Page 17 - The Problem of the Inner Wall
Having made such good progress with the outer wall, the inner wall provides a greater challenge, and one that I have been unable to model mathematically.
The main problem is that the advantage that an outer ring has over the mid-wall, which we discussed on the previous page, turns into a disadvantage for layers deep to the mid-wall. If unaided by some other mechanism, the deeper layers should not be able to keep pace with the mid-wall if they were circumferential, even less if they were angulated. Despite this, the dissections clearly show the deeper layers at an angle, in the opposite direction to the superficial helical angle.
There is a mechanism that can be invoked. It refers back to the fact that the models show that the mean systolic diameter of the cavity is a function of the diastolic diameter, the thickness of the wall, and the amplitude of outer rim shortening, the combination of which is the hydraulic effect on the endocardium. The inner mean diameter is a geometric result that is not a function of the tissue that comprises it. To make this point, look back on page 11. The inner ring shortening for our standard ventricle is 24%. Just suppose that the power of the outer wall was enough to manage the 15% shortening at the mid-wall, and that the inner 4.5mm of the wall was fat. The inner rim would still diminish by 24%. As stated earlier, this is quite counter-intuitive, but the maths is convincing.
Though I find it difficult to put numbers to it, I think the hydraulic effect is synergistic with cell contraction in these deeper layers, and the cells can be at an angle and not suffer a mechanical disadvantage. I suspect that the transition of the myocardium into a crenated and trabeculated structure on its endocardial surface is a mechanism to further accommodate the stresses involved.
Finally, there are the subendocardial longitudinal myocytes. It does not matter to them that the endocardial rim is contracting, indeed they are ideally aligned to cope with centripetal movement and reorganisation.
It is sometimes said that the 24% endocardial shortening indicates that the subendocardial cells are working harder than the rest. I submit that the hydraulic effect explains most of the change, and that this area works no harder than the rest.