DIAGNOSTIC METHODS

COMPUTER-ASSISTED TOMOGRAPHY

The usefulness of x-ray computed tomography for

the diagnosis of myocardial infarction
YOSHIAKI MASUDA, M.D., HIDEO YOSHIDA, M.D., NOBUHIRO MOROOKA, M.D.,
SHIGERU WATANABE, M.D., AND YOSHIAKI INAGAKI, M.D.

ABSTRACT Conventional and enhanced computed tomographic (CT) examinations were performed
in 103 patients with myocardial infarction for evaluation of the diagnostic usefulness of CT. After
intravenous bolus injection of contrast material, an initial filling defect and late enhancement of the
infarcted myocardium appeared on the cardiac CT images. These two findings were direct evidence of
myocardial infarction; the former was found mostly in the patient with recent myocardial infarctions,
and the latter was recognized both in those with recent and those with "remote" infarctions. Wall
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thinning at the site of infarction was found by enhanced CT mostly in patients with anteroseptal or
extensive anterior infarctions, and was rarely found in patients with inferoposterior infarctions. Left
ventricular aneurysms and ventricular thrombi were found by enhanced CT in 39 and 23 of the 103
subjects, respectively, and the sensitivity of CT in detecting intracardiac thrombi was higher than that
of two-dimensional echocardiography. Calcification of the myocardium and pericardial effusion asso-
ciated with myocardial infarction were also detected by conventional nonenhanced CT. Thus, cardiac
CT was found to be a useful test in evaluating patients with myocardial infarction.
Circulation 70, No. 2, 217-225, 1984.

