🧵Having previously tweeted on the post ejection LV velocities and the relation to aortic valve closure mechanics,
from findings in our recent paper
I will now take a look on the isovolumic relaxation.
1/ In the paper pubmed.ncbi.nlm.nih.gov/34184410/ we found a consistent finding of isovolumic apical lengthening and basal shortening
2/ This, of course, indicates a volume short, from base to apex, even if total volume is constant.
3/ The relaxation in the apex, is probably related to the apical "untwisting". The basal shortening is probably due to prolonged tension, interaction with the apical relaxation.
4/ This volume shift causes an apically directed intraventricular flow, as know for some time. pubmed.ncbi.nlm.nih.gov/3624661/
5/ This can now also be demonstrated, both with colour M-mode, showing consistent apical flow both we-tally and laterally during IVR, as well as flow vector imaging. pubmed.ncbi.nlm.nih.gov/34620522/
6/ This, of course, means that the intraventricular blood pool already has an apically directed momentum before MVO, adding to the momentum of early filling.
7/ which means that IVC contributes to the kinetic energy of filling, as shown by this diagram, there is kinetic energy already at the start of LV filling (E). Figure from pubmed.ncbi.nlm.nih.gov/34620522/ top row is kinetic energy, left one representative curve, right all study subjects
8/ And as the simultaneous shortening at the base and elongation of the apex has a clear physiological function, the notion that shortening during IVR is "wasted work" must be considered totally non-sensical.
9/ Vector flow imaging. Loop by Annichen S Daae.

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More from @strain_rate

31 Aug
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.
Read 13 tweets
26 Aug
1/ our paper elucidates the end ejection tissue velocity spike as well, and relation to AVC.
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.
The close relation between AVC and the end of the pre ejection spike has been shown before by phonocardiography pubmed.ncbi.nlm.nih.gov/16364793/ , and by high frame rate B-mode of the aortic valve pubmed.ncbi.nlm.nih.gov/20331696/ .
Read 12 tweets
20 Jul
1/ Our paper on pre- and post ejection tissue velocities by #EchoFirst in relation to valve closures and openings is out: onlinelibrary.wiley.com/doi/epdf/10.11…
2/ 22 healthy subjects, Valve openings and closures timed by Doppler flow, and transewfrred to Tissue Doppler recordings. Image
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. Image
Read 12 tweets
19 Mar
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?
Read 7 tweets
27 Jan
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.
Read 10 tweets
7 Oct 20
1/ It's a pity that the publication perpetuate the error that myocardial work is load independent. imaging.onlinejacc.org/content/13/7/1…
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.
Read 6 tweets

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