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DOI: 10.1161/01.CIR.0000065249.69988.AA published online Apr 7, 2003; Circulation

Frank A. Flachskampf Reulbach, Uwe Nixdorff, Günther Platsch, Torsten Kuwert, Werner G. Daniel and Jens-Uwe Voigt, Bert Exner;, Kristin Schmiedehausen, Cord Huchzermeyer;, Udo

Objective Evidence of Inducible IschemiaStrain-Rate Imaging During Dobutamine Stress Echocardiography Provides

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Strain-Rate Imaging During Dobutamine StressEchocardiography Provides Objective Evidence

of Inducible IschemiaJens-Uwe Voigt, MD; Bert Exner; Kristin Schmiedehausen, MD;

Cord Huchzermeyer; Udo Reulbach, MD; Uwe Nixdorff, MD, FESC; Günther Platsch, MD;Torsten Kuwert, MD; Werner G. Daniel, MD, FESC; Frank A. Flachskampf, MD, FESC

Background—Interpretation of dobutamine stress echocardiography (DSE) is subjective and strongly dependent on theskills of the reader. Strain-rate imaging (SRI) by tissue Doppler may objectively analyze regional myocardial function.This study investigated SRI markers of stress-induced ischemia and analyzed their applicability in a clinical setting.

Methods and Results—DSE was performed in 44 patients with known or suspected coronary artery disease. Simultaneousperfusion scintigraphy served as a “gold standard” to define regional ischemia. All patients underwent coronaryangiography. Segmental strain and strain rate were analyzed at all stress levels by measuring amplitude and timing ofdeformation and visual curved M-mode analysis. Results were compared with conventional stress echo reading. Innonischemic segments, peak systolic strain rate increased significantly with dobutamine stress (21.660.6 s21 versus23.461.4 s21, P,0.01), whereas strain during ejection time changed only minimally (21766% versus21669%,P,0.05). During DSE, 47 myocardial segments in 19 patients developed scintigraphy-proven ischemia. Strain-rateincrease (21.660.8 s21 versus 22.061.1 s21, P,0.05) and strain (21667% versus21068%, P,0.05) weresignificantly reduced (bothP,0.01 compared with nonischemic). Postsystolic shortening (PSS) was found in allischemic segments. The ratio of PSS to maximal segmental deformation was the best quantitative parameter to identifystress-induced ischemia. Compared with conventional readings, SRI curved M-mode assessment improved sensitivity/specificity from 81%/82% to 86%/90%.

Conclusions—During DSE, SRI quantitatively and qualitatively differentiates ischemic and nonischemic regionalmyocardial response to dobutamine stress. The ratio of PSS to maximal strain may be used as an objective marker ofischemia during DSE.(Circulation. 2003;107:2120-2126.)

Key Words: stressn ischemian echocardiographyn coronary diseasen scintigraphy

Dobutamine stress echocardiography (DSE) is well estab-lished for detecting inducible ischemia. Ischemia is

defined by a regional reduction or deterioration of myocardialthickening or inward motion of the endocardial border.1–3

Reading DSE is subjective and strongly dependent on expe-rience, making more objective markers desirable.4–6 In ani-mal and human studies, myocardial ischemia also caused adelayed onset and termination of systolic shortening.7–10

However, it is difficult to visually assess this potential sign ofischemia during DSE.11

Echocardiographic strain-rate imaging (SRI)12 reliablymeasures regional myocardial deformation (strain,e) anddeformation rate (strain rate, SR) compared with sonomi-crometry.13 Left ventricular wall motion is depicted accu-rately at rest and during acute and chronic ischemia,14–16

including dobutamine-induced ischemia in animal mod-els.17–19 Recent reports on the use of SRI during DSE forviability and ischemia are promising.20,21

Thus, this study investigates regional myocardial strain rateand strain response during DSE in patients and compares theresults with conventional DSE reading, perfusion scintigra-phy, and coronary angiography.