RECENTLY x-ray computed tomography (CT) has
been validated as a useful noninvasive diagnostic
method for use in patients with various cardiac dis-
eases. As far as the application of CT in patients with
myocardial infarction is concerned, since the report by
Adams et al. ,' which demonstrated that the CT find-
ings in infarcted myocardium differed from those in
normal myocardium whether or not contrast enhance-
ment was used, the possibility of detection of myocar-
dial infarction and of evaluating its extent and the stage
by this technique has drawn much interest.
To date there have been many reports of the CT
findings in animals with experimentally produced in-
farction.2 6 Several studies reported that the infarcted
myocardium appeared as an area of poor enhancement
on the x-ray during the first few minutes of the intrave-
nous administration of contrast material.", 1016 Subse-
quently there was a greater degree of enhancement of
the infarcted area compared with the normal myocardi-
um. This phenomenon was called late enhancement of
the myocardium and it was noted to be persistent for
From the Third Clinical Department of Internal Medicine, Chiba
University School of Medicine, Chiba, Japan.
Address for correspondence: Dr. Yoshiaki Masuda, The Third Clini-
cal Department of Internal Medicine, Chiba University School of Medi-
cine, 1-8-1 Inohana, Chiba City 280, Japan.
Received Aug. 15, 1983; revision accepted April 5, 1984.
Vol. 70, No. 2, August 1984
several minutes to 1/2 hr after the injection of contrast
material.
In spite of these excellent results from fundamental
studies, the clinical application of CT in the diagnosis
of myocardial infarction has not become popular thus
far. We have been studying the clinical value of CT in
the evaluation of patients with myocardial infarction.
In previous articles we reported the abnormality of
regional wall movement in the infarcted heart detected
by electrocardiographically gated CT'7 and the in-
crease in CT values in the congestive lung resulting
from myocardial infarction.'8 The purpose of this re-
port is to describe other CT diagnostic findings in
patients with myocardial infarction.
Methods
Subjects. One hundred and three patients with recent and
"remote" transmural infarctions, including 86 men and 17
women with an age range of from 33 to 84 years, were studied.
According to the electrocardiographic criteria for infarct loca-
tion,19 they were classified into three groups; group A included
56 patients with anteroseptal or apical infarctions, group B 24
patients with extensive anterior infarctions, and group C 23
patients with inferior (diaphragmatic) or inferoposterior iiifarc-
tions. Patients with multiple sites of infarction in differenit loca-
tions were excluded for simplification of the study. Those with
reinfarction and subendocardial infarction were also excluded.
In addition to this anatomic classification the patients were
divided into a recent infarction group (infarction occurring less
217
 MASUDA et al.
than 1 month before study) and a remote infarction group (in-
farction occurring more than 1 month before study).
The diagnosis of myocardial infarction was based on the
following criteria.
Recent myocardial infarction was diagnosed if the patientt had
(1) a history of typical prolonged chest pain, (2)electrocardio-
graphic changes indicative of acute myocardial infarction, and
(3) characteristic elevation of serum enzyme levels (creatine
kinase, glutamic-oxaloacetic transaminase, lactic acid dehydro-
genase).
Remote myocardial infarction was diagnosed if the patient
had (I) a history of previous myocardial infarction, (2) diagnos-
tic Q waves- on the electrocardiogram, and (3) normal enzyme
levels during the observation period.
All patients with recent myocardial infarction had been ad-
mitted to our service, and CT scan in those patients with acute
myocardial infarction were performed 3 to 30 days after onset of
the disease, when the patient was considered fit to be moved to
the radiologic laboratory.
Procedures. In most cases a GE CT/T 8800 was used for the
study, but a Siemens Somatom 2 was also sometimes used. Data
were stored on magnetic tapes so that CT images could be
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displayed on a television monitor for investigation at any time.
The record of CT images was obtained on x-ray films by a
multiformat camera. The pixel size of both the GE CT/T and
Siemens Somatom was 1 x 1 mm, and the CT value of each
pixel was presented as a number ranging from + 1000 to
-1000 Hounsfield units (HU). All subjects were examined
while they were in the supine position during a full inspiratory
breath hold.
The routine CT examination was done in the following man-
ner. First, conventional nonenhanced scans were done with
cm thick slices from the level of the aortic arch to the diaphragm
with an exposure time of approximately 10 sec for each scan.
These images were useful not only for the determination of the
left ventricular slice levels, but also for the detection of peri-
cardial effusion and calcification in the heart and vessels. Three
or four early scans were then obtained at the various left ventric-
ular levels immediately after each bolus intravenous administra-
tion of 15 to 20 ml of Renografin 76 (76% meglumine diatri-
zoate) in order to obtain enhanced CT images. The injection was
made manually into the antecubital vein of each subject through
an 18-gauge plastic cannula within several seconds.
In 23 selected subjects delayed scans at the levels of the left
ventricle were performed 10 to 15 min after the bolus injection
of the contrast material to evaluate late enhancement of the
infarcted myocardium; in 12 subjects electrocardiographically
gated CT scans with contrast enhancement were obtained to
evaluate regional ventricular wall motion abnormalities.
Two-dimensional echocardiography, left ventriculography,
and coronary angiography were carried out in most of the sub-
jects within a week of the CT scans. Two-dimensional echocar-
diography was performed with a Toshiba electronic sector scan-
ner (model 1 lA) and the parasternal long- and short-axis and
apical four-chamber views were obtained at the standard trans-
ducer position and recorded on videotapes or 8 mm cine films.
Left ventriculography and angiography were performed with a
biplane Siemens image-intensifier system. Left ventriculo-
grams were obtained in the 30 degree right anterior oblique and
60 degree left anterior oblique views. Both the ventriculograms
and coronary angiograms were recorded on 35 mm film at a rate
of 30 frames/sec.
CT images, two-dimensional echocardiograms, and left ven-
triculograms were interpreted independently by well-trained ob-
servers. The agreement of all observers was required for each
determination and when agreement was not possible after dis-
cussion the finding was judged to be questionable.
218
Definitions. The CT, left ventriculographic, and two-dimen-
sional echocardiographic terms used in this report were defined
as follows:
CT terms. Filling defect was a region with a decreased x-ray
attenuation coefficient compared with the surrounding normal
myocardium within the first few minutes after intravenous ad-
ministration of the contrast material.
Late enhancement was an increase in attenuation coefficient
compared with that for the normal myocardium after 10 to 15
min of administration of contrast material.
Wall thinning was reductionof left ventricular wall thickness
beyond normal values (9 + 2 mm) on CT images.
A left ventricular aneurysm was a localized protrusion of
pericardium and endocardium with wall thinning.
Left ventricular thrombi were filling defects between the left
ventricular cavity and myocardium on enhanced CT images.
Thrombi could be differentiated from filling defects because CT
values in the former were not increased by contrast enhance-
ment, but those in the latter were increased for from several
minutes to 1/2 hr after administration of the contrast material. A
small filling defect (less than 25 mm2 in size) that was seen in
only one slice of the CT scan was not considered a thrombus,
because a low-density fleck owing to artifacts might have con-
fused the diagnosis.
Calcification was considered to be present at the site at which
CT values were extremely high (>100 HU) on the conventional
CT image.
Pericardial effusion was considered to be present in the zone
surrounding the heart in which CT values ranged from 10 to 40
HU; this zone was not enhanced by contrast material.
Left ventriculographic terms. Left ventricular aneurysm was
a localized, permanent, abnormal, blood-filled dilatation of the
left ventricle and/or paradoxical movement of the left ventricu-
lar endocardium.20. 21
Left ventricular thrombus was a filling defect attached to the
left ventricular wall in the left ventricular cavity.22
Echocardiographic term. Left ventricular thrombus was a
distinct mass of echos in the left ventricular cavity that was seen
clearly throughout the cardiac cycle in at least two different
echocardiographic views. 23
Statistical analysis. All data are expressed as mean + SD.
Comparisons were made with a simple analysis of variance, and
p < .05 was considered significant.
Results
Filling defect and late enhancement of the myocardium.
Filling defects and the late enhancement of the myo-
cardium after administration of contrast material were
documented frequently in patients with myocardial in-
farction. When CT scans were obtained immediately
after the bolus injection of contrast material, the site of
myocardial infarction was observed as an area for
which CT values were decreased due to decreased
staining of the myocardium (figures 1 and 2). The
infarcted area gradually picked up the contrast material
and the CT values for the area were increased beyond
those of the normal myocardium; this lasted for up to
/2 hr after the injection (figures 1 and 2).
The incidences of filling defect and late enhance-
ment of the myocardium in the subjects who had myo-
cardial infarctions at various times before the study are
summarized in tables 1 and 2.
CIRCULATION
 DIAGNOSTIC METHODS-COMPUTER-ASSISTED TOMOGRAPHY

