Br Heart J 1991;66:359-63

Estimating the size of myocardial infarction bymagnetic resonance imaging

L W Turnbull, J P Ridgway, J J Nicoll, D Bell, J J K Best, A L Muir

AbstractObjective-To develop a method to

measure myocardial infarct size bymagnetic resonance imaging and tocompare the results with pyrophosphatescanning by single photon emission com-puted tomography.Design-All patients underwent mag-

netic resonance imaging and pyrophos-phate scanning 5-7 days after the onsetof symptoms. Both measurements ofinfarct size were compared with therelease of creatine kinase MB and withventricular performance estimated byradionuclide ventriculography.Patients-19 patients (age 40-68 years)

who had sustained their first uncom-plicated myocardial infarction and whohad not been treated with thrombolytictherapy.Results-The site of infarction was

clearly shown by both imaging tech-niques and was identical in each patient.The volume of infarcted tissue measuredby magnetic resonance imaging agreedwell with the infarct size measured bysingle photon emission tomography(mean difference 2 7 cm3). Correlations ofboth imaging techniques with the releaseof creatine kinase MB were best whentotal release rather than peak releasewas used. Both imaging techniquescorrelated closely with the subsequentventricular performance.Conclusions-Magnetic resonance

imaging after acute infarction allowsmeasurement of infarct size and thismay prove useful in assessing new treat-ments designed to salvage myocardium.

Prognosis after acute myocardial infarctiondepends on the extent of myocardial damageand on residual left ventricular function.Salvage of acutely ischaemic but reversiblydamaged myocardium is widely accepted to beresponsible for the preservation of ventricularfunction and for improved survival afterthrombolytic therapy.' 2 However, there arediscrepancies between survival after reper-fusion and residual left ventricular function,3and it has been suggested that the beneficialeffects of thrombolysis may be more complexthan a simple reduction in infarct size.Currently, ventricular function is used as anindirect indicator of the mass of ventricleinfarcted, but in patients with previous infarc-tion this relation is distorted. More direct

measurements of infarct size are required toclarify the effects of intervention.Of the other standard techniques (including

ST segment and R wave mapping, cardiacenzyme release, and echocardiography) onlyradionuclide imaging with infarct avid agentsattempts directly to measure the mass ofdamaged myocardium. Recent reports suggestthat magnetic resonance imaging may offerconsiderable advantages for direct measure-ment of infarct size.45 Studies in both animalsand humans have shown that infarcted musclecan be recognised on gated magnetic reso-nance images and we showed that there is anincrease in the relaxation parameter, Ti, inpatients after acute infarction.6 In animalstudies there was a close relation betweeninfarct size measured from areas of increasedpixel intensity on magnetic resonance imagesand anatomical estimates of myocardial injuryidentified histochemically.'To extend these observations to humans we

examined myocardial infarct size with a lowfield magnetic resonance imaging system andcompared the estimated injury with singlephoton emission tomographic images of 99m-technetium pyrophosphate uptake, withrelease of the enzyme creatine kinase MB,and with residual left ventricular functionmeasured by radionuclide ventriculography.

Patients and methodsPATIENTSWe studied 19 patients (14 men and fivewomen) who had sustained their first myocar-dial infarction and who had not been treatedwith thrombolytic drugs. Myocardial infarc-tion was diagnosed on the basis of history andtypical electrocardiographic or cardiac enzymechanges or both. At the time of the examina-tion all patients were clinically stable with noevidence of either acute pulmonary oedema orlow output cardiogenic shock. The patientswere all in sinus rhythm and gave informedconsent before entering the study. None of thepatients gave a history of previous cardiacdisease or of other chronic medical conditions.

