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

Jul 25, 2024
🧵Atrial strain 1/ In Norway, we have an idiom: “The north wind is just as cold, from wherever it blows”, meaning the basic properties of something doesn’t change with the perspective you apply. Image
2/ AV-plane motion exerts opposite effects on the ventricles and atria: LV shortening vs Atrial elongation in systole, LV elongation and atrial expansion during early and late LV diastole. Thus, both LV and LA strain are inseparable from AV-plane motion. Image
3/ Global left ventricular systolic strain (GLS) is the relative shortening of the LV (wall) by the longitudinal contraction of the LV, the physiological interpretation is as a measure of myocardial systolic function. Image
Read 10 tweets
Jun 18, 2024
🧵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, 2024
🧵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, 2024
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, 2024
🧵 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, 2024
🧵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

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