MethodsStudy PopulationThe study population (Table 1) comprised 44 consecutive patientsreferred for DSE to detect the presence or absence of inducibleischemia. Fifteen patients had moderate regional wall-motion abnor-malities at rest because of previous infarction. Medication was notdiscontinued. Patients not in sinus rhythm, with bundle-branch block

Received November 12, 2002; revision received February 7, 2003; accepted February 7, 2003.From the Medizinische Klinik II (J.-U.V., B.E., C.H., U.N., W.G.D., F.A.F.), Nuklearmedizinische Klinik (K.S., G.P., T.K.), and Institut für

Medizininformatik, Biometrie, und Epidemiologie (U.R.), Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.Presented in part at the 74th Scientific Sessions of the American Heart Association, Anaheim, Calif, November 11–14, 2001, and published in abstract

form (Circulation. 2001;104[suppl II]:II-627, II-751).Correspondence to Dr Jens-Uwe Voigt, Medizinische Klinik II, Friedrich-Alexander-Universität Erlangen-Nürnberg, Ulmenweg 18, 91054 Erlangen,

Germany. E-mail [email protected]© 2003 American Heart Association, Inc.

Circulation is available at http://www.circulationaha.org DOI: 10.1161/01.CIR.0000065249.69988.AA

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or more than mild valvular heart disease, were excluded. Allparticipants gave written informed consent before the examinations.

Dobutamine ChallengePatients underwent a standard DSE protocol2 with incrementaldobutamine infusion rates of 10, 20, 30, and 40mg · kg21 · min21 for3 minutes each and up to 2 mg of atropine if necessary. Criteria forterminating the test were achievement of target heart rate of(2202age)30.85 bpm, development or deterioration of wall-motionabnormalities, angina, ischemic ECG changes, systolic blood pres-sure increase to.240 mm Hg or decrease to,100 mm Hg, andsevere ventricular or supraventricular arrhythmias.

Echocardiographic Image AcquisitionPatients were scanned in the left supine position from an apicalwindow with a Vivid Five ultrasound scanner (GE Vingmed). Atbaseline, at each step of the DSE, and during recovery, 3 heart cyclesof the apical 4-, 3-, and 2-chamber views were captured in conven-tional 2D and color tissue Doppler mode. The image sector was setas narrow as possible, which resulted in a color tissue Doppler framerate between 133 and 147 frames per second (temporal resolution,7.5 to 6.8 ms). Echo data were stored digitally for subsequent offlineanalysis.

Tissue Doppler Data ProcessingA detailed description of the data processing and its theoreticalbackground is provided by Heimdal et al12 and Voigt et al.14,22 Weused dedicated research software (TVI 6.0, GE Vingmed, and TVA,J.U. Voigt, University of Erlangen, Germany). Longitudinal strainand strain rate were calculated from color tissue Doppler velocitydata (calculation distance, 8 mm). Color-coded strain-rate curvedM-modes were reconstructed from each myocardial wall (septal,anteroseptal, anterior, lateral, posterior, and inferior). Wall motionwas tracked manually to maintain midwall position. Strain andstrain-rate curves were obtained from the middle of the basal, mid,and apical segments of each wall. Thus, an 18-segment model of theleft ventricle was used for all further analysis. Three heart cycleswere averaged temporally to improve signal-to-noise ratio of thecurves. Strain curves were baseline-corrected. Timing of aortic andmitral valve opening (AVO, MVO) and closure (AVC, MVC) wasderived from the echo recordings.15

MeasurementsWe measured peak systolic strain rate (SRpeak sys), the maximumlength change during the entire heart cycle (emax), strain during

ejection time (eet), and postsystolic strain (eps), defined as themaximum length change between AVC and the regional onset ofmyocardial lengthening caused by early mitral filling (Figure 1).Values are expressed in seconds21 (strain rate) and percent (strain)and are negative in shortening and positive in lengthening myocar-dium. To account for systolic shortening and overall curve ampli-tude, the ratioseps/eet andeps/emax were calculated.

The beginning of myocardial shortening (tbos) and timing ofpeak systolic strain rate (tpsr) were measured relative to AVO and theend of shortening (teos) relative to AVC. Values are given inmilliseconds and as percentage of ejection time.