Filling defects and late enhancement of the myocar-

dium were usually obvious in the patients with antero-
septal or apical infarctions, and their location
coincided with the infarcted area estimated by electro-
cardiography, thallium-201 scintigraphy, two-dimen-
sional echocardiography, left ventriculography, and
angiography. However, these CT findings were rarely
documented at the inferior or posterior wall, even in
the cases in which obvious inferior or inferoposterior
infarction was demonstrated by the other methods. It
seemed that both filling defects and late enhancement
of the myocardium indicated the area of infarction, but
the mechanism of these phenomena appeared to be
somewhat different. The area of the filling defect was
always smaller than that of late enhancement, and the
-difference between them was increased with increasing
amounts of time after onset of myocardial infarction.
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FIGURE 1. Contrast-enhanced CT images from the middle level of the

left ventricle of a 45-year-old man with anteroseptal myocardial infarc-
tion 9 days after the onset. To/v After a holus injection of the contrast
Imledium1, a filling detect (arrows) appeared in the infarcted region.
Bottom, Ten minutes after the injection, late enhancement of the nmvo-
carditimllappeared in the same region. RV right ventricle: [.V left
ventricle.

Among 16 subjects from group A and seven from

group B, all of whom had recent myocardial infarc-
tions, a filling defect was noted on the early scans of 14
(88%) and six subjects (85%), respectively. In the
subjects with remote infarction a filling defect was
documented in only six (15%) of 40 subjects from
group A and three (1 8%) of 17 from group B. In group
C filling defects were rarely seen in either those with
recent or remote infarction, and only three question-
able cases among the 23 subjects were found.
Late enhancement of the myocardium was detected FIGURE 2. Cardiac CT iniages from a 66-year-oldnman with antero-
septal myocardial infarcti'on 3 weeks after the onset. A, A small tilling
in about half of the subjects from groups A and B,
detect was demonstrated in the anterior wall of the heft ventricle imnie-
regardless the time course of infarction, but late en- diately after a bolus inicction of contrast material. B. Fen minutes after
hancement of the myocardium was not documented in the injection, late enhanccment of the anteroseptal wall appeared and
group C. the enhanced area was larger than that of the tillinig defect.

