the assessment of left ventricular twist in anterior wall myocardial infarction using...

The Assessment of Left Ventricular Twistin Anterior Wall Myocardial Infarction UsingTwo-dimensional Speckle Tracking Imaging

Masaaki Takeuchi, MD, Tomoko Nishikage, RDCS, Hiromi Nakai, RDCS,Michiko Kokumai, MS, Shinichiro Otani, MD, and Roberto M. Lang, MD,

Osaka, Japan, and Chicago, Illinois

Background: Two-dimensional speckle tracking im-aging allows noninvasive measurement of left ventric-ular (LV) strain, rotation, and displacement. We inves-tigated whether LV twist would be depressed inanterior wall myocardial infarction (MI) as a result ofreduced apical rotation.Methods: Basal and apical LV short-axis imageswere acquired in 30 patients with anterior wall MI.Using commercially available 2-dimensional strainsoftware, time domain speckle tracking was per-formed, and regional LV strain, rotation, and radialdisplacement were obtained in each plane. LV twistwas defined as apical LV rotation relative to the base.Patients were divided into two groups according toglobal LV systolic function (normal LV ejection frac-tion [LVEF] group [LVEF > 45%, n � 16] and abnor-mal LVEF group [LVEF < 45%, n � 14]).Results: Circumferential strain in the apex was signif-

doi:10.1016/j.echo.2006.06.019

36

with normal LVEF group (�7.3 � 2.6 vs �13.5 � 4.1,P < .001). Peak LV twist was significantly reduced inabnormal LVEF group (5.6 � 2.6 vs 9.8 � 4.0 degrees,P < .005) mainly because of reduced apical rotation.Peak positive and negative twist velocity was alsosignificantly depressed (38.8 � 11.3 vs 52.1 � 19.3degree/s, P < .05, and �42.6 � 17.8 vs �63.4 � 28.0degree/s, P < .05, respectively). Significant correlationwas noted between peak twist and LVEF (r � 0.73, P <.001) and LV end-systolic volume (r � 0.56, P < .001).The twist-displacement loop was markedly distortedin abnormal LVEF group.Conclusions: Systolic twist was decreased and dia-stolic untwisting was depressed in accordance withLV systolic dysfunction in anterior wall MI. Theseresults suggest the significant impact of global LVsystolic function on LV twist and twist-displacementloops in patients with anterior wall MI. (J Am Soc

icantly reduced in abnormal LVEF group compared Echocardiogr 2007;20:36-44.)

Left ventricular (LV) torsional deformation, definedas the wringing motion of the heart as the apex rotateswith respect to the base around the LV long axis, hasan important role for both LV systolic and diastolicfunction.1-3 Abnormalities of torsional motion of theLV have been reported in patients with cardiomyop-athy,4-7 aortic stenosis,8-11 myocardial ischemia, andmyocardial infarction (MI)12,13 using tagged mag-netic resonance imaging (MRI). This technique,which is capable of assessing 3-dimensional motionof the heart noninvasively, has limited availability,thus, precluding its use in routine clinical practice.

The recent development of 2-dimensional (2D)ultrasound speckle tracking imaging has allowed LV

From the Department of Cardiology and Internal Medicine, TaneGeneral Hospital, Osaka, Japan, and Section of Cardiology, Uni-versity of Chicago Medical Center (R.M.L.).Reprint requests: Masaaki Takeuchi, MD, Department of Cardiologyand Internal Medicine, Tane General Hospital, 1-2-31 Sakaigawa,Nishi-ku, Osaka, 550-0024, Japan (E-mail: [email protected]).0894-7317/$32.00Copyright 2007 by the American Society of Echocardiography.

strain, rotation, and displacement to be evaluatednoninvasively.14-19 LV twist can be measured byrotation data in basal and apical short-axis views.Thus, this technique provides not only LV regionalstrain value but also an opportunity for the nonin-vasive construction of twist-displacement loops.20

Anterior wall MI is accompanied with regional wall-motion abnormalities in the LV apex. Because LV twistis predominantly generated from apical rotation, wehypothesized that LV twist might be depressed, andthe profile of twist-displacement loop could be dis-torted in patients with anterior wall MI. Thus, the aimof this study was to assess the influence of global LVcontraction on LV twist and twist-displacement loopsin patients with anterior wall MI.