MAGNETIC RESONANCE IMAGINGTechniqueIn all patients magnetic resonance imagingwas carried out five to seven days after theonset of chest pain with a low field system(M & D Technology) operating at 0-08 T.Patients with either temporary or permanentcardiac pacemakers, prosthetic heart valves, or

previous intracranial surgery had already been

UniversityDepartment ofMedical Radiology,Royal Infirmary,EdinburghLW TurnbullJ J K BestUniversityDepartment ofMedical Physics andMedical Engineering,Royal Infirmary,EdinburghJ P RidgwayJ J NicollUniversityDepartment ofMedicine, RoyalInfirmary, EdinburghD BellAL MuirCorrespondence toDr LW Turnbull,Academic Departnent ofRadiology, RoyalHallamshire Hospital,Sheffield S1O 2JF.Accepted for publication25 June 1991

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Turnbull, Ridgway, Nicoll, Bell, Best, Muir

Figure 1 (A) Tl map ofan angled transverse imageobtained through theventricles showing a largesemicircular area ofreduced signal intensityinvolving theinterventricular septumand adjacent anterior leftventricular wall secondaryto infarction. (B) Areaswithin the myocardiumwith a Tl value twostandard deviations ormore above the mean Tivalue for normalmyocardium are shown inwhite.

excluded from the study. Scout images were

initially carried out in the coronal plane tovisualise the long axis of the ventricles. Theseimages were obtained with a field of view of384 mm, a matrix of 128 x 64, a short repeti-tion time (TR) of 240 ms, and a field echo timeof 22 ms. Four slices were obtained with a

16 mm slice thickness and separation. Fromthese images, short axis views of the ventricu-lar chambers were aligned. We used a cardiacgating technique with carbon fibre electrodes(Abingdon Instruments, Abingdon, Oxford)placed on the left anterolateral and the rightparasternal chest wall.8 The downslope of theelectrocardiographic T wave was used to syn-chronise data acquisition during end systole atapproximately 110 ms after the upstroke ofthe T wave. An interleaved saturationrecovery-inversion recovery pulse sequencewas used with a TI of 42 ms and a variableTR, depending on the RR interval. Eight to10 slices (12 mm thick) were acquired as fouracquisitions to obtain multiple images frombelow the cardiac apex to the level of theaortic arch. Two slices with a 42 ms timeseparation were obtained with each acquisi-tion which consisted of two averages of 64phase encoding steps and 128 frequencyencoding steps resulting in a pixel size of3 x 6 mm. These data were interpolated to a

128 x 128 matrix (3 x 3 mm) and smoothed on

the final display monitor for image analysis.

AnalysisThe calculated Ti map showed good contrastbetween normal myocardium, ischaemic myo-cardium, and chamber contents, and was usedto define the myocardial border (fig 1A). Theoutlines of the endocardial and epicardialinterfaces of the left ventricle, including the

interventricular septum, were defined inter-actively by using image analysis software todraw an irregular region of interest. Owing topartial volume effects from pericardial fat theTi values of the extreme apical segment werefrequently higher than those of the normalmyocardium, and these images were thereforeexcluded from analysis. The TI calculations9were based on a look-up table that was gen-erated from the saturation recovery and "dif-ference" image signals when a repetition timeof 1000 ms was assumed. However, because itwas shown from phantom experiments thatour measurements of Ti values, which arebased on these look-up tables, varied con-siderably with heart rate it was necessary tocalculate an upper limit of normal for eachindividual patient. This was done by takingthe mean Ti value plus two standard devia-tions from regions of a fixed size (approxi-mately 2 cm3) placed within normal myocar-dium on all the slices that included the leftventricle. These regions of interest were asremote as possible from the areas of increasedsignal and were retrospectively confirmed tobe separate from regions of increased pyro-phosphate uptake. An average TI value wasobtained for all the slices measured. Regionswithin the myocardium with a Ti valuegreater than this limit were then generated bythe computer (fig 1B) and their areasmeasured. These values were multiplied bythe slice thickness to obtain the volume of theinfarcted myocardium on each slice, and thenthese volumes were summed to obtain thetotal volume of infarcted myocardium.

REPRODUCIBILITYThe reproducibility of the technique was affec-ted by the measurement of both the mean andstandard deviation of normal myocardium andby identification of the endocardial and epicar-dial borders of the left ventricle. To determinethe intra and inter observer variability twoindependent observers performed measure-ments on the same four patient examinationson three separate occasions.The volume of infarcted myocardial tissue

varied by 10-1% between observers and theintra observer variability was 6-8 and 10-4%.This variation was primarily attributable tothe difference of 8-8% between the twomeasurements of the upper threshold limit fornormal myocardium (mean (2 SD)).

