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?
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.
3/ It is also dubious that the peak protodiastolic velocity is the peak velocity of unloaded shortening. Protodiastolic motion is terminated by MVC, which will influence the peak. Thus it is unlikely to be useful.
4/ What about IVC duration? As shown, it can be measured by TDI, although older publications have got it wrong, by including protosystole. Remember, true IVC is measured by Doppler flow. with sample volume between LVPT and mitral orifice.
5/ IVC duration, is inversely related to the (mean) rate of tension (pressure) development, and directly related to the SBP, as, for a given rate of force development, it takes longer time to reach a higher pressure. Thus, IVC is both pre- and afterload dependent.
6/ The closest measure to contractility, is the peak rate of force development, which can be measured by peak dP/dt. It occurs during IVC. As this is before AVO, it is actually afterload independent, but still, of course preload dependent by the Frank-Starling mechanism.
7/ Remember, if there is a small MR, it is measurable by Doppler, as long as the MR do not cause LA pressure rise.
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/
🧵 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/
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?
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/
🧵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.
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.
🧵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.
🧵 On early diastole. 1/ It is important to differentiate relaxation and myocyte elongation. Relaxation means tension devolution, due to the removal of Ca, and dissolution of actin/myosin cross bridges. Elongation means volume expansion. They are not simultaneous.
2/ Myoccyte relaxation actually starts during ejection at the time of peak pressure, the decreasing pressure during ejection shows decreasing myocyte tension. pubmed.ncbi.nlm.nih.gov/6227428/
3/ Simultaneously, ejection continues, chiefly due to inertia, until overcome by the Ao-LV pressure gradient, when AV closes. Thus, there is simultaneous myocyte relaxation (tension↓) and volume ↓ (= myocyte shortening). Here is blood flow / myocardial deformation interaction
🧵1/ The E/A fusion in mitral flow with higher HR is well known, normally occurring around HR 100.
2/ also, it should be well known that this occurs because the diastole shortens more with high HR than systole. But why?
3/ In an early study of intervals during exercise, we showed that the RR-interval and DFP, but not LVET shortened in parallel < HR 100. > HR 100 (< RR 600) Both LVET, DFP and RR interval shortened in paralell, but at a slower rate. pubmed.ncbi.nlm.nih.gov/14611824/