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.
4/ This is why I have not considered MW (nor indeed myocardial power- being MW/time) especially useful, most businesses lok at supply (SV) vs demand BP, not supply x demand.
5/ Myocardial efficiency may be interesting, though, because it addressed how energy is utilised - another supply vs demand, but at the metabolic level. But far from clinical utility, however, and the inverse role of BP must be understood.
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.
Our last paper is out: Left ventricular longitudinal shortening: relation to stroke volume and ejection fraction in ageing, blood pressure, body size and gender in the HUNT3 study openheart.bmj.com/content/7/2/e0…
I'll discuss some of the findings and their implications in a thread
2/ 1266 subjects without history of HT, heart disease or diabetes, LV linear measurements of systolic and diast. wall thickness, length, and diameters, entered into an ellipsoid LV model.
3/ This gave us the possibility to look at age dependent changes in both volumes and functional measures, but with the two main limitations of the cross sectional nature of the study and for volumes the limitations of geometric model itself. There are still non-resolved issues.
1/ Tweetorial. Prompted by a question of "layer strain", I'd like to go into that, as the concept is based on a completely erroneous perception of strain components somehow related to the directional fibre shortening. This is not the case.
2/ The three normal strains are longitudinal, circumferential and transmural (or radial). The relations between all three major strains are explored in the HUNT study: openheart.bmj.com/content/openhr…
3/ Transmural (radial) strain is simply wall thickening, while circumferential strain is fractional circumferential shortening, which, as the circumference is 3.14*diameter, equals fractional diameter shortening.
1/ #GLS is not an objective measure, it's totally method dependent, and therefore with no gold standard, and no possibility of validating measurements. Why is this?
2/ Let's go into the definition of strain. The Lagrangian definition is S = (L-L0)/L0, change in length divided by original length. For GLS, that means (roughly) longitudinal shortening / end diastolic length.
3/ Since longitudinal shortening can be measured by longitudinal M-mode as MAPSE, this means GLS can be measured as MAPSE / end diastolic length.
1/ In the HUNT3 study, EF and GLS was highest in women, S' in men, while MAPSE showed no sex difference. The effect was present in all age groups. pubmed.ncbi.nlm.nih.gov/29399886/
2/ Sex difference was also independent of method for GLS. But it was a simple effect of body (heart) size, while MAPSE was BSA and sex independent. folk.ntnu.no/stoylen/strain…
3/ Why is this? We also found in the HUNT study that the LV length/external diameter ratio was BSA independent, so bigger LVs were both longer AND wider. pubmed.ncbi.nlm.nih.gov/27752332/
1/ I could go into the specifics of GLS (and perhaps I will later),but this pertains to imaging in general, not only GLS. Very few #echofirst measures have been evaluated as part of a treatment strategy, newer technology mainly in observational prognostic studies.
2/ But when treatment strategy is evaluated, we turn to the oldest measures, because that's where we have basic prognostic data. In valvular disease, we have pressures and stenosis areas, where intervention cut offs have been transferred from invasive to Doppler data
3/ But for ventricular function, even newer studies return to EF!! So EF have been evaluated as treatment guide for CABG, CRT, ACEI. And even in the present days, EF is the inclusion criterion for an ongoing post MI study of beta blocker treatment (EF>40).