METHODS

Study Participants

Thirty patients with chronic (duration � 1 month) ante-rior wall MI (mean age 69 � 11 years, 23 men) and 15
age-matched asymptomatic healthy volunteers (mean age

Journal of the American Society of EchocardiographyVolume 20 Number 1 Takeuchi et al 37

64 � 8 years, 8 men) were studied. MI was defined by theAmerican College of Cardiology/American Heart Associa-tion guidelines.21 The institutional review board of thehospital approved the study, and all study participantsprovided informed consent before participation.

Echocardiography

Echocardiography was performed using a commerciallyavailable ultrasound transducer and equipment (M3Sprobe, Vivid 7, GE Healthcare, Milwaukee, Wis). All 2Dgray-scale echocardiographic images were obtained usingsecond harmonic mode. LV volume and LV ejectionfraction (LVEF) were assessed using the modified Simpsonmethod from apical 4- and 2-chamber views. For theassessment of LV twist, two LV short-axis planes wereobtained at basal and apical levels at high frame rates(mean 78 � 6 frame/s, range 67-99). Care was taken toensure that the basal short-axis plane contained the mitralvalve, and that the apical plane was acquired distally to thepapillary muscles. At each plane, 3 consecutive cardiaccycles were acquired during a breath hold, and digitallystored in a hard disk for offline analysis. For the determi-nation of timing of cardiac events, mitral inflow and LVoutflow were recorded using pulsed Doppler echocardi-ography.

LV Strain, Rotation, and Rotational Velocity

From the basal and apical short-axis data sets, one cardiaccycle was selected for subsequent analysis. Using com-mercially available 2D strain software (Echopac PC,Version 4.03, GE Healthcare), the endocardial border ofeach short axis in the end-systolic frame was manuallytraced. A region of interest was then drawn to includethe entire myocardium. The software algorithm thenautomatically segmented the LV short axis into 6 equidis-tant segments (11-1 o’clock, anteroseptal; 1-3 o’clock,anterior; 3-5 o’clock, lateral; 5-7 o’clock, posterior; 7-9o’clock, inferior wall; and 9-11 o’clock, interventricularseptum) and selected suitable speckles for tracking. Oncecompleted, the software algorithm searched for specklepattern on a frame-by-frame basis using the sum of abso-lute difference algorithm. The speckle-tracking algorithmprovided a tracking score, representing the reliability oftracking based on the degree of decorrelation of the block-matching algorithm. The individual regional tracking scoreswere scored with values ranging from 1 (excellent) to 3(poor). Segments with a score of 3 were excluded from theanalysis. Finally, the software automatically defined theventricular centroid for the midmyocardial line on aframe-by-frame basis, and calculated the time domain LVstrain (radial and circumferential), rotation, rotationalvelocity, and radial displacement profiles for each seg-ment in both short-axis planes.

Regional strain curves were then analyzed, and peakradial strain and peak circumferential strain were mea-sured for each segment at both planes.

Counterclockwise rotation, as viewed from the LV apex,
was expressed as a positive value, whereas a clockwise
rotation was denoted as a negative value. Data pointsdepicting the basal and apical LV rotation and rotationalvelocities were exported to a spreadsheet program (Mi-crosoft Excel, Microsoft Corp, Seattle, Wash) to calculateLV twist and twist velocity. The averaged LV rotation androtational velocity profile from segments that could beanalyzed were used for the calculation of LV twist andtwist velocity. LV twist and twist velocity were calcu-lated as apical LV twist and twist velocity relative to thebase. To adjust for intersubject differences in heart rate,the time sequence were normalized to the percentage ofsystolic duration (ie, at end systole, t was 100%) anddiastolic duration (ie, at end diastole, t was 200%). Endsystole was defined as the time of aortic valve closure. Inaddition to the twist versus time profiles, peak twist, peakpositive twist velocity, peak negative twist velocity, andtime interval between the R wave on the electrocardio-gram and peak positive (negative) twist velocity weremeasured.

