during ejection where flow is mainly laminar, except at the very end where a slight apical momentum is imparted by the apical AV-plane motion.
12/ - and finally reaching minimum as the volume shift during iVR imparts a unidirectional flow gradient before early filling.
12/ VO is a new measure, and findings seems consistent with the qualitative evaluation of vortex formation, as well as colour flow and pw Doppler, so the physiology is credible.
13/ Caveats:
A:Actual peak values will differ with method.
B: There is no gold standard, ref. method will also be methodologically different, phantom validation might be possible though.
14/ I don't see the value of research stampeding along trying to run VO through the "sausage factory" of generating normal values or comparing patients with controls just because this is a new (and "sexy"?) method.
15/ so far, VO has confirmed what we see from flow patterns, and qualitative evaluation of the patterns and curve forms / timing, may give new information (like strain and strain rate) about physiology and pathophysiology, I'm specially optimistic about load.
16/ As you see, there are more measures available from the method, I'll probably return with a new thread about pressure gradients and maybe energy loss later.

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More from @strain_rate

Jul 25, 2024
🧵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. Image
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. Image
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. Image
Read 10 tweets
Jun 18, 2024
🧵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. Image
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.
#1 The atrioventricular pressure curves cross over in the middle of atrial systole, reversing the gradient from positive to negative, as documented by
Carmeliet;
Appleton: pubmed.ncbi.nlm.nih.gov/2208210/
pubmed.ncbi.nlm.nih.gov/9362417/
Image
Read 15 tweets
Jun 6, 2024
🧵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. Image
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/
Image
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 Image
Read 10 tweets
Apr 18, 2024
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/
Image
2/ Peak RFD corresponds to peak dP/dt, which is during IVC,m but closest to the AVO. pubmed.ncbi.nlm.nih.gov/5561416/
Image
Read 13 tweets
Apr 14, 2024
🧵 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/
Image
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? Image
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/
Read 12 tweets
Apr 10, 2024
🧵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. Image
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.
Read 11 tweets

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