99M-TECHNETIUM PYROPHOSPHATE SCANNINGRadioisotope scanning with 99m-technetiumpyrophosphate was performed with a Maxi-Camera 400AT Gamma Camera equippedwith a low energy, general purpose, parallelhole collimator (International GeneralElectric) and a MicroDelta Plus computersystem (Siemens Gammasonics). Patientswere imaged between 24 and 36 hours afteradmission to hospital and two hours afteradministration of 600 MBq 99m-technetiumpyrophosphate. Patients were positionedsupine with both arms beside the head. Singlephoton emission tomography was performedwith a set of sixty four, 64 x 64 images taken

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Estimating the size of myocardial infarction by magnetic resonance imaging

over a 3600 arc with the radius of rotationselected to minimise the distance from thedetector to the chest wall. Each image wascollected for a preset time of 10 seconds and,in addition to the "auto-tune" facility, thecamera was further corrected for uniformity(using a 30 million count 99mTc flood) and forthe centre of rotation. Transverse images, onepixel thick, were reconstructed "on line" witha Butterworth filter of order 5 and a cut-offfrequency of 0-5 Nyquist. The myocardialuptake of pyrophosphate was determinedfrom the transverse images by a simple threedimensional thresholding procedure operatingat 65% of the peak voxel value within theinfarct volume. The threshold value of 65%has been shown'0 from phantom studies to bethe optimal value. The peak value in thevolume of interest was found after eachtransverse slice had been smoothed twice by anine point filter. Myocardial uptake wasanalysed by drawing a cuboid region ofinterest around the heart and counting thenumber of voxels >65% of the peak valuewithin that volume (fig 2). The number ofinfarct voxels was then summed and the sizeof infarction determined by multiplying bythe voxel size (0-24 cm'/voxel).

Before we calculated infarct volume wereviewed each transverse image, and if neces-sary, modified the region of interest to excludeareas of non-cardiac uptake such as the ster-num or ribs.

SERUM CREATINE KINASE MBSerum creatine kinase MB was measured byan optimised kinetic spectrophotometer assay.In 11 of the 19 patients, 4-8 blood sampleswere obtained from eight to 48 hours after theonset of symptoms. This allowed calculationof the total creatine kinase released. In theremaining eight patients only three blood

Figure 2 Single photon emission tomographic images of "'Tc-pyrophosphate uptake inthe myocardium of the same patient as fig 1. A and B show an extensive anteriorinfarction. (A) coronal section; (B) sagittal section; (C) transverse section; (D) scoutimage roughly equating to a planar anterior view.

samples were obtained and we used the high-est value to express a "peak" creatine kinaserelease. Both the total and the peak creatinekinase release were used in our correlations.

RADIONUCLIDE VENTRICULOGRAPHYThis was carried out on the day before dis-charge from hospital (mean 7 days), when thepatient was clinically and radiologically clearof heart failure. All the patients were studiedin the supine position and cardiac imaging wasperformed in approximately a 300 left anterioroblique projection with a 100 caudal tilt. Theprecise angle was chosen to optimise theseparation of the ventricles. After injection of700 MBq 99mTc human serum albumin, imag-ing was carried out with a Siemens low energymobile gamma camera and the data werecollected by a Micro Delta computer. Theejection fraction was calculated by a gatedblood pool technique."

STATISTICAL ANALYSISStatistical analysis was performed with theSPSS/PC + computer programme.