LV Twist-displacement Loop

At end diastole, displacement was 0. The moving distancefrom tracking point in the midmyocardial line at enddiastole to the corresponding point at the next frame wasmeasured on a frame-by-frame basis throughout one car-diac cycle. Radial displacement toward the LV centroidwas expressed as a positive value. Averaged radial dis-placement data at basal and apical short-axis planes weresummed, and divided by two to obtain a mean valueduring the entire cardiac cycle. By plotting twist-displace-ment data during one cardiac cycle, twist-displacementloops were created for each participant.20 To createaverage twist-displacement loops in different groups ofpatients, the time sequences were normalized to thepercentage of systolic and diastolic duration. Averagedtwist-displacement loops were plotted at 10% incrementpoints during the systolic period (ie, 0% end diastole,100% end systole) and at 5% increment points during thediastolic period (105% first 5% of diastolic period, 200%end diastole).

Statistical Analysis

Data are expressed as mean � SD. Data were analyzed usinganalysis of variance to compare the degree of rotation,twist, and its related variables applying a Boferroni’scorrection among the 3 groups. When comparing contin-uous data between two groups, the Student t test wasused. A P value of less than .05 was considered significant.

Interobserver measurement variability was determinedby having a second observer measure LV twist and radialdisplacement in 7 randomly selected patients. Intraob-server variability was determined by having one observerremeasure LV twist and radial displacement in 7 patients 1month apart. Interobserver and intraobserver variabilitieswere calculated as the absolute difference between thecorresponding repeated measurements as a percent of
their mean.

rvention

olumicentricul

Journal of the American Society of Echocardiography38 Takeuchi et al January 2007

RESULTS

Patients with anterior wall MI were subdivided intotwo groups according to LV systolic function (LVEF� 45%, n � 16, and LVEF � 45%, n � 14). Clinicalcharacteristics of the study patients are shown inTable 1. LV volumes, LVEF, and pulsed Dopplerechocardiography data in patients with anterior wallMI and age-matched healthy volunteers are depicted

Table 1 Clinical characteristics of the study patients

All patients (n � 30)

Medical historyHypertension 19 (63%)Hypercholesterolemia 16 (53%)Diabetes 9 (30%)

Characteristic of MIS-T elevation infarct 30 (100%)Pathologic Q waves 11 (37%)

Angiographic dataSVD 16 (53%)2VD 9 (30%)3VD 2 (7%)No CAG 3 (10%)

Revascularization therapyPrimary PCI 26 (86%)CAG without PCI 1 (3%)

MedicationsBeta-blockers 20 (67%)Ca antagonists 10 (33%)Nitrates 10 (33%)ARB or ACE inhibitors 21 (70%)Diuretics 7 (23%)

ACE, Angiotensin-converting enzyme; ARB, angiotensin II receptor bMI, myocardial infarction; ns, not significant; PCI, percutaneous coronary inte

Table 2 Left ventricular volume and pulsed Doppler data inhealthy volunteers

Control

(n � 15)Age, y 64 � 8Male 8 (53%)HR, beats/min 67 � 11LVEDV, mL 73 � 17LVESV, mL 25 � 8LVEF, % 67 � 6LVH 0 (0%)E velocity, cm/s 61 � 13A velocity, cm/s 63 � 13E/A 1.00 � 0.33DcT, ms 233 � 62IVCT, ms 46 � 21IVRT, ms 93 � 23

A, Peak velocity of the late filling wave; AMI, anterior wall myocardial infarctfilling wave; HR, heart rate; IVCT, isovolumic contraction time; IVRT, isovend-diastolic volume; LVEF, left ventricular ejection fraction; LVESV, left v

in Table 2. The number of segments excluded from

the study because of inadequate tracking (trackingscore � 3) were 1.1 � 1.7 segments of 12 segmentsin patients with anterior wall MI and 0.6 � 0.7segments of 12 segments of age-matched controlsubjects (P � not significant).

LV Rotation, Twist, and Twist Velocityin Control Subjects

As seen from the apex, the LV in healthy volunteers

> 45% (n � 16) LVEF < 45% (n � 14) P value

13 6 �.058 8 ns5 4 ns

16 14 ns6 5 ns

9 7 ns6 30 21 2

15 11 ns0 1 ns

9 11 ns5 5 ns5 5 ns

12 9 ns2 5 ns

CAG, coronary angiography; LVEF, left ventricular ejection fraction;; SVD, single-vessel disease; 2VD, 2-vessel disease; 3VD, 3-vessel disease.

s with anterior wall myocardial infarction and age-matched

I with

> 45%

AMI with

LVEF < 45% P

16) (n � 14)� 11 72 � 10 ns(94%) 8 (57%) �.05� 14 70 � 12 ns� 21 111 � 47 �.01� 14 73 � 46 �.001� 8 37 � 9 �.001(13%) 4 (29%) ns� 18 50 � 19 ns� 17 81 � 25 ns� 0.30 0.74 � 0.56 ns� 55 215 � 79 ns� 26 78 � 43 �.05� 22 128 � 44 �.05

, deceleration time of the E wave velocity; E, peak velocity of the early rapidrelaxation time; LVH, left ventricular hypertrophy; LVEDV, left ventricularar end-systolic volume; ns, not significant.

