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.
🧵What is GLS? 1/ It is evident that it is some measure of the systolic LV longitudinal shortening, normalised for the diastolic LV length, after the basic Lagrangian formula S = (L-L0)/L0
But how do we chose the numerator and denominator? 2/ The simplest measure would be LV systolic shortening / LV end diastolic length. In the HUNT 3 study, strain by this method was -17.1%. pubmed.ncbi.nlm.nih.gov/32978265/
LV shortening can be approximated by MAPSE, so GLS is similar to MAPSE normalised for LV diastolic length. Average MAPSE of sep-lat was similar to average of sep-ant-lat-inf within the measurement accuracy in the HUNT3 study. pubmed.ncbi.nlm.nih.gov/29399886/
1/ During pre ejection, the vortex is seen to persist after MVC, and the septal part aligns with left ventricular outflow. This adds momentum and kinetic energy to the ejection flow.
2/ During ejection, however, the vortex seems to disappear, outflow more or less filling the whole apex, as flow in the lateral part is recruited by the rapid flow into the LVOT.
1/ The intraventricular vortex fills the ventricle, and the downwards flow in the septal part, will close the anterior MV leaflet. This also isolates the vortex in the ventricle, which may conserve the kinetic energy in the vortex
2/ At the end of diastasis, the lateral part of the vortex, with apical flow, is aligned with the incoming inflow in atrial systole, adding momentum and kinetic energy to the inflow during atrial systole.
🧵In our paper Intraventricular Vector Flow Imaging with Blood Speckle Tracking in Adults: Feasibility, Normal Physiology and Mech… we use a new method, not only BST, and can be applied on adult probes. pubmed.ncbi.nlm.nih.gov/34620522/
The main aim was to investigate the normal adult, intraventricular blood flow throughout the whole cardiac cycle, to compare with pw and colour Doppler M-mode and wall mechanics. (2D images courtesy of AS Daae).
As tweeted before, during IVR, there is simultaneous shortening of the base and elongation of the apex, inducing a volume shift with intraventricular apical flow, imparting a momentum and kinetic energy towards apex before start of early filling. This is thus *not* "wasted work"
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.