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.