ResultsThe location of the infarct was clearly demon-strated and was identical by both pyrophos-phate scanning and magnetic resonance imag-ing in 17 ofthe 19 patients. No abnormality wasshown by either imaging technique in onepatient, while in a second pyrophosphate imag-ing showed only a very small area of increaseduptake anteriorly, but magnetic resonanceimaging failed to demonstrate any abnormality.In the first of these two patients the electrocar-diogram was normal and in the second it wasindeterminate owing to the presence of leftbundle branch block. Both patients showedonly a minor rise in the peak serum creatinekinase MB values of 172 and 522 U/I respec-tively.We compared the myocardial infarct size

measured by pyrophosphate scanning andmagnetic resonance imaging by plotting thedifference between the two values against themean infarct size obtained from both methods'2(fig 3). This showed amean difference of2 7 cm3(magnetic resonance infarct size minus pyro-phosphate infarct size), while the standarddeviation of the difference was 9-9 cm'. Thelimits of agreement were - 22-5 and 17 1 cm'and the standard error of the mean was2-27 cm3. Hence the 95% confidence intervalfor the lower limit of agreement was - 30-8 to- 14-3 cm', while for the upper limit ofagreement the 95% confidence interval was8-9 to 25-4 cm'. These intervals showedmoderately good agreement between the twomethods, with reasonable consistency over therange of values encountered, although discrep-ancies were noted with infarct sizes > 80 cm3.The table shows the correlations between

infarct size, creatine kinaseMB release, and leftventricular ejection fraction. The creatinekinase MB release curves could be calculated inonly 11 patients, but there was a good correla-tion between the peak and total creatine kinase

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~~~~~~~~~~~~~~~~~~~~~~~~Turnbull,Ridgway, Nicoll, Bell, Best, Muir

E 20-

-a15-

+1 10-

0

-15

m

a c -25-0

Mean

+2SD

0

0*

0

-Mean

0~~~~~~

MMean-2SD

6 10o 30 40 50 60 7'0 810Average myocardial infarct size measured by MR I and PYP (cm)

Figure 3 Diference in myocardial infarct size between magnetic resonance imaging

(MRI) and 01'Tc-pyrophosphate scanning (PYP) plotted against the average value

measured by these techniques.

values. The size of the infarct measured by peak

creatine kinase correlated only moderately with

the volume of the infarct measured by pyro-

phosphate (r = 0.53, 0-02 > p > O-O1) and by

magnetic resonance imaging (r = 0-52, -O5 >

p > 0-02). The correlations were weakened by

the presence of two particularly high creatine

kinase results (6955 and 6255) that were con-

siderably greater than the other values.

However, the total creatine kinase release,

which included these two values, correlated

well with the infarct size measured by both

pyrophosphate (r = 0-75, 0*01 > p > 0-O01)and magnetic resonance imaging (r = 0-62,O-O5 > p > 0-02). The residual left ventricular

function measured by radionuclide ventricu-

lography correlated significantly with the

volume of infarct measured by both magnetic

resonance (r = 0-79, p < O0O01) and pyro-

phosphate imaging (r = 0-79, p < 0-001).

There was also a good correlation between the

left ventricular ejection fraction and the peak

creatine kinase release (r = 0-63, 0-O1 >p>O-O01), but a better correlation was obtained

with the total creatine kinase release

(r = 0-78, 0.01 > p > 0-OO1).

Discussion

The primary determinant of prognosis after

acute myocardial infarction is the size of the

area of infarction.13-5 However, despite its

importance, routine clinical measurement of

infarct size has not been achieved. The tech-

niques currently used are indirect and may be

misleading after thrombolytic therapy. Peak

serum creatine kinase values are more impor-

tant. Analysis of creatine kinase MB release

curves correlates well with histological infarct

size and provides prognostic information.""'However, after thrombolytic therapy there is

an early accelerated "washout" of cardiac

enzymes, presumably when blood flow is re-

stored through partially necrotic myocar-

dium.'9 Electrocardiographic techniques are

used to map the extent of infarction but are

inaccurate in assessing small non-transmural

or posterior lesions.""2 Echocardiography is

mainly of use in determining areas of wall

thinning, dyskinesis, or akinesis, and hence

also has major limitations. Residual ventricular

function gives an indication of myocardial

damage but is unreliable when there has been

previous infarction. Tissue characterisation by

any imaging technique remains an elusive goal.Since the introduction of single photon emis-

sion tomography, pyrophosphate imaging has

been considered a sensitive method for the

diagnosis and measurement of acute myocar-

dial infarcts.22 The use of single photon emis-

sion tomography has allowed more accurate

detection of posterior, inferior, and small

subendocardial infarcts, particularly after the

addition of blood pool overlay."3 These data

correlated well with the histological findings in

animals,23 and with analysis of serum creatine

kinase MB release and residual left ventricular

function in humans.

