A Practical Approach to Clinical Echocardiography 1st Edition

Chapter 15. Rotation, Twist and Torsion


The study of vectors of motion of the heart provides new insight into the intricate functioning of the heart muscle and detection of subclinical disease. In the left ventricle (LV), fibers in the subepicardium run in a left-handed direction, fibers in the midlayer run circumferentially and fibers in the subendocardium run in a right-handed direction. These myocardial fibers are connected to each other, with a smooth transition from subendocardium to midlayer, and then to subepicardium, about the long axis. Helical orientation of the heart muscle fibers creates several vectors of motion. Rotation is one of these along its long axis. Rotation is angular movement about the center of the mass in the left ventricular short-axis image. If a longitudinal structure like the LV has two ends, which rotate in different directions, the net angular movement is called twist. The LV twists in systole and untwists in diastole. Twisting produces ejection and also storage of potential energy. Untwisting is the recoil of twisted muscle due to release of potential energy. The terms 'torsion' and 'twist' refer to the same phenomenon and define the base-to-apex gradient in rotation. Torsion is the net twist angle divided by the long-axis dimension. Ejection is predominantly a result of the twist as longitudinal shortening is not capable of ejecting a normal stroke volume. Twist and torsion are gaining grounds as robust and valid mechanisms of the heart muscle function. Although of limited clinical utility at the moment, it is necessary to understand these vectors

of motion for greater future applications. Disturbed LV torsion may be considered as a marker for cardiac disease. In addition, quantification of LV torsion might be helpful in clinical decision making. It might indicate proper timing of aortic valve replacement or response to cardiac resynchronization therapy. Also, it could be used to monitor the effect of therapy.

Rotation is angular movement about the center of the mass in the left ventricular short-axis image. Looking from the apex, counterclockwise rotation is expressed with positive values and clockwise rotation with negative values, in units of degrees. Rotation of two ends (base and apex) occurs in opposite direction and this wringing motion is called twist. Torsion is more accurately defined as the base-to-apex gradient in rotation angle along the long axis of the LV, expressed in degrees/cm. Others express torsion as the axial gradient in rotation angle multiplied by the average of the outer radii of apical and basal planes. In echocardiographic examinations, torsion is nothing but net twist angle.


Torsion is the stress or deformation caused when one end of an elastic object is twisted in one direction and the other end is either held constant or rotated in the opposite direction (Fig. 15.1).

T orsion of the LV is the wringing motion of the ventricle around its long axis, induced by contracting myofibers in the wall.

Fig. 15.1: Graphical depiction of torsion when the twisting force is applied at two ends of an elastic object in different directions.

Fig. 15.2: Arrangement of myocardial fibers. The muscle fibers descend longitudinally from the base in the subendocardium and make a Fig. of ‘8' near the apex before starting the ascent subepicardially (helical configuration). In the middle, the fibers are arranged circumferentially.1-4

Fig. 15.3: Graphical depiction of the left ventricle short axis at the base (left side) and at the apex (right side). When viewed from the apex, the base rotates clockwise in systole and the apex rotates counterclockwise. The net difference in the angular movements (radians) is the twist.

A flexible elastic structure like myocardium stores mechanical energy when it is twisted. It also exerts a force in the opposite direction. The twisting force is proportionate to the angle it is twisted at. the stored energy is released during untwisting like a spring. Thus, the left ventricular muscle is like a helical torsion spring due to the arrangement of its muscle fibers (Fig. 15.2).

Subendocardial fibers are right-handed and have smaller radii than the subepicardial fibers, which are left- handed.1-3 the two helixes rotate in opposite direction, but

the rotation of the subepicardial fibers dominates because of greater angular amplitude. The arrangement of fibers is such that subendocardial fibers rotate clockwise at the apex during ejection but are overpowered by the subepicardial fibers with bigger radii, which rotate counterclockwise.2 At the base, the phenomenon gets reversed (Figs 15.3 to 15.7). During initial isovolumic contraction, the apex and the base both rotate in a counterclockwise direction when viewed from apex to base.

ttese muscle mechanics can be studied either by tagged magnetic resonance imaging (MRI) or by twodimensional (2D) or three-dimensional (3D) echocardio- graphic strain imaging using acoustic speckle tracking algorithms. Although considered more accurate, MRI requires considerably more time for acquisition, has less temporal resolution and is less affordable and accessible in most research and clinical environments. Indeed, the recent surge in interest evaluating LV rotation has coincided with the arrival of ultrasound tissue tracking.

