#Cardiotwitter@fpmorcerf Thread. The end ejection is also a complex series of events, with interaction between the aortic and mitral valves that is reflected in the septal and ring motions.
1/ The determining AVC by Tissue Doppler has been subject to confusion. In the septum, just after the ejection, there is a short negative spike. This was assumed to be IVR, among other things based on the proximity to peak negative dP/dt, which, however only is a proxy for AVC.
2/ This negative velocity is seen in both septal M-mode, spectral Tissue Doppler, colour TDI, and even as a septal elongation in strain rate. It was visual even in colour TDI of the mitral valve. Thus, AVC was assumed to be at the start of this event.
4/ and it is easily seen by transferring valve motions from Doppler flow to Tissue Doppler recordings, where it seems that this negative velocity is mainly septal.
5/ so just as in the pre ejection spike, this is not IVR, and the true IVR (AVC to MVO) is from the end of the spike to start of mitral flow.
6/ But is this interesting? Yes, firstly for correct measuring of IVRT by using TDI. Secondly, because this in itself gives information about aortic valve closure. Myocyte relaxation, in the meaning of tensjon development, starts at peak LV systolic pressure.
7/ Shortening, continues, under decreasing tension, due to continuing, but decreasing outflow. At end of flow, there is no shortening, but continuing relaxation. This implies elongation with open aortic valve.
8/ The motion of the aortic root in a stationary blood column will in itself be a mechanism for closing the valve, and the valve closure itself be a mechanism for termination of this protodiastolic motion, but also the aortic orifice will "capture) a small volume at end ejection
9/ This has been shown experimentally, pubmed.ncbi.nlm.nih.gov/18606917/, both the volume increase before AVC, and that stenting of the aortic valve abolished the protodiastolic spike.
10/The protodiastolic motion of the mitral ring may be asymmetric, as the open aortic orifice will offer less resistance to the basal motion than the closed mitral valve
🧵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.