There are certain limitations to.- pyrophos-

phate imaging. The delivery of the radio-

nuclide to the centre of a large infarct may be

incomplete.2 Our single photon emission

tomographic technique overcomes this by

measuring the volume defined by pyrophos-

phate rather than by quantifying the amount of

isotope concentrated in the unevenly perfused

tissue. More uniform labelling can be achieved

by antimyosin antibodies, labelled with

indium, but the poorer imaging characteristics

of indium offset this advantage. Radionuclide

imaging also involves exposure to a significant

radiation dose and is only useful for up to five

days after infarction, whereas our own work,

performed in human subjects, showed that the

maximum increase in TI is not obtained for up

to five days after infarction and persists for a

long time thereafter.2

To determine the extent of myocardial

Correlations between measurements of infarct size, left ventricular ejection fraction (%), and release of creatine kinaseMB (Ull)

MRI 4-'"Tc PYP LV ejection Peak creatineinfarct size infarct size fraction kinase

LV ejection fraction n =18 n =18r =-0-79 r =-0-79p < 0*001 p < 0-001

Peak creatine kinase n 18 n =18 n =17r=0-52 r=0-53 r= -0-630-05>p >0O02 0-02 > p>OOOl0 0.01 >p > 0OO

Total creatine kinase n =11 n =11 n =11 n = 11r 0-62 r 0-75 r= -0-78 r =0-930-05 > p > 0-02 0-01 > p > 0-001 0-01 > p > 0-001 p < 00001

LV, left ventricle; MRI, magnetic resonance imaging; PYP, pyrophoaphate.

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Estimating the size of myocardial infarction by magnetic resonance imaging

infarction by magnetic resonance imaging, wehad to define Ti values for normal myocar-dium. Because the measured TI valuesobtained from our system varied with repeti-tion time it was essential to define a thresholdlimit for each individual patient. Althoughnormal myocardium was identified subjectivelythe inter observer variability of 101% suggeststhat this is an acceptable method. In this studywe related the volume of infarcted myocardiummeasured by magnetic resonance imaging fiveto seven days after infarction to several vari-ables that also reflect infarct size.We chose to obtain the magnetic resonance

images at this stage because our previous workhad shown this to be the time of maximalchange. We studied patients with their firstmyocardial infarction so that preservation ofventricular function after infarction wouldnegatively correlate with infarct size. In addi-tion, because our patients were not treatedwith thrombolytic therapy the creatine kinasekinetics would be unaltered. Our results indi-cate that with a low field magnetic resonanceimaging system Ti maps provide estimates ofinfarct size that agree closely with other tech-niques. We found a good agreement betweenmagnetic resonance and pyrophosphate imag-ing and both these techniques correlated wellwith depressed ventricular function measuredafter infarction. Poorer correlations wereobtained with peak creatine kinase but thesewere improved in the group of patients forwhom enough data points were available tocalculate the total release of creatine kinaseMB.We expect that the use of a 128 x 128 pixel

matrix and a reduced slice thickness willimprove the precision of infarct size measure-ment by magnetic resonance imaging althoughit will increase the examination time. Manyfactors, such as the field strength and theimaging pulse sequence, can alter the ability todetect myocardial damage. Currently thesecond or third echo of a multiple spin echosequence is widely used to detect myocardialinfarction, but particularly at high fieldstrengths a paramagnetic contrast agent, suchas gadolinium diethylenetriamine pentaaceticacid may then be required to demonstrate areas

of damage.26 This study shows the ability of a

low field system with a saturation recovery-inversion recovery plus sequence to measure

human infarct size and avoid the routine use

of paramagnetic contrast agents. Because Tivalues remain raised for the first three monthsafter infarction,25 this technique will provideinformation on infarct size in the convalescentperiod.

We thank Mrs R H B Armstrong and Miss F Taddei for theirexcellent technical help. This work was supported in part by theBritish Heart Foundation.

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