Torsional deformation is sensitive to changes in endocardial and epicardial contraction, concentric remodeling and the fibrous architecture of the heart.

ttree factors govern rotation and torsion, and alteration in any of these will disturb twisting.

• Arrangement of muscle fibers as two helixes running down and up from the apex each separated by about 60° angle from the long axis.4

• Inotropy and lusitropy of muscle fibers and all the factors that affect these like preload, afterload, catecholamines, and so on.5

Figs 15.4A and B: (A) Rotation of the base-to-apex from end diastole to end systole; (B) Angular motion of the left ventricle long axis. Normally, near base, it rotates about 4° clockwise, while at apex, it rotates 12° counterclockwise in systole producing a net twist of 16°.

Fig. 15.5: Twist depicted graphically with simultaneous shortening in circumferential (C-C') and longitudinal (L-L') planes along with the net shortening in oblique plane (O-O'). Net shortening is greater than longitudinal or circumferential shortening and correlates with ejection fraction. Net twist is 90°-a.

• Relative balance between subepicardial versus subendocardial muscle fibers.

tterefore, distorted anatomy, reduced contraction and nontransmural involvement in a diseased process will all affect torsion.

As mentioned previously, subepicardial myocardial fibers run in a left-handed direction, and contraction of these fibers causes the base to rotate in a clockwise direction and the apex to rotate in a counterclockwise direction. Myocardial fibers in the subendocardial region run in a right-handed direction, and contraction of these

fibers causes the base to rotate in a counterclockwise direction and the apex to rotate in a clockwise direction (Figs 15.4 and 15.5). Radius of rotation of the subepi- cardium is greater than that of subendocardium and hence normally, the net effect is dominated by the action of subepicardial fibers. Conditions like constrictive pericarditis, which predominantly affect subepicardial fibers, produce hyporotation,6 while initial stages of pathological hypertrophy, which mainly affects subendocardium will result in hyper-rotation.7

Torsion gives rise to a principal shortening direction (i.e. direction of maximum contraction, O in Figure 15.5), which is oriented obliquely to the short-axis plane, in the approximate direction of the subepicardial muscle fibers. The direction of the principal shortening is relatively constant across the wall, despite the large change in fiber angle, so that the maximum contraction in the subendocardial wall is approximately orthogonal to the fiber direction. There is a constant relationship between torsion and shortening. Torsion to shortening relationship is a measure of intrinsic contractility and is load-independent7 (Figs 15.6 to 15.8).

Acoustic speckle tracking has made estimation of twist and torsion easy.8 However, before LV torsion can be used as a clinical tool, the physiology of the torsional deformation should be well understood. Mean values for systolic peak rotation, systolic basal and apical rotation, peak systolic twist, twist rate, peak torsion, diastolic peak untwist, untwist rate and time-to-peak untwist are usually measured.

Fig. 15.6: Basal rotation (mauve color) versus apical rotation (green color) giving rise to net twist (white color) throughout a cardiac cycle in a normal subject. Clockwise rotation is shown below the baseline (negative) and the counterclockwise rotation is shown above the baseline (positive). Net twist is 16° [11°-(-5°)]. Also note that during isovolumic contraction, the rotation vectors are opposite to that seen during ejection.

Fig. 15.7: Rotation of the left ventricle base in a normal subject by velocity vector imaging. Radians of all four segments are shown below baseline (negative) during ejection, indicating clockwise rotation. Note the heterogeneity of segments.

Fig. 15.8: Rotation of the left ventricle apex by velocity vector imaging. All segments show counterclockwise rotation (above the baseline) during systole.

• Torsion represents the myocardial rotation gradient from the base to apex of the LV.

• LV systolic torsion is an important mechanism of wall thickening and a primary component of normal systolic function. Mere longitudinal shortening of 15-20% cannot produce ejection fraction of 60-70%.• *

• It acts to normalize LV wall stress by minimizing transmural gradients of fiber strain and thereby, increase energy efficiency by reducing oxygen demand.

• Greater torsion occurs in the presence of increased concentricity (decreased radius/thickness ratio) due to increased mechanical torque advantage of subepicardial fibers over subendocardial fibers.

• LV torsion is followed by rapid isovolumic untwisting of the ventricle. During contraction, potential elastic energy is stored in the collagen matrix and cytoskeletal proteins (titin); its release (recoil) causes rapid untwisting and contributes to active suction of blood from the atria.9

• Normalized twist can be twist divided by distance from base to apex or individual rotation divided by corresponding radii.

• LV torsion is directly related to the circumferential- longitudinal shear angle.

