Page 7 - The Diastolic Shell - part 2
This page is pivotal in the solution to the conundrum. It is a vertical long axis view of a normal MRI, the same case as in page 6, with the diastolic epicardial shell again superimposed on the right hand systolic image.
Again, the epicardial surface has retreated from the diastolic shell (noting that the retreat at the apex is minimal, and the greatest movement at the basal (inlet) end, see page 19). A moment's thought will tell us that the volume of the green gap must equal the stroke volume of the cavity, as the volume of the myocardium is constant (well, near enough constant, it may expel up to 4% of its volume due to pressure on its vascular bed, but this is not enough to derail the argument).
And so it follows that the ventricular myocardium has to repack itself into a smaller space, and that as a direct consequence its walls must thicken. Furthermore, the degree of mean wall thickening has a direct and fixed relation to the diastolic volume of the cavity and the total volume of cavity plus the wall and the amount of inward movement of the epicardium. The images on this page show that the greatest change in space happens at the base. However the basal wall has no muscle. The repacking has to occur in the rest of the ventricle, and this is the main reason why the wall thickening is more apparent in the short axis views of the mid cavity.
In fact, it matters not what the constitution of the ventricular wall is; so long as it has enough contractility to move the epicardium inwards by the desired stroke volume, the mean wall thickening will be the same. If the walls were made of clay and you squeezed the stroke volume out with your hands, the wall thickening would be exactly the same as when the same stroke volume is ejected by the efforts of the wall itself. Indeed, the disproportion between myocyte thickening and wall thickening only appears to be a conundrum: there is no direct relationship between the two. The real question is: how does the myocardium manage to repack itself into the reduced space when it has become a turgid mass of contracting myocytes? The MRI tagging on page 6 has shown us the gross reorganisation it achieves, but does not show how the required movement of cell against cell is allowed. I think some of it must take place in the thin plates of connective tissue seen on page 2, and LeGrice has observed radial clefts in the collagen matrix which would allow considerable radial re-organisation. I am not qualified to comment further on the histology of the matrix: my task is to make some anatomic observations that are valid enough to have to be taken into account when the finer details of myocardial structure are investigated.
I hope I have made my point here. You might find it a novel way of thinking about wall thickening, and not particularly intuitive at that. It can be expressed in a mathematical way, making a couple of justifiable assumptions at the outset, and this I will do in the following pages. In the process, some interesting properties of the outer oblique myocardium will emerge.