The negative velocity post ejection spike had an average duration of 35 ms, ending about 10 ms after AVC in the septum. Thus, this spike is not isovolumic relaxation, and the true IVR (AVC to MVO) is from the end of the spike to start of mitral flow.
In the lateral wall, neither by velocity, strain rate, strain nor annular displacement, the post ejection lengthening was not so prevalent, and relation to AVC not so clear. This is important for correct measuring of IVRT by using TDI, it can only be done in the septum
5/ Relaxation is tension devolution, starting at peak LV pressure; last part of ejection being driven by pressure and inertial flow. At end of flow, there is no shortening, but continuing relaxation results in wall elongation, the post ejection velocity /displacement.
6/ This motion will be asymmetric, the open aortic valve offer less resistance than the closed mitral valve. The motion of the aortic root in a stationary blood column will in itself be a mechanism for closing the valve.
7/ the presence of vortices in the sinus valsalvae, will assist in separating the cusps from the aortic wall, reducing the energy necessary for AVC pubmed.ncbi.nlm.nih.gov/5635642/
8/ Also, this motion will cause the aortic annulus to move along, “capturing” a small volume that increases the LV volume, as has been shown experimentally. pubmed.ncbi.nlm.nih.gov/18606917
And the time course of AVC is concomitant with the post ejection lengthening (velocity spike), as shown in the paper and illustrated here in a skewed M-mode
through septum, aortic valve and posterior aortic annular rim.
10/ Lengthening before AVC also will give a more rapid AO pressure drop as shown by Wiggers (1921 Studies on the consecutive phases of the cardiac
cycle. American Journal of Physiology-Legacy
Content, 56, 415–438), termed by him "protodiastole", which thus is duration of AVC.
11/ The final closure of AV, will give an abrupt increase in resistance, stopping the post ejection motion: end of spike in vel/SR and notch in displacement/strain:
Apart from the physiological implications, what are the consequences of this study onlinelibrary.wiley.com/doi/epdf/10.11… for timing of valve openings and closures by tissue Doppler?
1/ Valve closures can be timed by tissue Doppler and mitral ring motion. However, only the septal motion will reliably show AVC.
2/ MVO is close to the END of the pre ejection spike. Timing MVC by the start of the pre ejection spike will result in an error of about 40 ms too early. Timing by the peak R wave will result in about the same error.
2/ 22 healthy subjects, Valve openings and closures timed by Doppler flow, and transewfrred to Tissue Doppler recordings.
3/ Pre ejection velocities started 24.8 ms after start QRS, with a duration of 51.5 ms, ending about 11.5 ms after MVC. Thus, both electromechanical delay and pre ejection velocity occurs *before* onset of IVC, and are not a measure of IVC or Isovolumic acceleration.
1/ Man ca 30, exertional dyspnea, CPET with normal VO2max, but pulmonologist concerned about possible drop in CO at peak exercise. Normal resting echo, no LVOT obstruction or gradient, no MR. Dobutamine stress: Chordal SAM, no regional ischemia
2/ Intraventricular gradient
3/ shown by CMM to be mid ventricular, moving towards apex in systole. No concomitant MR.
What next?
1/ #LBBB generates often a classical pattern on #EchoFirst. The pattern is very distinctive in Tissue Doppler of the septum.
The classical pattern arises from the time lapse of the activation and relaxation of the two walls, creating a pattern of interaction due to a sequence temporal imbalances of the tension between the two walls.
2/ As the septum is activated first, it contracts (shortening - septal flash) without activation of the lateral wall, which stretches. This generates slower pressure build up than a normal IVC, which then is prolonged.
It's the ratio of SV and BP that's closest to afterload dependence. MW being the *product* of SV (and hence also preload dependent) is very afterload dependent (although an inverted U relation can be hypothetisized.
3/ Thus, if SV ⬇️, MW⬇️, but if LVEDV also ⬇️, EF will ➡️. Sp far so good. But if BP ⬆️, MW⬆️, even if SV and GLS ⬇️ and EF➡️, as shown in pubmed.ncbi.nlm.nih.gov/32966690/, meaning that the demand increased while performance (SV) decreased, both due to increased afterload.
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.