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🇳🇴🇩🇰Asbjørn Støylen 🇺🇦🇵🇸 Profile picture
@strain_rate
Oct 21, 2021 • 6 tweets • 3 min read • Read on X
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And the final short 🧵 from pubmed.ncbi.nlm.nih.gov/34620522/ about the findings in the ejection phase, continuing 🧵🧵
and
dealing with ejection.
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.
3/ At the same time, the AV plane with the closed mitral valve moves towards the apex. It seems that some of this recruited flow hits the mitral valve and is diverted back towards the apex, creating a basolateral momentum towards the apex again.
4/ -which after AVC leads into the IVC deformation creating a stronger momentum towards the apex before the start of early filling. Finding of a functional regional differential function (not "wasted work"), shows that Tau do not tell the whole truth about IVR.
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More from @strain_rate

🇳🇴🇩🇰Asbjørn Støylen 🇺🇦🇵🇸 Profile picture
Jun 18
🧵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
🇳🇴🇩🇰Asbjørn Støylen 🇺🇦🇵🇸 Profile picture
Jun 6
🧵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
🇳🇴🇩🇰Asbjørn Støylen 🇺🇦🇵🇸 Profile picture
Apr 18
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
🇳🇴🇩🇰Asbjørn Støylen 🇺🇦🇵🇸 Profile picture
Apr 14
🧵 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
🇳🇴🇩🇰Asbjørn Støylen 🇺🇦🇵🇸 Profile picture
Apr 10
🧵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
🇳🇴🇩🇰Asbjørn Støylen 🇺🇦🇵🇸 Profile picture
Apr 10
🧵1/ 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 wave prpagation velocity.
3/ Secondly, AS patients may have a higher wall/cavity pressure at end systole than controls, and thus higher pressure related stiffness.
Read 7 tweets

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