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J Am Coll Cardiol Img, 2008; 1:366-376, doi:10.1016/j.jcmg.2008.02.006
© 2008 by the American College of Cardiology Foundation
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Twist Mechanics of the Left Ventricle

Principles and Application

Partho P. Sengupta, MBBS, MD, DM*, A. Jamil Tajik, MD, Krishnaswamy Chandrasekaran, MD, Bijoy K. Khandheria, MD

Division of Cardiovascular Diseases, Mayo Clinic Arizona, Scottsdale, Arizona.


Figure 1
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Figure 1 Temporal Sequences of LV Twist During a Cardiac Cycle

The left ventricular (LV) rotation from apical and basal cross-sections of LV has been obtained by speckle tracking of B-mode cardiac ultrasound images (GE Healthcare, Milwaukee, Wisconsin) in a normal healthy subject. The difference between the 2 rotations provides an estimate of net LV twist angle (black line). During isovolumic contraction (phase 1), the apex shows a brief clockwise rotation and the base shows a brief counterclockwise rotation. During ejection (phase 2), the direction of rotation changes to counterclockwise at the LV apex and clockwise at the LV base, respectively. Torsional recoil occurs predominantly during the phase of isovolumic relaxation (phase 3) and early diastolic filling (phase 4).

 

Figure 2
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Figure 2 Myofiber Architecture of LV and Models for Understanding LV Twist Dynamics

Myofiber orientation in the left ventricular (LV) changes smoothly from a left-handed helix in the subepicardium to a right-handed helix in the subendocardium (A, left). Thick-walled cylindrical myofibers models proposed by Ingels et al. (A, right) and Taber et al. (B), showing the subendocardial fiber wrapped in a right-handed helix and a subepicardial fiber wrapped in a left-handed helix. Arrows (A) depict the circumferential components of force that results from force development in each fiber direction. The radii (R1 for subendocardium and R2 for the subepicardium) are the lever arms, which convert these circumferential components of force into torque about the long axis of the cylinder. The subepicardial fibers have a longer arm of moment than the subendocardial fibers (R1< R2). Figure illustration done by Rob Flewell.

 

Figure 3
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Figure 3 Sequence of Twist Mechanics Explained in an Experimental Animal Model

Electric and mechanical activation are initiated in the apical subendocardial region. During isovolumic contraction (IVC) (A), the subendocardial myofibers (right-handed helix) shorten with stretching of the subepicardial myofibers (left-handed helix), producing a brief clockwise rotation of the apex and a counterclockwise rotation of the left ventricular base. During ejection (B), the subendocardial and subepicardial layers shorten simultaneously, with shortening strains near the apex exceeding those of the base. The larger arm of moment of the subepicardial fibers dominates the direction of twist, causing rotation of the apex and base in counterclockwise and clockwise directions, respectively. During isovolumic relaxation (IVR) (C), subepicardium lengthens from the base toward the apex and the subendocardium from the apex toward the base. The subsequent period of diastole is characterized by relaxation in both layers with minimum untwisting (D). This figure refers to the experimental model that was used in Sengupta et al. (22). Figure illustration done by Rob Flewell.

 

Figure 4
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Figure 4 LV Twist in Health and Disease

Rotation of the left ventricular (LV) apex, the LV base, and the net LV twist angle (shown in red, green, and black colors, respectively) are assessed by speckle-tracking echocardiography in a normal subject (A), a patient with dilated cardiomyopathy with systolic heart failure (B), a patient with cardiac amyloidosis presenting as heart failure with normal ejection fraction (diastolic heart failure) (C), and a patient with constrictive pericarditis (D). Net ventricular twist is negative in dilated cardiomyopathy because of complete reversal of the LV apex rotation (B). In contrast, a patient with amyloid cardiomyopathy shows relatively preserved magnitude of net LV twist angle. In a normal subject, the onset of untwisting occurs just before the aortic valve closure (AVC) (A); however, in the patient with amyloid cardiomyopathy, the onset of untwisting is delayed after AVC (C). The patient with constrictive pericarditis (D) shows reduced magnitude of net ventricular twist and marked delay in the onset of untwisting. Phases 1 through 4 are defined in the Figure 3 legend.

 




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