Implications of the Mechanics of Torsion and Detorsion.
There is morphological agreement that the architecture of the LV muscle fibers produces systolic twists during ejection, with differential rotation of the LV base (clockwise) and apex (counterclockwise). The torsion phenomenon refers to the change in its angle of rotation, along the longitudinal axis of the LV. The intrinsic muscular mechanisms responsible for this phenomenon have only been deduced.
The helical architecture generates LV torsion when the DS contracts turning the base clockwise and when the AS co-contracts the apex counterclockwise, causing the torsion to be generated ”between the segments of the helicoid” 29,41. The interactions between torsion and recoil are independent of the maximum value of torsion because prolonged torsion delays unwinding, a process necessary to develop suction, affecting ventricular performance. The torsion ends when the DS stops contracting, since the unwinding by the AS cannot start until that happens (the isovolumetric relaxation phase), this process of prolonged torsion will eventually become a precursor of diastolic dysfunction. This interdependence between torsion and recoil emphasizes why diastolic dysfunction cannot be thought to exist in a patient whose ejection fraction is considered normal and healthy.
The evidence of septal deformation confirms the displacement in different longitudinal directions and the transition of the functionally overlapping fibers that pass along its septal hyperechoic line, where the longitudinal tension of the AS during pre-ejection and ejection shows the positive deformation (elongation) continuing during recoil, as shown by sonomicrometric and magnetic resonance imaging20,21. During cardiac resynchronization therapies, therapeutics should approach returning to the myocardium the mechanisms of myocardial torsion and detorsion, seeking better anatomical sites for LV stimulation, as we have discussed in this review, the movement of the heart is sequential, during an experimental study Liakopoulos etal43 evaluated ventricular torsion after isolated ventricular or biventricular stimulation and the torsion was inconsistent, finding that the interruption of the DS and AS contraction sequence explains the mechanisms of asynchronous ventricular shortening. On the other hand, the same study group showed that when the His-Purkinje conduction system is stimulated, the torsion phenomenon is restored44. This can be explained because the speed of electrical propagation is 10 times faster through the natural His-Purkinje fiber conduction system (3 m/s) than through direct stimulation of the ventricular muscle (0.3 m/s)45therefore the helical arrangement must be taken into account.