LVEF

locker;

patient

AM

LVEF

(n �6615688638562

5971

0.8321847

101

ion; DcT

performs a systolic wringing motion with a clock-


wise rotation at the base and counterclockwiserotation at the LV apex (Figure 1, A and B). Thesystolic rotation attains peak motion at the end ofsystole in both the basal and apical planes. Thus,peak twist develops near the end of systole (9.3 �3.6 degrees, 98 � 8% of end systole) (Figure 1, C).During early diastole, a rapid recoil motion is ob-served that is directed in opposite direction to thesystolic rotation. Twist velocity, defined as the netdifference of rotational velocities between the basaland apical plane, depicted a systolic positive velocity(peak positive velocity: 54.8 � 23.7 degree/s) and adiastolic negative velocity (peak negative velocity:�56.8 � 20.9 degree/s) (Figure 1, D).

LV Strain, Rotation, Twist, and Twist Velocityin Patients with Anterior Wall MI

Peak radial strain and peak circumferential strainin each segment at both planes between twogroups and those with age-matched control sub-jects are shown in Table 3. No significant differenceof average peak radial strain in the apex was noted

Figure 1 Left ventricular basal rotation (A), apiccurve in age-matched healthy volunteers. All data(�100%) and end diastole (�200%). Mean � Srotation; values below x-axis, clockwise rotation a

between patients with LVEF less than 45% (abnor-

mal LVEF group) and those with LVEF 45% or greater(normal LVEF group) (12.8 � 5.4 vs 16.5 � 9.0, P �not significant). However, average peak circumfer-ential strain in the apex was significantly depressedin abnormal LVEF group (�7.3 � 2.6 vs �13.5 �4.1, P � .001).

Differently to normal LVEF group, peak LV twistwas significantly reduced in abnormal LVEF group(5.6 � 2.6 vs 9.8 � 4.0 degrees, P � .05) (Table 4),mainly as a result of reduced apical rotation (Figure2, A-C). Peak positive twist velocity was also signif-icantly reduced in abnormal LVEF group (Figure 2,D, and Table 4). Peak negative twist velocity wasreduced and time to peak negative twist velocitywas delayed in abnormal LVEF group resulting inreduced and prolonged diastolic untwisting (Figure2, D, and Table 4).

Significant correlations were noted between peaktwist and LVEF (r � 0.73, P � .001), LV end-diastolicvolume (r � 0.50, P � .001), and LV end-systolicvolume (r � 0.56, P � .001) in patients with

tion (B), twist (C), and twist velocity (D) profiletted as function of time normalized to end systoleshown. Values above x-axis, Counterclockwise

d from apex.

al rotaare ploD are

s viewe

anterior wall MI.


Twist-displacement Loops

Twist-displacement loop in patients with anteriorwall MI and age-matched healthy volunteers areshown in Figure 3. In control subjects, there is asmall initial clockwise twist at the beginning ofejection followed by a linearly increasing, prolongedcounterclockwise twist with extends throughoutsystole. A tight linear correlation between twist andradial displacement during systole was noted inevery participant (r � 0.99 � 0.01). The rate ofsystolic twist with respect to radial displacement,determined by the slope of systolic loop, was 2.14 �0.82 degree/mm. During early diastolic filling, thetwist and radial displacement loop depicted thatan inflection point with a substantial degree ofuntwisting occurred despite a small early diastolic

Table 3 Regional strain data in patients with myocardial in

Control

Ant

(LVE

Radial strainBasal

AS 39.3 � 14.8 21.3Ant 50.8 � 13.8 34.5Lat 59.1 � 14.3 48.4Post 63.7 � 12.4 47.4Inf 57.8 � 11.6 43.6IVS 45.8 � 13.3 29.0Average 52.8 � 11.5 35.8

ApexAS 26.4 � 14.0 15.3Ant 24.7 � 14.3 14.8Lat 25.3 � 14.6 15.3Post 26.4 � 14.1 17.1Inf 28.8 � 14.6 18.4IVS 25.8 � 9.4 18.3Average 26.5 � 13.5 16.5

Circumferential strainBasal

AS �20.5 � 4.9 �12.6Ant �18.0 � 4.8 �14.1Lat �11.0 � 3.2 �13.5Post �10.1 � 5.3 �12.6Inf �15.4 � 4.0 �15.4IVS �19.7 � 4.5 �15.6Average �16.2 � 3.4 �13.7

ApexAS �18.8 � 4.5 �8.4Ant �20.5 � 3.7 �11.6Lat �20.1 � 4.3 �16.5Post �21.6 � 4.1 �18.4Inf �21.7 � 3.2 �15.7IVS �21.2 � 3.1 �10.8Average �20.6 � 3.3 �13.5

ANOVA, Analysis of variance; Ant, anterior; AS, anteroseptal; Inf, inferiorMI, myocardial infarction; ns, not significant; Post, posterior.*P � .05, control vs Ant MI (LVEF � 45%).†P � .05, control vs Ant MI (LVEF � 45%).‡P � .05, Ant MI (LVEF �45%) vs Ant MI (LVEF � 45%).

reversal of systolic radial displacement. If the slope

of the loop from end systole to the first 20% ofdiastolic period (t � 120%) was defined as the earlydiastolic slope, a linear correlation was noted (r �0.93 � 0.11). This early diastolic slope was signifi-cantly steeper than the one observed during systole(8.45 � 10.32 degree/mm, P � .05). During middleto late diastole, the magnitude of untwisting wassmall despite a large reversal of systolic radial dis-placement.

Although maximal twist and radial displacementwere reduced in abnormal LVEF group, a linearrelation between systolic twist and radial displace-ment was maintained, with a mean slope of 2.00 �1.18 degree/mm, which overlapped with that notedin control subjects (Figure 3, A). However, in thesepatients, there was no obvious inflection point

n and healthy volunteers

I

)

Anterior MI

(LVEF < 45%) P, ANOVA

.4* 13.0 � 8.2† �.001

.4* 26.5 � 11.7† �.001

.0 38.8 � 15.6† �.05

.1* 42.8 � 14.3† �.005

.0* 35.0 � 15.1† �.001

.8* 21.1 � 11.0† �.001

.7* 27.4 � 10.3† �.001

.2* 10.0 � 5.0† �.005

.3 11.3 � 5.0† �.05

.9 13.4 � 5.8† �.05

.4 14.3 � 7.0† �.05* 15.3 � 7.5† �.01.9 14.0 � 8.7† �.05* 12.8 � 5.4† �.005

* �8.4 � 4.8† �.001�9.2 � 5.6† �.001

�11.0 � 7.0 ns�14.9 � 7.3 ns�13.4 � 7.3 ns�10.8 � 6.0†‡ �.001�10.7 � 5.1† �.005

* �4.1 � 4.0†‡ �.001* �6.8 � 3.1†‡ �.001

�9.4 � 2.5†‡ �.001* �11.2 � 4.4†‡ �.001* �9.4 � 3.7†‡ �.001* �3.9 � 5.5†‡ �.001* �7.3 � 2.6†‡ �.001

terventricular septum; Lat, lateral; LVEF, left ventricular ejection fraction;

farctio

erior M

F > 45%

� 11� 12� 15� 15� 12� 10� 10

� 12� 11� 10� 10� 9.9� 10� 9.0

� 6.5� 6.3� 5.1� 3.4� 4.3� 4.1� 4.0

� 5.3� 5.6� 4.9� 4.6� 4.5� 5.1� 4.1

; IVS, in

observed during early diastole, and diastolic untwist-

g to L


ing occurred simultaneously with a considerable rever-sal of systolic radial displacement, resulting in a re-duced early diastolic slope (3.65 � 5.80 degree/mm).There was no significant difference between systolicslope and diastolic slope in abnormal LVEF group.

In contrast, the configuration of twist-displace-ment loop was maintained in normal LVEF group(Figure 3, B). The slope of twist against radial

Figure 2 Left ventricular (LV) basal rotation ((D) profile curve in patients with anterior wall mof time normalized to end systole (�100%) aPatients were divided into two groups accordin

Table 4 Left ventricular twist data in patients with anterio

Control (n � 15)

AM

Peak twist, degree 9.3 � 3.6Twist at AVC, degree 9.0 � 3.7Twist at MVO, degree 5.5 � 3.1PPTV, degree/s 54.8 � 23.7PNTV, degree/s �56.8 � 20.9Time to PPTV, ms 164 � 37Time to PNTV, ms 438 � 53

AMI, Anterior wall myocardial infarction; AVC, aortic valve closure; LVEFPNTV, peak negative twist velocity; PPTV, peak positive twist velocity.*P � .05, control vs anterior MI with LVEF � 45%.†P � .05, AMI with LVEF � 45% vs AMI with LVEF � 45%.

displacement during systole in normal LVEF group

(3.02 � 1.27 degree/mm) was significantly steeperthan that in abnormal LVEF group (P � .05), andtended to be larger than that noted in controlsubjects. The early diastolic slope in normal LVEFgroup was 7.75 � 9.78 degree/mm. No difference ofearly diastolic slope was noted among the 3 groupsas a result of large SD. No significant difference wasnoted between systolic slope and diastolic slope in

ical rotation (B), twist (C), and twist velocityrdial infarction. All data are plotted as functiond diastole (�200%). Mean � SD are shown.V ejection fraction.

myocardial infarction and age-matched healthy volunteers

VEF > 45%

16)

AMI with LVEF < 45%

(n � 14) P

� 4.0 5.6 � 2.6*† �.005� 4.0 5.3 � 2.7*† �.005� 2.5 3.8 � 2.0 ns� 19.3 37.5 � 10.6 �.05� 28.0 �43.8 � 17.9 ns� 56 185 � 152 ns� 124 650 � 244*† �.005

ntricular ejection fraction; MVO, mitral valve opening; ns, not significant;

A), apyoca

nd en

r wall

I with L

(n �

9.89.55.4

52.1�63.4

128471

, left ve

normal LVEF group.


Measurement Variability

The interobserver variability was 6% for peak twistand 6% for radial displacement. Intraobsever vari-ability was 6% for peak twist and 5% for radialdisplacement.

DISCUSSION

The major findings in this study were as follows.First, when viewed from the apex, the normal LVperforms a systolic wringing motion with a clock-wise rotation at the base and a counterclockwiserotation at the apex. The majority of diastolic un-twisting occurs in early diastole, followed by a mildgradual untwisting during the remainder of diastole.These findings were consistent with previous stud-ies using tagged MRI.8,12 Second, peak circumferen-tial strain in the apex was significantly depressedin anterior wall MI with LV systolic dysfunction(LVEF � 45% group) compared with those withpreserved systolic function (normal LVEF group).Third, LV twist is severely depressed in abnormalLVEF group, mainly because of reduced LV apicalrotation. Diastolic untwisting is also reduced anddelayed. Twist-displacement loops clearly demon-strate delayed untwisting occurring simultaneouslywith diastolic cavity enlargement. Finally, LV twist

Figure 3 Averaged twist-displacement loop obta(AMI) with depressed left ventricular (LV) systocontrol subjects (A), and between AMI with nosubjects (B). For adjustment of intersubject diffepercentage of systolic and diastolic duration. Aincrement points during systolic period (ie, 0% eincrement points were used for the diastolic perioFirst 20% of diastolic period.

behavior is maintained in normal LVEF group.

LV Rotation and Twist in Anterior Wall MI

Systolic twist was significantly depressed in patientswith anterior wall MI and LVEF less than 45%. Thisabnormality can be predominantly attributed toreduced apical rotation. These results are similar toprevious studies that used an optical device andtagged MRI1,12,22 to quantify apical motion. LV sys-tolic dysfunction in patients with anterior wall MI ismainly attributed with transmural infarction result-ing in severe reduction of circumferential strain inthe apex. These severe impairments of apical straincannot generate sufficient apical rotational move-ment, which is the main determinant of LV systolictwist.