• Both twist and shear angles were counterclockwise as seen from the apex and greater in anterolateral regions than in posteroseptal regions.

• Rotation occurs around the center of mass of the entire heart, which would be located more toward the inferoseptal region, instead of only around a centroid in the LV.

• Besides the magnitude of rotation, its timing also provides physiological information.9

• There is a positive relation between torsion and stroke volume, and ejection fraction. However, contraction and torsion are two independent phenomena.

Fig. 15.9: Graphical depiction of twisting rate (100°/s) and untwisting rate (138°/s) in a normal subject.

Fig. 15.10: Rotation of base and apex in opposite directions during ejection with net twist in white by acoustic speckle tracking.

Fig. 15.11: Apical rotation (counterclockwise, shown above baseline) by velocity vector imaging. Note the lack of smoothening of curves.

• LV untwisting rate is related to the peak twisting angle and the LV end-systolic volume, both in patients with decreased ejection fraction and in patients with diastolic dysfunction.10

• Left ventricular untwisting is the dominant deformation during relaxation and links systole with early diastolic recoil. ttere is a relationship between the LV pressure drop during isovolumic relaxation (recoiling), which generates diastolic suction, and untwisting.9,10

• Significant amount of untwisting occurs prior to the opening of mitral valve. Relaxation of torsion is a direct measure of the deactivation of myocytes and release of stored elastic energy, both of which facilitate rapid filling (Fig. 15.9).


Myocardial tissue velocities can be tracked at the base and apex in the short-axis plane, allowing for the determination of rotational velocities by tissue Doppler imaging (TDI).

the tissue Doppler technique of assessing torsion has been shown to correlate quite well with MRI; however, as with all Doppler recordings, there is concern about angle dependency. tterefore, torsion estimation using TDI is rarely used in clinical practice.

Rotation, twist or torsion can be studied by two different algorithms of 2D strain.

1. Acoustic speckle tracking (which tracks acoustic reflectors of a region of interest in time and space).

2. Velocity vector imaging (incorporates myocardial featuring, which tracks speckle as well as endocardial border simultaneously).

the values derived by the two methods have modest correlation with each other and can not be used interchangeably.11 ttere is a better validation of acoustic speckle tracking against tagged MRI. the speckles are tracked throughout the cardiac cycle to quantify the rotational displacement of the myocardium (Figs 15.10 and 15.11).

Methodological Details

• Short-axis 2D images are acquired at the apex and base (mitral valve level) using frame rates of 50-100 Hz and at least three cardiac cycles are stored. the width of the region of interest is adjusted as required to fit the wall thickness.

Fig. 15.12: Counterclockwise rotation of the six equidistant apical segments in degrees with the average value shown as dotted line curve in a normal subject.

Fig. 15.13: Difference in apical rotation values at true apex (17°, left panel) versus near the apex (11°, right panel).

Fig. 15.14: Net twist in a healthy elderly person 70 years of age. Note that net twist is increased (24°) with increased basal rotation.

• After manually tracing the endocardial boarder, computer software is used to automatically select 'speckles' and then track them frame by frame using the sum of absolute difference algorithm. Verify visually adequate tracking quality of endocardial and epicardial borders by the system.

• Circumferential motion (in degrees) and rates of rotation (degrees/s) are provided by the software for both a mean measure and for six equidistant regions around the circumference (Fig. 15.12).

• The software depicts net twist in degrees with time- activity curve as well as rotational velocities.

• Using the algorithm, twisting and untwisting rate can be easily estimated (mean as well as segment-wise) as shown in Figure 15.9.

• Rotational deformation delay is determined and defined as the magnitude of the time difference between time-to-peak basal rotation and time-to-peak apical rotation.

• It is also possible to estimate transmural torsion (endocardium, midmyocardium and epicardium). However, it has limited clinical utility.

• With low frame rates, the myocardial motion is too large frame to frame, and with frame rates that are too high, the opposite occurs.

• Speckle tracking-derived torsion and twist depend on numerous factors that require technical care, making the acquisition of high-quality images at the appropriate LV levels susceptible to error.

Limitations of Speckle tracking Method to Assess torsion

• High-quality images are required, which are not always possible.

• 2D strain suffers from limitation of through-plane motion.

• Imaging true apex remains a challenge (Fig. 15.13).

clinical applications of torsion

Torsion is an important index of cardiac function and provides additional information on myocardial performance over and above standard pump function indices. However, there are no large valid and robust clinical studies and the most information is in the realm of research, physiology and hypothesis-generating. The importance of measuring LV rotation lies in its potential

Fig. 15.15: Increased torsion of 25° in a subject with nonobstructive hypertrophic cardiomyopathy.

