Asbjørn Støylen 🇳🇴🇩🇰 Profile picture
Oct 3, 2020 18 tweets 7 min read Read on X
1/ Thread on myocardial work. What does it actually mean, and is it really useful? It is a spin-off from pressure-volume loops, which are an illustration to visualise the relation between stroke volume, pressure and contractility, and to assess physiology in animal experiments.
2/ The area of the PV-loop is LV ejection work. The height of the PV-loop is the SBP-LVDBP difference, the width is the SV. Mean SBP and mean LVDBP ((blue dotted rectangle), shows the relation in an easy way. GMW is SV x (mean SBP - mean LVDBP).
3/ This, of course means that it is definitely preload dependent, as increased preload increases SV. Increased afterload, on the other hand increases pressure work, but as afterload decreases SV, the relation is somewhat more uncertain.
4/ Physiological experiments show pre- and afterload dependence of GMW. But GMW is not a measure of contractility, but LV energy expenditure. Contractility is the *ratio* of pressure and volume, roughly BP/SV, while work is the *product* of pressure and volume, roughly BP*SV
5/ GLS, is a measure closely related to SV. Longitudinal shortening accounts for between 60 and 75% of SV, and this fraction seems to be fairly constant across ages and reduced function:
pubmed.ncbi.nlm.nih.gov/17098822/
openheart.bmj.com/content/7/2/e0… and
6/ Regional pressure strain loops are similar to global PV-loops, and shows regional oxygen consumption in animal experiments. pubmed.ncbi.nlm.nih.gov/7932236/.
7/ Using GLS and LV pressure gives a global pressure-strain loop; a proxy of true GMW. Longitudinal shortening contributes only a fraction to SV, this GMW proxy should be a fraction of the true GMW, although compensated somewhat by ST derived strain overestimating GLS somewhat.
8/ Non-invasive pressure can be obtained from standardised pressure curve, time-calibrated by valve closures and openings, pressure calibrated by brach. cuff pressure. There is 1: No assessment of pressure augmentation and 2: LVDBP from a standard curve, is assumed normal.
9/ It can still be valid for comparisons where these systematic errors may be assumed constant. But what does it mean physiologically, and what value clinically? Physiologically it is myocardial work (energy expenditure). But this increases by both output (SV) and load (demand)
10/ In an observational study, GMW correlated with both SBP and GLS, but a correlation between a compound measure and its components is hardly surprising. It
also correlated with SV, EF, MAPSE, and diastolic measures, also unsurprising.
pubmed.ncbi.nlm.nih.gov/31408147/
11/ In HFrEF, lower GMW predicted a poor prognosis, slightly better than GLS alone. pubmed.ncbi.nlm.nih.gov/32820318/ In this study, despite (lower) BP being significant in univariate analysis, it was taken out of the multivariate analysis.So then........
12/ But more hilarious: In a study of hypertension and diabetes, pubmed.ncbi.nlm.nih.gov/32966690/, GMW increased from normal to HT pts. (hardly surprising), and even more in pts. with HTR + diabetes, despite lower numerical GLS. So now, it seems that a *high* GMW is suddenly bad for you.
13/ So, it's not a measure of LV myocardial capacity, but a combination of performance and demand. Useful?......
But regional myocardial work was the start of it in the 70ies, it could probably be used to compare different regions of the LV. pubmed.ncbi.nlm.nih.gov/22315346/
14/ In this case, imitations of pressure curves are the same in all segments and do not matter. But so is the same with the pressure curve itself. It's the same pressure curve for all segments. So any difference in loops between segments, is only the difference in strain.
15/ The width of the loop at AVC = end systolic strain, and with the same pressure input, all differences in loop shape and area are due to differences in regional strain. This is true whether this is due to schema, conduction, or other regional discrepancies.
16/ But what about the wasted work concept? Wasted work can be seen in the strain - pressure loops, but has been demonstrated just as well by strain analysis alone, logical since only strain is different. pubmed.ncbi.nlm.nih.gov/22520537/
In my opinion, contractility is equivalent with supply (SV) vs demand (load = BP) - the ratio. Work is equivalent with supply x demand, what business finds this useful?

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More from @strain_rate

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
Apr 4
🧵 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. Image
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
Read 17 tweets
Mar 25
🧵1/ The E/A fusion in mitral flow with higher HR is well known, normally occurring around HR 100. Image
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/

Image
Image
Read 8 tweets

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