Visual AssessmentConventional 2D recordings were read by an experienced readerblinded to all patient data using a quad screen with synchronizeddisplay of baseline, low-dose, peak, and recovery stage. Ischemiawas defined as regional reduction or deterioration of radial myocar-dial thickening in$1 segment. Subsequently, curved M-modes oflongitudinal strain rate were assessed visually. Delayed onset ofsystolic shortening of.20 to 23 ms (3 frames) after AVC, visibledeterioration of systolic shortening, and development of postsystolicshortening (PSS) were considered an ischemic response. Artifactswere identified by their band-like shape (Figure 2).

Scintigraphic Image Acquisition and Data ProcessingDuring DSE, the radioactive tracer (99mTc-tracer, Cardiolite, Bristol-Meyers-Squibb) was injected at peak stress, and dobutamine wascontinued for 2 minutes. Scintigraphic images were acquired within1 hour. Baseline perfusion scintigraphy was performed before thestress test or the day after. Single-photon emission computedtomography (SPECT) was performed with a Multi-SPECT 3 scanner(Siemens) with a low-energy, high-resolution collimator and a gatedacquisition protocol. SPECT data were reconstructed with filteredbackprojection and visualized with 20% background correction.Corrected tracer uptake at baseline and at peak stress was quantifiedand compared (ECT-Tool Box, Siemens). As in echocardiography,18 myocardial segments were defined and assigned as nonischemic,ischemic, or scarred by an experienced reader blinded to DSE resultsand other patient data.

Coronary AngiographyCoronary angiograms were obtained within 4621 days from thestress echo study, and stenosed vessels were quantified (QCAQuantcor, Siemens). A diameter stenosis of.50% was consideredinductive of stress ischemia. To account for variable coronaryanatomy, a blinded reader experienced in both coronary angiographyand echocardiography assigned myocardial segments to the pre-sumed perfusion territories of stenosed vessels, considering the leftcoronary to generally supply anterior, anteroseptal, and mid andapical septal segments, the circumflex to supply the lateral wall, andthe right coronary artery the basal septal and basal and mid inferiorsegments. The remaining segments were assigned depending on therelative size of the 3 coronaries and their branches.

StatisticsIn this study, scintigraphy was the “gold standard” for definingischemia. Segments with scintigraphic evidence of scar or echocar-diographic wall-motion abnormalities at baseline were excludedfrom the analysis.

If not stated otherwise, all data analysis and comparisons betweenimaging modalities were performed on a segmental level. Continu-ous parameters are expressed as mean6SD. Grouped data weretested for normal (gaussian) distribution and equality of SD (Bartlett,Kolmogorov, and Smirnov) and compared by use of a 2-tailedt test.For .2 groups, ANOVA was used. Probability values ofP,0.05were considered statistically significant. Receiver operating charac-teristics (ROCs) were analyzed for SRI and timing parameters.kstatistics were used to compare 2D echo and strain-rate readings withscintigraphy. Sensitivities and specificities were calculated for 2Decho readings and SRI parameters.

TABLE 1. Characteristics of Patients With and WithoutIschemic Response During Dobutamine Stress

Nonischemic Ischemic P

No. of patients 25 (57) 19 (43)

Age, y 62610 6369 NS

b-Blocker 18 (72) 13 (68) NS

Nitrate 3 (12) 8 (42) NS

Hypertension 19 (76) 15 (79) NS

Diabetes 7 (28) 7 (37) NS

Smoking 8 (32) 9 (47) NS

Ejection fraction, % 6466 6164 NS

Baseline WMA 6 (14) 9 (20) NS

Ischemic segments 0 47 (7.3)

Ischemic segments/patient 0 2.562.1

Baseline BP, mm Hg 132/77 134/73 NS/NS

Peak stress BP, mm Hg 146/79 158/73 NS/NS

Values are n (%) or mean6SD. WMA indicates wall motion abnormalities;BP, blood pressure.