Fig. 15.16: Increased torsion (28°) in an asymptomatic patient with aortic stenosis.

for early detection of pathology. Systolic twist acts to limit myocardial energy expenditure by creating high intraventricular systolic pressures with minimal muscle shortening, resulting in efficient LV contraction. Reduced twist will, then, be associated with inefficient contraction. Increased torsion or twist, on the other hand, may be a compensatory phenomena or just a reflection of an imbalance between subepicardial versus subendocardial muscle fiber function.


Aging is associated with increased LV torsion secondary to reduced rotational deformation delay and increased peak basal rotation.12 Aging is associated with a decrease of contractile function in the subendocardium relative to that in the subepicardium without changes in ejection fraction. ttis impairment of subendocardial contractile function may be secondary to subendocardial fibrosis, asymptomatic subendocardial infarction or reduced subendocardial perfusion. The net effect is increased LV torsion due to unopposed action of subepicardial fibers and the preservation of ejection fraction in the elderly and reduced myocardial oxygen demand. Time-to-peak apical rotation occurs later in systole and closer to the timing of peak basal rotation with advancing age (Fig. 15.14).

Torsion may represent a compensatory mechanism to maintain an adequate stroke volume and cardiac output in the face of progressively reduced LV volumes and myocardial shortening associated with aging.


Elevated torsion and/or torsion-shortening ratios have been detected almost exclusively in patients with LV hypertrophy13 caused by increased hemodynamic loading conditions (i.e. aortic valve stenosis or hypertension), and in patients with hypertrophic cardiomyopathy (Figs 15.15 and 15.16). However, elderly patients with normal LV wall dimensions also show increased left ventricular torsion, indicating that age-related myocardial alterations contribute to changes in the pattern of contraction in this population.

Increased torsion is generally regarded as the result of impaired contraction of predominantly subendocardial myofibers (due to relative hypoperfusion of the thickened wall), leading to increased counteraction of contracting epicardial fibers, which have a longer lever arm. However, increased basal rotation has been observed more often in hypertrophic cardiomyopathy (Fig. 15.15).

A similar observation of increased LV torsion with unaltered circumferential strain in asymptomatic type I diabetes mellitus patients without morphological evidence of cardiac disease, contributes to the idea that intrinsic disease-related pathology might be responsible for differences in myocardial deformation.14

Increased torsional deformation also exists in healthy mutation carriers of hypertrophic cardiomyopathy, even in the absence of hypertrophy.15

Fig. 15.17: Dilated cardiomyopathy in a young male showing reduced rotation and torsion. There is prolonged unidirectional counterclockwise rotation during isovolumic contraction.

Fig. 15.18: Torsion in a 63-year-old male with heart failure with normal ejection fraction and Class IV symptoms. Note that rotation and net twist are maintained.

Fig. 15.19: Solid body rotation in a patient with left ventricle noncompaction cardiomyopathy.

Fig. 15.20: Negative net twist of -4° in a patient with end-stage systolic heart failure. Note reversed rotation of the base and the apex.


Torsion differentiates two phenotypes of heart failure. Torsional deformation is reduced in heart failure with reduced systolic function (Fig. 15.17) but is preserved in patients with normal ejection fraction (Fig. 15.18).

Heart failure with LV dilatation and reduced ejection fraction is characterized by spherical remodeling. This results in greater angle between the LV long axis and the helixes. Torsion is reduced as a result of more transverse orientation of the muscle fibers.16

Heart failure with normal ejection fraction (HFnEF) is characterized by normal torsion, although untwisting rate may be slowed in some cases.17

In advanced heart failure with spherically remodeled hearts, rotation at the two ends may be in the same direction with no net twist (Figs 15.19 and 15.20). This phenomenon is called solid body rotation.18,19 Solid body rotation was initially considered specific for genetic cardiomyopathy like noncompaction, mitochondrial myopathy, etcetera, but of late has been shown to exist in any advanced heart failure.

Other patterns of rotation in heart failure are being explored (Figs 15.21 to 15.23).


Constrictive pericarditis may have involvement of subepicardial muscle fibers either by fibrosis and

Fig. 15.21: Unusual biphasic rotation in heart failure with reduced ejection fraction due to markedly prolonged isovolumic contraction phase.

Fig. 15.22: Noncompaction left ventricle cardiomyopathy showing reduced twist and markedly prolonged time-to-peak twist.

