🧵In our paper Intraventricular Vector Flow Imaging with Blood Speckle Tracking in Adults: Feasibility, Normal Physiology and Mech… we use a new method, not only BST, and can be applied on adult probes. pubmed.ncbi.nlm.nih.gov/34620522/
The main aim was to investigate the normal adult, intraventricular blood flow throughout the whole cardiac cycle, to compare with pw and colour Doppler M-mode and wall mechanics. (2D images courtesy of AS Daae).
As tweeted before, during IVR, there is simultaneous shortening of the base and elongation of the apex, inducing a volume shift with intraventricular apical flow, imparting a momentum and kinetic energy towards apex before start of early filling. This is thus *not* "wasted work"
1/ At the time of MVO and start of inflow, the AV plane also starts to move basally. This expands the space in the LVOT and behind the mitral ring, thus diverting inflowing blood laterally.
2/ This motion diverts blood flow downwards, creating vortices, counterclockwise in the LVOT, clockwise in the lateral part when viewed in a conventional 4-chamber view. The LVOT vortex is the largest as there is more room here.
3/ This diversion of blood flow, and start of diastolic vortex, is due to the ventricle being wider than the orifice, plus the expansion of the basal space, and thus starts near the LV base, as can be easily seen by CMM.
4/ The diverted flow into the LVOT is easily seen by pw Doppler, if you look for it, and is thus a normal phenomenon, although the E/A ratio in the LVOT will reflect the mitral E/A ratio, so a low E/A gives rise to the J-wave, which in reality is a high ALVOT.
5/ contrary to what has been published previously, this is not return flow from the apex. In our study, there was no delay between mitral E and e', while ELVOT had a delay of 116 ms. With an E of 82 cm/s, return flow from the apex would arrive after about 2 s.
6/ during early filling, the lateral vortex being smaller and clockwise, seem to be extinguished, while the counterclockwise LVOT vortex expands (LVOT continuing to expand basally and more blood being diverted basally, as well as inflowing blood being diverted closer to the apex)
7/ This has previously been described as vortex propagation pubmed.ncbi.nlm.nih.gov/7867035/
but is actually an expansion, and apical propagation can be seen by colour M-mode; both negative vectors along the septum and positive vectors along the mid-lateral ventricle.

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More from @strain_rate

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
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
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
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
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
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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