#Cardiotwitter, thread no IV on mitral annular dynamics, still in the ejection phase, going rom early to late ejection (which was defined already by Wiggers).
1/ Early ejection measures;, peak flow velocity, peak annular velocity and peak global SR are all afterload dependent, by the peak determined by the early termination by the rise in afterload. Thus, peak velocities (or acceleration) are not measures of peak force.
2/Peak strain rate is velocity normalised for length apical velocity is near zero, they are equivalent in terms of contractility and load.
3/Even though strain rate is normalised for heart length, this do not give a better normalisation to body size, contrarywise, it increases the BSA dependency, and do not reduce biological variability. strain rate should be reserved for regional function. ncbi.nlm.nih.gov/pubmed/32154940
4/As ejection continues through the whole phase, the volume decreases, the wall shortens, despite the second part of the ejection phase has decreasing tension (relaxation), Thus we have myocardial shortening, but at the same time relaxation.
5/The end ejection measures are SV, EF, MAPSE and GLS. They are all closely related to the total ejection (but not pressure) work performed by the ventricle during the ejection phase, and they are all afterload dependent to the same degree.
6/As peak strain is annular displacement normalised for length, the apical displacement being near zero, they are equivalent in terms of contractility and load.
7/ Even though strain is normalised for heart length, this do not give a better normalisation to body size, contrarywise, it increases the BSA dependency induced sex dependency, which is is only due to body size. Strain should be for regional function ncbi.nlm.nih.gov/pubmed/29399886
8/Why is this? Annular displacement contributes 60 to 80% to the total stroke volume. Ventricular diameter and length increase proportionally with BSA openheart.bmj.com/content/3/2/e0…
Thus, even with equal MAPSE, a larger ventricle has larger SV. So MAPSE is less BSA dependent.
🧵 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/
🧵 As for MAPSE, we showed in HUNT3 thatpwTDI S' varies between mitral ring sites. LV global S' must be averaged, but we have shown that the difference between mean of septal/lateral and of septal/anterior/lateral/inferior is negligible.
2/ Values are age dependent, and in fact mean of 2 walls was 8.37 cm/s, and of four walls 8.4 cm/s, the difference was statistically significant, but totally un interesting as lower measurement limit of pwTDI is 0.1 cm/s. folk.ntnu.no/stoylen/strain…
3/ But what about diastolic velocities? variation of e' between sites is present as for S', as shown previously in HUNT3. It is common to average lateral/septal, but I haven't found any comparisons between two and four sites, so I looked at that in HUNT3 and found: