doi:10.1016/j.e

262

Prognostic Value of Longitudinal Strain After PrimaryReperfusion Therapy in Patients with Anterior-wall

Acute Myocardial InfarctionYong Hyun Park, MD, Soo-Jin Kang, MD, Jae-Kwan Song, MD,

Eun Young Lee, RDCS, Jong-Min Song, MD Duk-Hyun Kang, MD, Young-Hak Kim, MD,Cheol Whan Lee, MD, Myeong-Ki Hong, MD, Jae-Joong Kim, MD,

Seong-Wook Park, MD, and Seung-Jung Park, MD, Seoul, South Korea

Objectives: We sought to test whether longitudinal strain (LS) can be a useful predictor of left ventricular (LV)remodeling after reperfusion therapy in acute myocardial infarction.

Background: Predicting LV remodeling based on quantification of regional contractility remains an elusivegoal of echocardiography.

Methods: In 50 patients with anterior-wall acute myocardial infarction, the peak systolic velocity and LS weremeasured by Doppler tissue imaging (LSDTI) and speckle tracking imaging (LS2D) at 7 LV segments of leftanterior descending coronary artery territory after primary reperfusion therapy. LV remodeling was defined asan increase in LV end-diastolic volume of greater than or equal to 15% at follow-up echocardiography.

Results: A total of 22 patients showed LV remodeling, who had significantly lower baseline ejection fraction,LSDTI, and LS2D, and higher wall-motion score index and peak creatine kinase-MB with shorter decelerationtime of early diastolic mitral inflow than those without LV remodeling. LS2D (odds ratio [OR] � 1.307, 95%confidence interval [CI] � 1.082-1.579, P � .005) and LSDTI (OR � 1.430, 95% CI � 1.152-1.776, P � .001)were independent predictors of LV remodeling. During clinical follow-up of 18.3 � 9.0 months, death orcongestive heart failure developed in 11 patients (22%); LS2D (OR � 1.455, 95% CI � 1.142-1.852, P � .002)and LSDTI (OR � 1.436, 95% CI � 1.093-1.888, P � .009) were independent predictors.

Conclusions: LS immediately after primary reperfusion therapy is an excellent predictor of LV remodeling and

adverse events in patients with anterior-wall acute myocardial infarction.

After successful reperfusion therapy in the hyperacute stage ofacute myocardial infarction (AMI), dysfunctional myocardial seg-ments subtended by the infarct-related artery can follow two differentnatural courses: functional recovery or irreversible remodeling.1 Todistinguishing these two entities, myocardial contrast echocardiogra-phy for estimating microvascular integrity and dobutamine stressechocardiography for evaluating contractile reserve are currentlypopular in routine clinical practice2-9 and these two techniques arebest regarded as complementary.10 Predicting functional recovery orremodeling based on quantification of regional contractility remainsan elusive goal of echocardiography. Measurement of ultrasonicintegrated backscatter and cyclic variation, predominantly reflectingthe intrinsic contractile performance of the myocardial segment, hasbeen reported to be a clinically useful index of functional recov-

From the Division of Cardiology, Asan Medical Center, University of Ulsan Collegeof Medicine, Seoul, South Korea.

Reprint requests: Jae-Kwan Song, MD, Asan Medical Center, University ofUlsan College of Medicine, 388-1 Poongnap-dong Songpa-ku, Seoul 138-736South Korea (E-mail: jksong@amc.seoul.kr).

0894-7317/$34.00

Copyright 2008 by the American Society of Echocardiography.

cho.2007.08.026

ery.11-13 However, as this technique is highly angle dependent, onlythe anterior septum and posterior wall at the parasternal long- orshort-axis view can be evaluated. Recent clinical introduction ofDoppler tissue imaging (DTI)14 and speckle tracking imaging (STI)yields deformation index representing the contractility of the myo-cardial segment15,16 and more diverse application has been possible.However, there are few data on the use of quantifying the localizedmyocardial contractility by DTI or STI in predicting functional recov-ery or unfavorable remodeling after reperfusion therapy in AMI. Wesought to address this issue in the current study.

METHODS

Patients and Two-dimensional EchocardiographyFifty consecutive patients with anterior-wall AMI who received pri-mary angioplasty or thrombolytic therapy within 12 hours after painonset were included in this prospective study. Six of the patientsreceived thrombolytic therapy in the hyperacute stage and under-went diagnostic coronary angiography and percutaneous interven-tion of the infarct-related artery within 24 hours. Stenting wasperformed in 49 of the patients, and the residual diameter stenosis ofthe infarct-related left anterior descending coronary artery (LAD) wasless than 20% in all patients. Patients with atrial fibrillation, significant

ventricular arrhythmia, valvular regurgitation, or prior myocardial

Journal of the American Society of Echocardiography Park et al 263Volume 21 Number 3

infarction were excluded. Nine patients with poor echocardiographicwindow and 7 with normal wall motion after successful reperfusiontherapy during study period were also excluded. All patients under-went comprehensive 2-dimensional (2D) and Doppler echocardiog-raphy including DTI, and STI within 48 hours after confirmation ofcomplete revascularization therapy using coronary angiography. Theconventional 16-segment model of the left ventricle (LV) was usedfor the analysis of segmental wall motion,17 which was categorized ineach of the predefined segments as being normal, hypokinetic,akinetic, dyskinetic, or aneurysmal (with scores of 1-5). The com-bined score of the 7 LV wall segments of the LAD territory at theapical 4-chamber view (mid septal, apical septal, and apical lateralsegment) and 2-chamber view (apical inferior, apical anterior, midanterior, and basal anterior segment) was divided by 7 to produce awall-motion score index (WMSI). LV systolic and diastolic volumeswere calculated by biplane Simpson’s method using two apical views.Doppler echocardiography was used to measure the diastolic param-eters including the peak velocity of early and late diastolic mitralinflow and deceleration time.

DTI and STIAfter reperfusion therapy, an ultrasound system (Vivid 7, GEMedicalSystems, Horten, Norway) with an M3S probe was used for both DTIand STI. For DTI, a color-coded apical 4-chamber view of the LV wasobtained and stored digitally in a cineloop format for subsequentoffline analysis (EchoPAC PC 6.0.0, GE Medical Systems). All mea-surements were blinded. In conventional color DTI, at least 3 samplevolumes were placed at each LV segment of LAD territory, andthe peak systolic velocity (Vpeak) and longitudinal strain (LS) (LSDTI)were measured. Strain was calculated as (L � Lo)/Lo, where Lo is theoriginal length at the end of diastole and L is the length at the end ofsystole; when acquired from the apex, a normally contracting myo-cardium has a negative LS. The offset distance for DTI measurementwas 8 mm and we tried our best to put interrogating points inside themyocardium. The mean of 7 LV segments of LAD territory was usedas a representative value. In the color DTI study the frame rate washigher than 100 frames/s and every effort was made to keep theregion of interest at the center of the ultrasound beam.

For STI, the second-harmonic B-mode images of both apical 4- and2-chamber views were obtained and digitally stored in cineloopformat for offline analysis (EchoPAC PC 6.0.0, GE Medical Systems).The frame rate was 52 � 17 frames/s. After selecting the best-qualitydigital 2D image of the cardiac cycle, the LV endocardial border wasmanually traced at the end-systolic frame, from which a speckletracking region of interest was automatically selected to approximatethe myocardium between the endocardium and epicardium. Thewidth of the region of interest was adjusted as necessary toaccommodate the total thickness of the LV wall. The computerautomatically tracked stable objects in each frame using the sum ofabsolute differences algorithm, which is verified by the computer:LV segments with verification were used for further analysis. Afterthese steps, the workstation computed and generated strain curves(Figure 1). The mean of 7 LV segment of LAD territory was usedas a representative value.

For analysis of both DTI and STI, significant postsystolic shorteningwas defined to be present if the peak negative systolic strain occurredafter aortic valve closure, and the peak negative value of strain curvebefore mitral valve opening (either before or after aortic valveclosure) was used as a representative value (Figure 1, A and B); if

strain curve showed predominant positive value before aortic valve

closure, suggesting systolic lengthening rather than shortening, thepeak positive value before aortic valve closure was used (Figure 1, C).

Follow-upClinical and echocardiographic follow-up was done in all patients.Follow-up echocardiography was performed at least 3 monthslater after AMI (14.7 � 8.4 months, mean � SD; range 3-47months) for LV volume measurement, and LV remodeling wasdefined as an increase in LV end-diastolic volume of greater thanor equal to 15%.7,9 In case of multiple follow-up echocardio-grams, the last one was taken as a representative study. Anyepisode of clinical events of death or development of AMI or heartfailure were recorded by attending cardiologists or clinical nursespecialists: development of heart failure was defined as worseningof exertional dyspnea with typical chest radiograph findings ofprogressive cardiomegaly or pulmonary edema, which requiredhospital admission or administration of new or different diuretics.Clinical follow-up data were obtained until June 2006 (18.3 � 9.0months, mean � SD; range 4-50 months). Follow-up diagnosticcoronary angiography was recommended 6 or 9 months afterstenting regardless of symptoms.

Statistical AnalysisAll data are presented as mean � SD values. Clinical and echo-cardiographic variables including Vpeak, LSDTI, and LS2D werecompared between patients who did and did not show thedevelopment of LV remodeling in follow-up echocardiography.Student t test was used for continuous variables, and Fisher’s exacttest or the �2 test was used for frequency variables. Multivariableanalysis was used to determine the factors associated with thedevelopment of LV remodeling or adverse clinical events afterreperfusion therapy; LS2D and LSDTI are separately tested bybackward logistic regression analysis including variables showing P

Figure 1 Representative 2-dimensional longitudinal straincurves measured by speckle tracking imaging. In patient whodid not show left ventricular (LV) remodeling (A and B), straincurve was almost identical and all 7 LV segments showednegative strain value; mean value was �15.6%. Other patientwho developed LV remodeling (C and D) showed variablepatterns of strain curves, and many segments showed positivepeak during systole, suggesting passive lengthening ratherthan active shortening; mean value of 7 segments was 1.7%.Arrowhead, Strain value of each segment; AVC, aortic valveclosure; MVO, mitral valve opening.

value less than .05 between patients who did and did not show the

264 Park et al Journal of the American Society of EchocardiographyMarch 2008

development of LV remodeling or adverse clinical events (timeinterval from chest pain onset to reperfusion, baseline WMSI,baseline ejection fraction, peak creatine kinase-MB level, anddeceleration time of early mitral inflow velocity). The interob-server and intraobserver variabilities were examined in a blindedfashion in 20 randomly selected patients, and are expressed hereas correlation coefficients between measurements of two investi-gators and two readings (�2 months apart). All of the statisticalanalyses were performed using software (SPSS, Version 12.0 forWindows, SPSS, Chicago, IL). A probability value of P less than .05was taken to indicate statistical significance in all analyses.

RESULTS

LV Remodeling After AMIThe patients were aged 56 � 13 years, and 82% of them weremale. Primary percutaneous coronary intervention of the infarct-related artery was performed in 44 patients (88%), and thrombo-lytic therapy was applied in the other 6 patients. LV remodelingwas evident in 22 patients (46%, group 2), whereas the remaining28 patients did not show progressive LV enlargement (group 1).Although the initial LV end-diastolic volume was similar in the twogroups (94.6 � 20.7 vs 95.6 � 20.2 mL, P � .05), the follow-upvolume was significantly larger in group 2 (91.4 � 17.8 vs 143.2 �40.4 mL, P � .01). Table 1 compares the demographic and baselineclinical variables between the groups. The frequency of risk factorsassociated with the development of atherosclerosis did not differsignificantly between the groups. Although the time to reperfusiontherapy, lesion site (proximal vs mid-to-distal LAD), and the fre-quency of final thrombolysis in myocardial infarction flow at grade 3did not differ significantly, the peak level of creatine kinase-MB wassignificantly higher in group 2 (193.0 � 163.8 vs 363.0 � 153.8ng/mL, P � .001).

Immediately after reperfusion therapy, patients in group 2 showed asignificantly lower baseline ejection fraction (49.8 � 8.6% vs 43.0 �7.0%, P � .004) and higher WMSI (2.03 � 0.47 vs 2.44 � 0.36, P �.001) (Table 2). In all LV segments, DTI measurement was possiblefor quantifying the systolic function of the apical septum, and tracking

Table 1 Comparison of demographic and clinical variables bet

Group 1 (n � 28) Remodelin

Age, y 55.5 � 12.1Male 25 (89.3%)Current smoker 14 (50.0%)Hypertension 14 (50.0%)Cholesterol � 240 mg/dL 7 (25.0%)Diabetes mellitus 8 (28.6%)Peak CK-MB, ng/mL 195.2 � 161.1Time to reperfusion, h 4.8 � 4.0Killip class on admission 1.41 � 0.67Primary PCI 24 (85.7%)Multi-/single-vessel disease 19/9Lesion siteProximal/mid-to-distal LAD 12/16Final TIMI flow, grade 3 26 (92.9%)Follow-up CAG 19 (67.9%)Restenosis 2/19 (10.5%)

CAG, Coronary angiography; CK, creatine kinase; LAD, left anterior dthrombolysis in myocardial infarction.

for STI analysis was possible in 347 among 350 LV segments (99%).

LS2D and LSDTI showed significant positive correlation (r � 0.69, P �.001). Vpeak did not differ significantly between the groups (2.18 �0.94 vs 2.34 � 1.30 cm/s, P � .622), whereas the degree of activelongitudinal shortening or strain measured either by conventionalDTI (LSDTI, �10.1 � 3.3% vs �5.8 � 3.9%, P � .001) or STI (LS2D,�11.6 � 3.9% vs �6.3 � 4.1%, P � .001) was significantly lower ingroup 2. Among the diastolic Doppler parameters, deceleration timeof early mitral inflow velocity was significantly shorter in group 2(194.3 � 43.5 vs 155.9 � 24.9 milliseconds, P � .001). The adjuvantmedical treatment was similar in the groups (Table 2).

LS2D (odds ratio per 1% decrease [OR] � 1.307, 95% confi-dence interval [CI] � 1.082-1.579, P � .005) and LSDTI (OR �1.430, 95% CI � 1.152-1.776, P � .001) were independentpredictors for LV remodeling, when these two variables wereincluded separately in the backward logistic regression analysis.The receiver operating characteristic curves of LS2D and LSDTI areshown in Figure 2. The area under the curve of LS2D was 0.85(95% CI � 0.73-0.97), which was not significantly different fromthat of LSDTI (0.81, 95% CI � 0.69-0.94, P � .569). The bestcut-off value of LS2D was �10.2%, with LS2D less than this valuepredicting LV remodeling with a diagnostic sensitivity and speci-ficity of 90.9% (20/22) and 85.7% (24/28), respectively.

Clinical Events During Follow-upDuring the clinical follow-up of 18.3 � 9.0 months, one patient diedas a result of heart failure 9 months after the initial event. Develop-ment of symptomatic congestive heart failure was documented in 10patients; 7 patients required hospital admission to control heartfailure symptoms and the other 3 patients needed new administra-tion of diuretics. Patients with these clinical events were more oftenfemale (11.3% vs 45.5%, P � .017), had higher baseline WMSI(2.13 � 0.48 vs 2.49 � 0.28, P � .004), had lower LSDTI (�9.3 �3.4 vs �4.3 � 4.4%, P � .001), and had lower LS2D (�10.6 � 4.3 vs�4.3 � 4.4%, P � .001) with longer time interval from chest pain toreperfusion (4.7 � 3.4 vs 8.1 � 2.5 hours, P � .008) than thosewithout clinical events. In multivariable analysis, LS2D (OR � 1.455,95% CI � 1.142-1.852, P � .002) and LSDTI (OR � 1.436, 95%CI � 1.093-1.888, P � .009) were independent predictors for

n the groups

Group 2 (n � 22) Remodeling (�) P

56.2 � 14.6 .84016 (72.7%) .13011 (50.0%) 1.00010 (45.5%) .749

4 (18.2%) .5634 (18.2%) .393

367.9 � 155.6 �.0016.1 � 2.8 .217

1.53 � 0.51 .54220 (90.9%) .575

10/12 .111

14/8 .14418 (82.8%) .23313 (59.1%) .522

2/13 (15.4%) 1.000

ding coronary artery; PCI, percutaneous coronary intervention; TIMI,

wee

g (–)

escen

development of adverse cardiovascular event. The area under the

er tis

re in

Journal of the American Society of Echocardiography Park et al 265Volume 21 Number 3

operating characteristic curves of LS2D was 0.86 (95% CI � 0.73-0.97), and the best cut-off value was �6.4% (Figure 2, B), with LS2Dless than this value predicting development of heart failure or deathwith a diagnostic sensitivity of 81.8% (9/11) and 84.6% (33/39),respectively.

Reproducibility of MeasurementIntraobserver and interobserver variability of LV volume was testedusing baseline echocardiography of 15 patients. The correlationcoefficient of intraobserver variability was 0.96 and the standard errorof estimation (SEE) was 2.2% (P � .001); the correlation coefficientand the SEE of interobserver variability was 0.92 and 2.5%, respec-tively (P � .001). For intraobserver measurements of LS, r was 0.78

Figure 2 Receiver operating characteristic curves testing diagremodeling (A) and adverse cardiovascular events (B) in patietherapy. CI, Confidence interval; LSDTI, LS measured by Doppl

Table 2 Comparison of echocardiographic variables and adjuv

Group 1 (n � 28) Remodelin

EchocardiographyBaseline WMSI 2.03 � 0.47Baseline EF, % 49.8 � 8.6Follow-up EF, % 54.9 � 6.8Vpeak, cm/s 2.18 � 0.94LSDTI, % –10.1 � 3.3No. of segments with PSSDTI 26/196 (13.3%)LS2D, % –11.6 � 3.9No. of segments with PSS2D 31/196 (15.8%)E peak, cm/s 67.5 � 15.9A peak, cm/s 70.4 � 17.3DT, ms 194.3 � 43.5MedicationsAspirin 28 (100%)Clopidogrel or cilostazol 27 (96.4%)�-Receptor blocker 24 (85.7%)ACE inhibitor or ARB 24 (85.7%)Lipid-lowering therapy 16 (57.1%)GP IIb/IIIa inhibitor 1 (3.6%)

ACE, Angiotensin-converting enzyme; ARB, aldosterone-receptor blockGP, glycoprotein; LSDTI, longitudinal strain measured by Doppler tisstracking imaging; PSS, postsystolic shortening exceeding –2.5% (in abthe cardiac cycle); Vpeak, peak systolic velocity; WMSI, wall-motion sco

for LSDTI (P � .001, SEE � 2.6%) and 0.94 for LS2D (P � .001,

SEE � 1.8%). For interobserver variability, r was 0.75 for LSDTI (P �.001, SEE � 3.9%) and 0.93 for LS2D (P � .001, SEE � 2.1%).

DISCUSSION

This study has demonstrated the variable systolic function of dysfunc-tional myocardial segments subtended by an infarct-related arteryeven after successful primary reperfusion therapy, and that LS isanother clinically useful predictor of LV remodeling in patients withanterior-wall AMI. The baseline LS data also provide importantprognostic information regarding the development of serious clinicalevents after AMI. Compared with dobutamine stress and myocardial

ic value of longitudinal strain (LS) in predicting left ventricularith anterior-wall acute myocardial infarction after reperfusion

sue imaging; LS2D, LS measured by speckle tracking imaging.

edical treatment between the groups

Group 2 (n � 22) Remodeling (�) P

2.44 � 0.36 .00143.0 � 7.0 .00441.1 � 9.1 .0002.34 � 1.30 .622–5.8 � 3.9 �.001

24/154 (16.1%) .538–6.3 � 4.1 �.001

16/151 (10.6%) .15961.2 � 18.7 .20668.9 � 21.0 .790

155.9 � 24.0 .001

22 (100%) 121 (95.5%) .86115 (68.2%) .13719 (86.4%) .94812 (54.5%) .8542 (9.1%) .576

T, deceleration time of early diastolic mitral inflow; EF, ejection fraction;aging; LS2D, 2-dimensional longitudinal strain measured by speckle

te value) or 20% (relative to the overall myocardial deformation duringdex.

nostnts w

ant m

g (–)

er; Due imsolu

contrast echocardiography, which need stress or sophisticated instru-

266 Park et al Journal of the American Society of EchocardiographyMarch 2008

ments and analysis, measurement of LS has strong advantages in riskstratification after AMI.

LS as a Predictor of LV RemodelingLV remodeling after AMI is an important precursor of the devel-opment of overt heart failure and is an important predictor ofmortality.18,19 Heterogeneous LV remodeling processes are re-ported to occur even after achievement of early flow in theinfarct-related artery, and post-AMI LV dilation still retains itsprognostic significance.20 The importance of optimal microvascu-lar flow and tissue perfusion in the dysfunctional myocardialsegment cannot be overemphasized, and quantifying segmentalLV function to assess intrinsic contractile performance remains anelusive goal of echocardiography.

The development of DTI has made it possible to determine themyocardial velocities of regional LV segments. However, the mea-sured velocity of a myocardial segment is influenced by regional wallthickening, cardiac displacement, cardiac movement, and tetheringcaused by contraction of the adjacent segments, which means thatthe velocity of a dyskinetic myocardial segment after AMI itselfcannot be used to differentiate between active contraction andpassive displacement.21,22 This can explain why Vpeak did not differsignificantly between patients with and without LV remodeling in thecurrent study. Normalized velocity, such as the strain rate or thestrain, has been recommended to overcome the inherent problems ofvelocity measurement21,23 and the usefulness of strain-rate imagingto define the transmurality of myocardial infarction was tested in ananimal experiment.24,25 LS can be easily measured by DTI. However,because of relatively noisy profiles and angle dependency ofDTI,26,27 clinical usefulness of LSDTI in patients with AMI has notbeen fully investigated.

Motion analysis by the newly developed STI technique is based onapplying autocorrelation search algorithms to the detection of thespeckle motion that is closely linked to underlying tissue motion; afterfiltering out random speckles, autocorrelation is applied to estimatethe motion of the stable structures. This angle-independent non-Doppler technique for quantifying regional function has recentlybeen validated,28 and its clinical usefulness in the measurement ofspatially complicated LV motion has been reported, such as for LVapical torsion.29 Leitman et al16 first reported the feasibility ofreal-time LS2D measurement in healthy control subjects and patientswith myocardial infarction. Tracking was possible in 87% of infarctsegments and the correlation coefficient between LS2D and LSDTI

was 0.74 (P � .0001). The authors concluded that measuring LS2Dwith novel non-Doppler-based software has the potential to becomea standard for the real-time automatic echocardiographic assessmentof cardiac function.

The current study has shown that both conventional DTI and STIare useful for assessing regional myocardial function after AMI. LS2Dand LSDTI were independent predictors of LV remodeling andprovided prognostic information regarding the development of clin-ical events including death or congestive heart failure. The correlationcoefficient between these two variables in our study (LSDTI �0.69LS2D � 1.79, r � 0.69, P � .001) was quite similar to theprevious report.16 One potential issue is measurement variability, asthis is another important factor when considering an optimal methodfor quantifying regional myocardial function. The SEEs for the in-traobserver and interobserver measurements of LS2D were 1.8% and2.1%, respectively, whereas those of LSDTI were 2.6% and 3.9%,respectively. With reference values of LSDTI (�20 � 9%)21 and LS2D

(�17.7 � 6.5%) in the normal apical septum,16 the coefficient of

variations of intraobserver and interobserver measurements of LSDTI

were 13.2% and 19.7%, respectively; those of LS2D were 10.2% and11.9%, respectively. As the DTI technique is totally angle depen-dent,27 the LV apical septum is not an ideal target for quantifyingsegmental contractility or measuring LSDTI, especially considering thegeometric deformity resulting from anterior-wall AMI. The highermeasurement reproducibility of LS2D by STI can be explained notonly by angle independency, but also by averaging several points andsubstantial smoothing.

According to the recent report by Chan et al,30 LS2D was notuseful to diagnose the transmurality of myocardial infarction andcircumferential strain could differentiate between subendocardialand transmural infarction. Thus, they concluded that the combinedassessment of both long- and short-axis function using 2D strain maybe useful to identify the transmural extent of myocardial infarction.They enrolled patients with chronic ischemic heart disease andperformed magnetic resonance imaging and dobutamine stress echo-cardiography for viability test. Thus, the patient population is quitedifferent from our study, in which early diagnosis of LV remodelingafter successful primary revascularization therapy in anterior wallAMI was an issue. However, we believe it is worthwhile to testwhether assessment of short-axis function can provide additive infor-mation in this selected group of patients.

Study Limitations

As a result of absence of gold standard against which both LS2D andLSDTI would be directly compared, the accuracy of both techniquescould not be determined in this study, and actually was not an issue.As validation of LS2D was not tested for various interrogation angleswith respect to the region of interest even in a well-controlledexperiment,26 there was no way to provide the best cut-off value ofLS2D in other patients with AMI that involved different vascularterritories, such as inferior or lateral walls. The predictive role of strainand potential difference among different kinds of strain includingradial, circumferential strain should be tested in additional studiesusing larger numbers of patients with various types of AMI.

The mechanism of relatively preserved regional contractility inpatients without LV remodeling is unclear at this moment; as otherfunctional imaging studies such as magnetic resonance imaging orpositive emission tomography were not done in this study, we couldnot separate preserved subendocardial function (stunned myocar-dium) versus subendocardial infarction. However, patients with LVremodeling in our study showed higher cardiac enzyme levels andWMSI with lower ejection fraction immediately after successfulreperfusion therapy, which might imply much larger myocardialdamage. The patency of the stenting site was not tested in all patients.Although no patient experienced another episode of anterior-wallAMI during the follow-up, the lack of follow-up coronary angiogra-phy data in all patients is an inherent limitation of this study thatshould be considered in the interpretation of our data.

Conclusions

The current study has validated the clinical usefulness of measure-ment of LS in patients with anterior-wall AMI immediately afterprimary reperfusion therapy. This novel clinical variable providesan excellent prediction of LV remodeling and adverse clinical

events in these selected patients.

Journal of the American Society of Echocardiography Park et al 267Volume 21 Number 3

REFERENCES

1. Solomon SD, Glynn RJ, Greaves S, Ajani U, Rouleau J-L, Menapace F, etal. Recovery of ventricular function after myocardial infarction in thereperfusion era: the healing and early afterload reducing therapy study.Ann Intern Med 2001;134:451-8.

2. Ito H, Tomooka T, Sakai N, Yu H, Higashino Y, Fujii K, et al. Lack ofmyocardial perfusion immediately after successful thrombolysis: a predic-tor of poor recovery of left ventricular function in anterior myocardialinfarction. Circulation 1992;85:1699-705.

3. Bologenese L, Antoniucci D, Rovai D, Buonamici P, Cerisano G, SantoroGM, et al. Myocardial contrast echocardiography versus dobutamineechocardiography for predicting functional recovery after acute myocar-dial infarction treated with primary coronary angioplasty. J Am CollCardiol 1996;28:1677-83.

4. Leclercq F, Messner-Pellenc P, Moragues C, Rivalland F, Carabasse D,Davy J-M, et al. Myocardial viability assessed by dobutamine echocardi-ography in acute myocardial infarction after successful primary coronaryangioplasty. Am J Cardiol 1997;80:6-10.

5. Swinburn JMA, Lahiri A, Senior R. Intravenous myocardial contrastechocardiography predicts recovery of dyssynergic myocardium earlyafter acute myocardial infarction. J Am Coll Cardiol 2001;38:19-25.

6. Main ML, Magalski A, Chee NK, Coen MM, Skolnick DG, Good TH.Full-motion pulse inversion power Doppler contrast echocardiogra-phy differentiates stunning from necrosis and predicts recovery of leftventricular function after acute myocardial infarction. J Am CollCardiol 2001;38:1390-4.

7. Lepper W, Kamp O, Vanoverschelde JL, Franke A, Sieswerda GT,Pasquet A, et al. Intravenous myocardial contrast echocardiographypredicts left ventricular remodeling in patients with acute myocardialinfarction. J Am Soc Echocardiogr 2002;15:849-56.

8. Hillis GS, Mulvagh SL, Gunda M, Hagen ME, Reeder G, Oh JK. Contrastechocardiography using intravenous octafluoropropane and real-timeperfusion imaging predicts functional recovery after acute myocardialinfarction. J Am Soc Echocardiogr 2003;16:638-45.

9. Main ML, Hannen MN, Kusnetzky LL, Martin JL, Coggins TR, Lanza PA,et al. Myocardial contrast echocardiographic estimates of infarct sizepredict likelihood of left ventricular remodeling after anterior wall myo-cardial infarction. J Am Soc Echocardiogr 2006;19:64-70.

10. Lim TK, Burden L, Janarhanan R, Dwivedi G, Ping C, Moon J, et al.Contrast echocardiography versus gated single photon emission com-puted tomography for the assessment of parameters of left ventricularremodeling after acute myocardial infarction. J Am Soc Echocardiogr2006;19:280-4.

11. Takiuchi S, Ito H, Iwakura K, Taniyama Y, Nishikawa N, Masuyama T, et al.Ultrasonic tissue characterization predictsmyocardial viability in early stage ofreperfused acute myocardial infarction. Circulation 1998;97:356-62.

12. Muro T, Ota T, Watanabe H, Teragaki M, Takeuchi K, Yoshikawa J.Prediction of contractile reserve by cyclic variation of integratedbackscatter of the myocardium in patients with chronic left ventriculardysfunction. Heart 2001;85:165-70.

13. Komuro K, Yamada S, Mikami T, Yoshinaga K, Noriyasu K, Goto K, et al.Sensitive detection of myocardial viability in chronic coronary arterydisease by ultrasonic backscatter analysis. J Am Soc Echocardiogr 2005;18:26-31.

14. Hatle A, Surtherland GR. Regional myocardial function–a new approach.

Eur Heart J 2000;35:1842-9.

15. Reisner SA, Lysyansky P, Agmon Y, Mutlak D, Lessick J, Friedman Z.Global longitudinal strain: a novel index of left ventricular systolicfunction. J Am Soc Echocardiogr 2004;17:630-3.

16. Leitman M, Lysyansky P, Sidenko S, Shir V, Peleg E, Binenbaum M, etal. Two-dimensional strain–a novel software for real-time quantitativeechocardiographic assessment of myocardial function. J Am SocEchocardiogr 2004;17:1021-9.

17. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigen-baum H, et al. Recommendations for quantitation of the left ventricle bytwo-dimensional echocardiography. J Am Soc Echocardiogr 1989;2:358-67.

18. Pfeffer MA, Braunwald E. Ventricular remodeling after myocardial infarc-tion: experimental observations and clinical implications. Circulation1990;81:1161-72.

19. St John SuttonM, Pfeffer MA, Plappert T, et al, for the SAVE Investigators.Quantitative two-dimensional Echocardiographic measurements are ma-jor predictors of adverse cardiovascular events after acute myocardialinfarction. Circulation 1994;89:68-75.

20. Bolognese L, Neskovic AN, Parodi G, Cerisano G, Buonamici P, SantoroGM, et al. Left ventricular remodeling after primary coronary angioplasty;patterns of left ventricular dilation and long-term prognostic implications.Circulation 2002;106:2351-7.

21. Jamal F, Kukulski T, Sutherland GR, Weidmann F, D’hooge J, Bijnens B, etal. Can change in systolic longitudinal deformation quantify regionalmyocardial function after an acute infarction? An ultrasonic strain rateand strain study. J Am Soc Echocardiogr 2002;15:723-30.

22. Yang HS, Kang SJ, Song JK, Moon DH, Song JM, Kang DH, et al.Diagnosis of viable myocardium using velocity data of Dopplermyocardial imaging: comparison with positron emission tomography.J Am Soc Echocardiogr 2004;17:933-40.

23. Urheim S, Edvardsen T, Torp H, Angelsen B, Smiseth OA. Myocardialstrain by Doppler echocardiography: validation of a new method toquantify regional myocardial function. Circulation 2000;102:1158-64.

24. Derumeaux G, Loufoua J, Pontier G, Cribier A, Ovize M. Tissue Dopplerimaging differentiates transmural from nontransmural acute myocardialinfarction after reperfusion therapy. Circulation 2001;103:589-96.

25. Weidemann F, Dommke C, Bijnens B, Claus P, D’hooge J, Mertens P, etal. Defining the transmurality of a chronic myocardial infarction byultrasound strain-rate imaging: implications for identifying intramuralviability: an experimental study. Circulation 2003;107:883-8.

26. Skulstad H, Edvardsen T, Urheim S, Rabben SI, Stugaard M, Lyseggen E,et al. Postsystolic thickening in ischemic myocardium: active contractionor passive recoil? Circulation 2002;106:718-24.

27. Marwick TH. Measurement of strain and strain rate by echocardiography.Ready for prime time? J Am Coll Cardiol 2006;47:1313-27.

28. Korinek J, Wang J, Sengupta PP, Miyazaki C, Kjaergaard J, McMahon E, etal. Two-dimensional strain–a Doppler-independent ultrasound methodfor quantitation of regional deformation: validation in vitro and in vivo.J Am Soc Echocardiogr 2005;18:1247-53.

29. Notomi Y, Lysyansky P, Setser RM, Shiota T, Popovic ZB, Martin-Miklovic MG, et al. Measurement of ventricular torsion by two-dimen-sional ultrasound speckle tracking imaging. J Am Coll Cardiol 2005;45:2034-41.

30. Chan J, Hanekom L, Wong C, Leano R, Cho GY, Marwick TH. Differ-entiation of subendocardial and transmural infarction using two-dimen-sional strain rate imaging to assess short-axis and long-axis myocardial

function. J Am Coll Cardiol 2006;48:2026-33.