However, in the HUNT study, we found no significant sex differences in MAPSE (although a trend, p=0.1), but in a large study of 1266 subjects, the difference was small < 0.05mm - far below measurement limit). pubmed.ncbi.nlm.nih.gov/29399886/ Why, when both are long axis function?
1/ In our study, we compared GLS derived from segmental values by our software, with MAPSE normalised for the corresponding end diastolic wall length (straight line) and non-normalised MAPSE pubmed.ncbi.nlm.nih.gov/29399886/
2/ Age was the most important source of biological variability in these normal subjects, declining with increasing age.
3/ MAPSE was weakly, related to body size, increasing with increasing BSA. More surprising, normalised MAPSE and GLS were both negatively correlated with BSA. Thus it seems to be normalisation for LV length per se, irrespective of method, that changes the relation with body size.
4/ Why? Firstly, we found previously that the ratio between wall length and diameter was independent of BSA and sex. This means, a longer ventricle also has a larger diameter. pubmed.ncbi.nlm.nih.gov/27752332/
5/ Secondly, MAPSE contributes between 60% pubmed.ncbi.nlm.nih.gov/17098822/ and 75% pubmed.ncbi.nlm.nih.gov/32978265/ (probably a little less than the latter) (Figure: If myocardium is incompressible, only outer contour change contributes to SV, as the myocardium inside don't change it's volume)
6/ As the main part of SV is MAPSE x area, larger area gives higher SV even with unchanged MAPSE. In the fig., a ventricle with 2x length, has 2x diameter and 4x area; increasing SV in proportion. At the same time the 2x length increases strain denominator, halving the strain.
7/ Thus it seems that the correction for length only, not diameter, which is done by strain, amounts to a systematic error that reverses and increases (absolute) the body size dependence of strain compared to MAPSE.
8/ In the HUNT study, BSA was significantly lower in women. In linear regression, sex was not significant for normalised MAPSE, and in three dimensional analysis of linear strain, sex was not significant for any of the strains pubmed.ncbi.nlm.nih.gov/31673384/.
9/ Thus it seems that sex differences in strain is mainly size differences, and the cause of this is the unidimensional nature of strain, which amounts to a systematic error.
🧵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.
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.
🧵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.
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/
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
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.