Page 26 - Summary
This series tries to take the simplest view of the mechanics without defying the restrictions of cardiac anatomy. With regard to twist, it does not (and was not intended to) detract from the clinical usefulness of disturbances of twist being sensitive indicators of disordered ventricular function. The opinions that I arrive at are:There is no direct relationship between myocyte thickening and ventricular wall thickening. The increase in wall thickness is predetermined by the ratio of wall thickness to cavity diameter and the degree of myocyte shortening achieved.
Ventricular twist is caused by the slight dominance of the outer (anticlockwise) oblique myocytes. Biphasic rotation of the basal third of the left ventricle could be due to the superimposition of general rotation of the ventricle in a clockwise direction
Twist does not directly contribute to overall contractility. The development of the oblique layers is designed to minimise twist.
Long axis contractility is mainly generated by a net longitudinal vector from the opposing outer and inner oblique layers.
The change in dimension of the short axis projection of the epicardial rim is as good guide to myocyte shortening as is the endocardial short axis, possibly better.
References:
Page 3 - R.H. Anderson, M. Smerup, D. Sanchez-Quintona, M. Loukas, P.P. Lunkenheimer. The Three-Dimensional Arrangement of the Myocytes in the Ventricular Walls. Clinical Anatomy 22:64-76. 2009
Page 5 - N.B. Ingels. Myocardial fiber architecture and left ventricular function. Technology and Health Care, no 5 pp 45-52, 1997.
Page 7 - I. LeGrice, Y. Takayama, and J. Covell. Transverse shear along myocardial cleavage planes provides a mechanism for normal systolic wall thickening. Circ. Res., vol. 77, no. 1, pp. 182-193, 1995.
Page 22 - I.G.. McDonald. The shape and movements of the human left ventricle during systole : A study by cineangiography and by cineradiography of epicardial markers. American Journal of Cardiology, Volume 26, Issue 3, pp 221-230. 1970