Voigt et al Strain-Rate Imaging in Stress Echocardiography 2121



ResultsNo adverse events occurred during DSE. DSE was terminatedbecause of signs of ischemia in 10 patients and after achiev-ing target heart rate in 34 patients. In total, 792 myocardialsegments on$4 stress levels each were analyzable (3786segments). Eighty segments (10.1%) were excluded becauseof scintigraphic evidence of scar, echocardiographic wall-motion abnormalities, or abnormal strain-rate patterns at rest.On scintigraphy, 19 of 44 patients (43%) had an ischemicresponse in 47 of 712 segments (7.3%). All patients withinducible ischemia on scintigraphy had significant stenosis(mean, 80618%) in the supplying coronary artery. No patientwithout scintigraphic ischemia had significant coronary ste-nosis. Patients with and without ischemic response did notdiffer significantly with respect to age, medication, riskfactors, baseline ejection fraction, or average blood pressureand heart rate at baseline and peak stress (Table 1).

FeasibilityConventional visual wall-motion assessment was possible in97% of the segments. Quantitative analysis of strain and

strain-rate curves was possible in only 85% of the segmentsbecause of noise and artifacts. Qualitative visual assessmentof curved M-modes, however, was achieved in 95% of thesegments. As reported previously, interobserver and intraob-server variability of strain and strain-rate measurementsranged from 5% to 10% in our laboratory.14 The variability oftime-interval measurements ranged from 10 to 15 ms.15

Quantitative DSE Analysis

Amplitude of Strain and Strain RateData are exemplified in Figures 1 and 2 and summarized inFigures 3 and 4 and Table 2. Baseline parameters of ischemicand nonischemic segments did not differ significantly. DuringDSE, SRpeak sysclearly increased in nonischemic segments. Incontrast to the slight changes in the averaged data (Figure 3b),individual emax and eet showed a biphasic response in mostnonischemic segments. In ischemic segments at peak stress,eet and increase in SRpeak syswere clearly reduced, whereasemax

remained almost constant.

Figure 1. Examples of ischemic and nonischemic stress response. Left, baseline; right, peak stress. Dotted vertical lines indicate MVC,AVO, AVC, and MVC. a, Two-chamber views with color-coded strain-rate overlay and perfusion scintigraphy images in matching orien-tation. Stress-induced inferoapical ischemia (red arrow). Markers “apical” and “basal” indicate origin of curves below. b, Strain rate.Typical nonischemic patterns at baseline and in basal curve at peak stress. In ischemic apical region, note delayed onset and end ofshortening and low peak systolic strain rate at peak stress. Measurements of SRpeak sys, tbos, and teos relative to AVO and AVC are illus-trated. c, Strain curves. Note early systolic bulging (arrow) and marked PSS in inferoapical curve at peak stress. Other curves showtypical nonischemic patterns. Measurements of emax, eet, and eps are illustrated. Note that in strain curves, position of zero line dependsonly on definition of “beginning” of cardiac cycle and, thus, is arbitrary. d, ECG, time scale.

2122 Circulation April 29, 2003



Timing of Myocardial Shortening and PSSData are provided in Table 2. In all segments at baseline,segmental systolic shortening began at approximately AVO.SRpeak sysoccurred in the first third of ejection time. In mostsegments, shortening at baseline was systolic only; in twofifths, however, PSS of minor amplitude was found. PSSamplitude did not correlate with blood pressure. At peakstress, nonischemic segments showed a similar pattern.

The ischemic response at peak stress differed significantly:Onset and peak of shortening were delayed, and all segmentsshowed a markedly delayed end of shortening. This ische-mia-induced PSS had a significantly higher amplitude than innonischemic segments.

By ROC analysis,eps/emax was the best parameter to identifyischemia (area under the curve, 0.899;P,0.05). An eps/emax

cutoff of 35% identified patients with ischemia with asensitivity of 82% and a specificity of 85%.eps/eet performedcomparably (area under the curve, 0.898; cutoff, 55%; sen-sitivity, 82%; specificity, 82%). All other SRI parameters hadsignificantly less discriminating power (see Figure 5).