Fig. 15.23: Mitochondrial cardiomyopathy in a 12-year-old boy showing solid body rotation in first half of systole followed by reduced torsion and prolonged time-to-peak torsion.

Fig. 15.24: Study of basal rotation in a patient with surgically proven constrictive pericarditis. Mean clockwise rotation is reduced (-1°) due to paradoxical counterclockwise rotation of the tethered left ventricle free wall segments.


• In patients with LV dyssynchrony due to heart failure, LV twist and torsion are negatively correlated with radial dyssynchrony.20

• Torsion improves after resynchronization (Fig. 15.28).

• Twist and torsion may be predictors of response to resynchronization therapy.21

• the difference in response may be due to lead placement, since LV leads positioned in midventricular

calcification or tethering.6 This can result in hyporotation and reduced twist (Figs 15.24 to 15.26).

Pericardium plays a significant role in maintaining myocardial muscle mechanics. Patchy involvement of pericardium with affliction of the underlying subepicardial fibers can produce several different patterns of rotation. Even unidirectional basal and apical rotation has been shown due to marked tethering at one or the other site (Fig. 15.26).

HFnEF has normal torsion but reduced longitudinal strain (Fig. 15.27).

Fig. 15.25: Reduced apical rotation (+6°) in a patient with constrictive pericarditis. Note significant reduction in counterclockwise rotation of the free wall segments. There is also post-systolic rotation.

Fig. 15.26: A 25-year-old male with constrictive pericarditis. Reduced twist due to both apex and base showing counterclockwise rotation. Ejection fraction was preserved due to normal apical counterclockwise rotation.

Fig. 15.27: Endomyocardial fibrosis in a 40-year-old female with heart failure. Note preserved twist despite restrictive mitral flow pattern.

Fig. 15.28: Apical rotation in a 60-year-old female with heart failure and left bundle branch block before (left panel) and after (right panel) resynchronization therapy. Apical rotation is shown, which improves significantly after therapy, although time-to-peak rotation is still prolonged.

and apical regions can exhibit a larger increase in systolic LV twist than LV leads positioned in the basal regions of the LV free wall.

acute and chronic ischemia

• In acute ischemia, apical rotation may be initially increased due to relative impairment of subendocardial fibers.22

• In regional ischemia or myocardial infarction, torsion is typically impaired in relation to the regional nature of the disease.

• In patients with myocardial infarction, twist is reduced and untwisting is delayed and prolonged.22

• Apical myocardial infarction can produce 'solid body rotation,' which tends to normalize after revascularization over time.

• Regional heterogeneity in ischemia can show varying patterns of twist and rotation.

Fig. 15.29: Apical hypertrophic cardiomyopathy with early diastolic dysfunction. Note enhanced torsion due to basal rotation.


dysfunction AND TWIST

• Significant increase in apical rotation, basal rotation, twist and twist rate occurs in those with Grade I diastolic dysfunction (impaired relaxation), while those with more severe diastolic dysfunction are not different from controls23(Fig. 15.29).

• Systolic-diastolic rotational coupling is always present. There are a variety of other cardiac conditions where

twist mechanisms are being studied to understand cardiac physiology and consequences of procedures, which alter the helical geometry of the LV like ventriculectomy, cardiac transplantation, and so on.

□ summary

Relative to end diastole, the apex of the LV rotates anticlockwise about its central axis, as viewed from the apex, at a relatively constant rate throughout systole, to a maximum value of approximately 10°. The base, initially rotating anticlockwise, reverses direction to give a net clockwise rotation by end systole of approximately 3°. The resulting end-systolic torsion is the difference between two rotations. During diastole, most untwisting or restoration of angular motion occurs in isovolumic relaxation.

LV torsion is circumferential-longitudinal shear angle corrected for length or radius. Amount and timing of LV torsion are directly related to the structure and function of the myocardium and myocytes. The proof of concept is there, but some methodological and validation issues still remain. Torsion has been calculated as relative rotation

(degrees), rotation per length (degrees/mm), torsional shear angle (degrees) and shear strain (dimensionless).

A unified way to describe LV torsion should be independent of the measurement method. Noninvasive measurement methods such as cardiovascular magnetic resonance tissue tagging and speckle tracking echocardiography must provide reproducible and comparable measurements of LV torsion, before they can be used as clinical tools for detection of myocardial dysfunction. It might be difficult to incorporate the circumferential- longitudinal shear angle approach in echocardiography, due to the lack of a reference coordinate system. However, new methods such as 3D speckle tracking might be able to overcome this problem.


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