#Cardiotwitter Prompted by a question earlier, I would like to go through the dynamics of the pre ejection dynamics of the mitral annular movements. 
1/ Electrical activation occurs earliest in mid septum and inferolateral base through the left anterior and posterior bundles, delay 5 - 15 ms. Additional elerctromechanical delay, 30 - 40 ms: Active contraction could be expected to start after about 50 ms; before the end of ECG.
2/ Pressure increase starts in accordance with this, before mitral valve closure, and as LV pressure at this point is low, some shortening would be expected too. By M-mode of the Mitral ring, a small, initial motion towards the apex can be seen.
3/ This, of course, is much easier to see in velocities, the pre ejection spike is a well known feature of Tissue Doppler. However, this is NOT the isovolumic contraction. Why not?
4/ The pre ejection spike occurs BEFORE MVC, as seen here (valve openings and closures from Doppler flow - different cycles). MVC is concomitant with the stop of apical motion.
This also verified with HFR IQ data, where both MV M-mode and TDI has been reconstructed from the same cycle. ncbi.nlm.nih.gov/pubmed/24210859
5/ This seems to indicate that the closure of the MV being the mechanism for the end of the pre ejection apical motion, and the other way around, the early contraction, after the end of blood inflow, is a mechanism for actually losing the mitral valve.
6/ Probably in addition to the vortex from late diastolic inflow, forming behind the anterior mitral leaflet, being delayed in relation to the inflow.
Basically, there is no ring motion during IVC, the ventricle being isovolumic, and concepts like isovolumic tissue velocity or acceleration are erroneous.