Qualitative DSE Analysis

Conventional 2D ReadingCompared with the scintigraphic gold standard, 78% of thereadable ischemic segments were detected by conventionalreading. With this, DSE sensitivity and specificity per patientwere 81% and 82%, respectively (k, 0.62).

Strain-Rate Curved M-Mode ReadingIn nonischemic segments, baseline and peak stress curvedM-mode patterns differed only in hues and the duration oftime intervals. The general sequence of lengthening andshortening events remained unchanged.

In stress-induced ischemia, reduction of systolic strain rate(color change) and changes in timing of events (particularlyoccurrence of PSS) were clearly visible. Of the ischemicsegments, 89% were identified, resulting in a DSE testsensitivity and specificity of 86% and 90%, respectively (k,0.74) (Figures 2 and 6).

DiscussionNormal Stress Response of Strain and Strain RateIn normally perfused myocardium, SRpeak sysclearly increasedwith increasing dobutamine dosage (Figure 3a). This is in

Figure 3. Averaged segmental values of a, SRpeak sys and b, eet,emax at rest, with incremental doses of dobutamine and atropine(atr.), and at recovery (rec.).

Figure 2. Perfusion scintigrams and color-coded strain-rate curved M-modes of a patient’s anteroseptal wall at baseline (left) and dur-ing dobutamine stress (right). a, Ischemic response. Note normal strain-rate patterns at rest and delayed onset of myocardial shorten-ing and marked PSS in apical region at peak stress (red arrows). b, Same patient after successful revascularization of the left anteriordescending coronary artery. Normal strain-rate patterns both at rest and at peak stress. Middle of lower left curved M-mode shows atypical artifact, identifiable by its band-like shaped color inversion (yellow/blue).




agreement with previous studies.17,18 In contrast, averagedemax andeet changed only little (see Figure 3b), although clearbiphasic responses were observed in individual patients. Thelatter is concordant with reports on animal experiments17,18

and comparable to human studies.23

Strain and Strain-Rate Amplitude inStress-Induced IschemiaNew or worsening abnormalities of radial wall thickening arethe classic echocardiographic signs of ischemia in DSE.Although SRI measures longitudinal deformation, in ourstudy, botheet and the increase in SRpeak syswere significantlyreduced in ischemic segments, confirming earlier stud-ies.8,13,17,18Interestingly,emax of ischemic segments remainedalmost constant because of the increasing or newly occurringPSS.

Timing of Regional Deformation and PSSOnly in ischemia, tbos and teos increased significantly becauseof delayed contraction and marked PSS (Figure 1). Both havebeen known for years to be markers of myocardial dysfunc-tion.9,10 The mere presence of PSS, however, is not specificfor ischemia, because it is often found at rest,8,15 in our studyin two fifths of all segments at baseline. At peak stress, PSSwas found in 100% of the ischemic but also in 47% of thenonischemic segments.

Criteria for Defining Stress-Induced IschemiaSimple amplitude cutoffs foreet or SRpeak sys to identifyischemia during DSE performed rather poorly (Figure 5).Reasons may be both noisy strain-rate signals and differingcontractile states of the individuals. Assessing timing by SRIis less sensitive to noise, which may explain the better

Figure 4. Myocardial strain and strain rate insegments with ischemic (gray) and nonischemic(black) stress response. All differences at peakstress are significant (P,0.01). a, SRpeak sys; b,eet; c, eps in segments with PSS.

