1/ In the paper pubmed.ncbi.nlm.nih.gov/34184410/ we found a consistent finding of isovolumic apical lengthening and basal shortening
2/ This, of course, indicates a volume short, from base to apex, even if total volume is constant.
3/ The relaxation in the apex, is probably related to the apical "untwisting". The basal shortening is probably due to prolonged tension, interaction with the apical relaxation.
5/ This can now also be demonstrated, both with colour M-mode, showing consistent apical flow both we-tally and laterally during IVR, as well as flow vector imaging. pubmed.ncbi.nlm.nih.gov/34620522/
6/ This, of course, means that the intraventricular blood pool already has an apically directed momentum before MVO, adding to the momentum of early filling.
7/ which means that IVC contributes to the kinetic energy of filling, as shown by this diagram, there is kinetic energy already at the start of LV filling (E). Figure from pubmed.ncbi.nlm.nih.gov/34620522/ top row is kinetic energy, left one representative curve, right all study subjects
8/ And as the simultaneous shortening at the base and elongation of the apex has a clear physiological function, the notion that shortening during IVR is "wasted work" must be considered totally non-sensical.
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/