In contrast, systolic twist was maintained in pa-tients with anterior wall MI with LVEF 45% orgreater. This is a result of the mild reduction ofcircumferential strain in the apex that may affect LVtwist behavior in a mild manner. It is known that themyocardial fiber orientation in the mammalian LVwall changes from a left-handed helix in the subepi-cardium to a right-handed helix in the subendocar-dium.22-25 Contraction of these obliquely orientedfibers creates a wringing or twisting motion of theLV. Torsional deformation is determined by the neteffect of positive torsional deformation forces devel-oping in the subepicardium and negative torsionaldeformation forces generating in the subendocardial

patients with anterior wall myocardial infarctionction (LV ejection fraction [LVEF] � 45%) andV systolic function (LVEF � 45%) and controlin heart rate, time sequence was normalized tod twist-displacement loop was plotted in 10%stole [ED], 100% end systole [ES]) whereas 5%5% first 5% of diastolic period, 200% ED). 120%,

ined inlic funrmal Lrencesveragend diad (10

fibers.22,24,25 Normal LV systolic function associated


with MI usually is the result of a small subendocar-dial infarction with preserved epicardial function.Thus, another possibility is that these counteractingforces generated by the subendocardial layer againstsubepicardial layer decreases in the setting of sub-endocardial dysfunction resulting in sufficient sub-epicardial fiber torque to drive torsional deforma-tion toward positive angles.

Twist-displacement Loops

Because 2D speckle tracking imaging provides si-multaneous information on both radial displacementand cardiac rotation throughout the entire cardiaccycle, twist-displacement loops can be constructednoninvasively.20 In this study, we tested whetherglobal LV twist was directly related to radial short-ening in healthy volunteers and patients with ante-rior wall MI. Our results confirm a strong linearrelation between twist and radial displacement dur-ing ejection in healthy volunteers. However, duringearly diastole, nearly 50% of the total amount ofuntwisting occurred despite less than a 15% changein radial displacement (Figure 3). Throughout theremainder of diastole, gradual continued untwistingoccurred, with much less untwisting per unit ofradial displacement change that had been presentduring systole. Thus, although there is a relationbetween twisting and radial contraction, this rela-tionship is modified by the phase of cardiac cycle.Similar observations have been reported in previousanimal and human studies.5,10,12,20,22,25,26

Even in patients with anterior wall MI who hadabnormal LV systolic function (LVEF � 45%), a linearrelation between systolic twist and radial displace-ment was maintained, which overlapped with thatobserved in control subjects. Thus, the absolutevalue of the slope during ejection does not reflectcontractile performance. However, radial displace-ment was less than normal and early diastolic un-twisting occurred simultaneously with radial dis-placement, resulting in distorted twist-displacementloops.

On the other hand, the morphology of the twist-displacement loops was maintained in patients withanterior wall MI and preserved LV systolic function(LVEF � 45%). The assessment of twist-displace-ment loops clearly depicts not only a linear relation-ship between twist and systolic shortening but alsoreduced and delayed untwisting in patients withanterior wall MI and impaired LV systolic function.

Limitations

In this study, no gold standard for measuring LVtwist and twist velocity was studied. However,previous studies have already validated the accuracyof 2D speckle tracking imaging versus taggedMRI.15,16,19 It seemed curious that radial strain in the
basal short-axis data in each segment is reduced not
only in anterior but also in the inferoposterior wallin patients with anterior wall MI. Small sample sizeand the stiffening of valvular plane in aged peoplemight be the cause of this discrepancy. Two-dimen-sional speckle tracking analysis cannot track the3-dimensional motion of the heart and, thus, cannoteliminate the errors introduced by through-planemotion, especially in the basal plane. However,previous studies have shown that LV rotation in-creases nonlinearly toward the apex,27,28 thus, lim-iting the impact of through-plane motion at the base.It should be noted that radial displacement valuesare not similar to endocardial values. Radial displace-ment does not directly reflect changes in chambervolume.

Conclusion

Noninvasive assessment of LV strain, rotation, anddisplacement was feasible in patients and age-matchedcontrol subjects using newly developed 2D speckletracking imaging. Systolic twist was depressed anddiastolic untwisting prolonged and delayed in pa-tients with anterior wall MI and abnormal LV systolicfunction. These abnormalities were related to re-duced apical rotation and associated with the reduc-tion of apical circumferential strain. Twist-displace-ment loops clearly demonstrated delayed untwistingoccurring simultaneously with diastolic cavity en-largement in patients with anterior wall MI andimpaired LV systolic function.

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