TABLE 2. Strain Rate Imaging Parameters in Segments With Nonischemic (n5665) and Ischemic (n547) ResponseDuring Dobutamine Stress

Baseline Peak Stress

Nonischemic Ischemic Nonischemic Ischemic

Sign.‡ Sign.§ Sign.‡ Sign.§

Heart rate, bpm 70612 65611 NS 134618 † 130620 NS †

SRpeak sys, 1/s 21.660.6 21.660.8 NS 23.461.4 † 22.061.1 † *

emax, % 22066 21968 NS 22369 † 220610 NS NS

eet, % 21766 21667 NS 21669 * 21068 † *

eps, % 0.963.4 0.963.5 NS 0.464.1 * 26.764.5 † †

eps/emax, % of emax 24616 22619 NS 22617 * 39630 † †

PSS, % of segment 39 43 47 100

eps, %i 22.161.4 22.461.5 NS 22.661.8 * 26.764.5 † †

eps/emax, % of emaxi 1068 15614 * 12614 NS 39630 † †

tbos, ms (tbos, % of ET) 9657 (3617) 18645 (6614) NS 12666 (7640) NS 47645 (28628) * *

tpsr, % of ET 31623 35625 NS 31643 NS 55638 * *

teos, ms (teos, % of ET) 24678 (8626) 32663 (11622) NS 24677 (15646) NS 79645 (47628) † †

ET indicates ejection time.*P,0.05, †P,0.01.‡Significance vs segments with nonischemic stress response.§Significance vs baseline.iSegments with PSS only.




performance of teos(as a measure of PSS) and the good curvedM-mode reading results. To separate “ischemic” from “nonis-chemic” PSS and to increase the specificity of this highlysensitive marker of ischemia, its amplitude relative to maxi-mum shortening (which incorporates systolic shortening) wasanalyzed. During ischemia,eps/emax increases because of PSSand reduced systolic shortening.eps/emax was the best quanti-tative parameter to define stress-induced ischemia in DSE(similar to eps/eet but significantly better than all otherparameters).

Clinical ImplicationsDSE is based on the visual assessment of regional myocardialfunction and thus is subjective. SRI is feasible in the clinicalsetting, measures longitudinal myocardial deformation di-rectly independently of translation, and offers parameterscomparable and possibly superior to the visually assessedregional (radial) wall thickening. PSS is a well-known sign ofischemia. Because of its relatively low amplitude and, inparticular, its short-lived nature, however, its visual recogni-

tion (known as “contraction asynchrony”) is difficult.11 SRIallowed us to quantify PSS and, with a cutoff value ofeps/emax

.35%, resulted in a sensitivity of 82% and specificity of 85%for the detection of stress-induced ischemia.

A particularly practical approach is the visual comparisonof color-coded strain-rate curved M-modes at baseline andduring stress, because they combine information on thedelayed onset of shortening and deterioration of systolicfunction (akinesia, yellow to green; dyskinesia, yellow toblue) and are highly sensitive to the occurrence of PSS. Ourdata suggest that visual interpretation of strain-rate curvedM-modes is more accurate than conventional visual DSEassessment (sensitivity, 86% versus 81%; specificity, 89%versus 82%; see Figure 6).

LimitationsStrain and strain-rate measurements are subject to noise,angle artifacts, and interindividual variability. Therefore,relative parameters (in particular,eps relative toemax or eet) andtime intervals should be preferred.

A further limitation of SRI is that currently, unlike visualor magnetic resonance analysis, only apical scanning offerscomparable information on all segments, which restrictsanalysis to longitudinal deformation only. However, the goodspatial and unrivaled temporal resolution of SRI make ituniquely suited to assess short-lived regional phenomena likePSS.

In our analysis, we omitted segments with wall-motionabnormalities at rest for the sake of clarity. Further studieswill be needed to address SRI characteristics of scar, partialscar, and dysfunctional but viable myocardium during DSE.

Although SRI analysis is currently still time consuming, itis clinically applicable, and with modest software improve-ments, measurements will be a matter of a few minutes atmost, similar to flow Doppler.

ConclusionsDoppler SRI is feasible and able to objectively differentiateischemic and nonischemic myocardium. In particular, thedelayed end of myocardial shortening after AVC (PSS)identifies stress-induced ischemia with high sensitivity and ifamplitude of PSS (eps/emax or eps/eet) is considered, goodspecificity, possibly superior to that of conventional visualDSE assessment.

AcknowledgmentsThis work was supported in part by the “ELAN-Programm” ofErlangen University.

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