Page 23 - Untwisting

The ventricle has to untwist and return to its diastolic resting configuration at the end of every cycle, or there would be the impossible situation of incremental rotation over successive beats. Untwisting is more than half complete during the isovolumetric phase of diastole.

It is easy enough to visualise the effect of tension imparted by systole into the framework of the myocardium (by general contraction and not just by twist) and into the compression of titin within the myocyte, such that the myocardium will try to "spring back" into its resting position. Delay in actin/myosin decoupling and fibrosis in the myocardium will detract from this springiness.

Classic wall anatomy and histology do not demonstrate a mechanism which could actively generate negative cavity pressure, i.e. "suck". Tangential myocytes cannot do it. It may well be that intruding myocytes, particularly in the subendocardial region, are increasingly angled downwards by the repacking process and so can provide a brief dilating force in early diastole.

These mechanisms will encourage early diastolic filling and assume greater importance during exercise. It is my opinion that they are still not the main mechanism of ventricular filling, which is the effect of a distending intracavitary pressure. I would submit that this pressure has been underestimated. In the clinical setting we measure it against a zero of atmospheric pressure. Surely it should be measured against the pressure immediately outside the ventricle, which is intrathoracic pressure, which is well below atmospheric?

I realise that manometry in the LV cavity can demonstrate shallow gradients during diastole, but I do wonder if they are inertial gradients and not driving gradients: the full Bernoulli equation has a section that caters for them.

On the subject of twisting in general, I must say that I have difficulty in seeing it ordinary MRI. I would have hoped that I could detect a 7 to 10 degree rotation of the apex for example. I can often see some, but not that much. I wonder if some of the rotational movement is due to irregular systolic repacking? Speckle tracking and MRI tagging might not be able to distinguish between rotation of part of the wall against other parts rather than rotation of the wall as a whole. Others will have to decide. What I do feel sure about is that the "wringing" action, even if it were true, is of such a slight degree that it cannot contribute significantly to systolic contractility.

Just for fun, perhaps the image below explains why I cannot see twist when it is present, as I can see twist in these illusions when it most certainly does not exist!