/1 Strain is relative deformation in three dimensions; simple linear measures of end diastolic and end systolic dimensions. Linear measures are vendor independent, with no need for advanced technology, but the measures are method dependent.
/2 Strain analysis of the LV myocardiumtreats the LV myocardium as ONE object deforming in three dimensions, longitudinal, transmural and circumferential.
The three normal LV strains; longitudinal, circumferential and transmural do not reflect directional fibre shortening, they are simply the three spatial coordinates of the total deformation of the three-dimensional object; the LV myocardium.
the xyz and longitudinal/transmural/circumferential coordinate systems are equivalent. Nobody would talk about three independent functions along the x/y/z axes, so why would it be along the l/t/c axes?
/3 The three strains are interrelated, indicating very little myocardial systolic compression. This means that the main information is carried by longitudinal strain. When an incompressible object deforms along ONE dimension, it has to deform along the other two as well.
When the LV shortens, it has to thicken. Wall thickening pushes both endocardial and midwall circumferences inwards so they shorten. Circumferential strain is the same as diameter shortening.
/4 There is a gradient of circumferential strain from outer to inner circumference. Outer circumferential shortening is the true circumferential fibre shortening, while the deeper circumferential strains are increasingly a function of wall thickening.
/5 All three strains are body size, gender and age dependent. Gender dependency is only due to body size. Both age and body size dependency is highest for longitudinal strain.
All there strains decline with age. Thus, there is no increase in short-axis (circumferential) function to compensate for the reduced longitudinal function, despite preserved EF by age.
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🧵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.
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.
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.
🧵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.