Vol. 701 No. 2. August 1984 219

 MASUDA et al.

TABLE 1
Appearance of filling defects on contrast-enhanced CT scans in 103 patients with myocardial infarction

Time from Group A Group B Group C

onset of disease n + n + - n

Within 1 week 7 6 1 2 2 0 2 1
I week to I month 9 8 1 5 4 1 7 2 5
I month to 3 months 13 4 9 6 2 4 5 0 5
3 months to 6 months 6 2 4 5 1 4 5 0 5
More than 6 months 21 0 21 6 0 6 4 0 4
Total 56 20 36 24 9 15 23 3 20

Furthermore, the filling defect was recognized only in
patients with relatively recent infarctions (attack with-
in 6 months), but late enhancement was seen in both
recent and remote myocardial infarctions (figures 1
through 3).
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each of 20 in group B, and each of three in group C,
and the detection rate of ventricular aneurysm in each
group was 28%, 83%, and 13%, respectively. These
results indicated that after myocardial infarction ven-
tricular aneurysm usually develops in the anterior wall

Wall thinning. Wall thinning in the left ventricle was
one of the indirect findings associated with the healing
process after myocardial infarction. Figure 4 shows the
left ventricular wall thicknesses from CT scans of nor-
mal subjects and the patients of each group. Wall thin-
ning at the site of infarction was clearly noted in pa-
tients in groups A and B. However, it was not
sufficiently recognized in group C because of the im-
proper slice angle of CT scans.
In 41 subjects in groups A and B who underwent CT
scans within 100 days after onset of myocardial infarc-
tion the relationship between the anterior wall thick-
ness and the length of time from infarction to the CT
study is demonstrated in figure 5. The wall thickness at
the site of infarction gradually decreased over time.
This was especially evident in certain patients (data
represented by solid line in figure 5).
Left ventricular aneurysm (figure 6). Marked localized
bulging in systole and akinesis or dyskinesis of particu-
lar segments were observed in all five patients with
aneurysms that underwent electrocardiographically
gated CT examination.
A left ventricular aneurysm was detected on the
enhanced CT image in each of 16 subjects in group A,
and sometimes extends to the apex.
Left ventriculography was performed in 78 subjects
within a week of CT scanning for comparison of the
findings obtained with both methods. The relationship
between the results of CT and left ventriculography
with regard to left ventricular aneurysms is summa-
rized in table 3. Among the 78 subjects, 36 subjects,
including 14 from group A, 19 from group B, and three
from group C, were determined by CT to have left
ventricular aneurysms. Among these 36 subjects, 25
were determined to have left ventricular aneurysms by
left ventriculography. In the other 1 1 subjects, local-
ized akinesis of the left ventricular wall at the infarcted
site was evident, but there was no evidence of aneu-
rysm. Among the 42 subjects in whom no ventricular
aneurysms were found by CT, eight were found to
have aneurysms by left ventriculography, and 34 were
found not to have ventricular aneurysms; localized
akinesis of the ventricular wall was found in 16 of the
34 subjects.
Ventricular thrombus. Enhanced CT was found to be
an excellent method for the detection of mural
thrombi, which were recognized as filling defects in
the ventricular cavity. Left ventricular thrombi were

TABLE 2
Appearance of late enhancement of the myocardium on delayed CT scans in the 23 patients with myocardial infarction

Time from Group A Group B Group C

onset of disease n + + - n + - n +

Within I week 1 0 1 0 0 0 0 0 0 0 0 0
I week to I month 6 2 2 2 2 1 1 0 1 0 0 1
1 month to 3 months 2 2 0 0 2 1 1 0 0 0 0 0
3 months to 6 months 3 1 0 2 0 0 0 0 1 0 0 1
More than 6 months 2 1 0 2 1 1 0 1 0 0
Total 14 6 4 4 6 3 3 0 3 0 0 3

220 CIRCULATION
 DIAGNOSTIC METHODS-COMPUTER-ASSISTED TOMOGRAPHY
found on CT images from 23 of the 103 patients Wall thickness n
mm
~~~~~~~~~~~~~~~group
55 A
(22%), including 12 (21%) from group A and 11 from *4- group B 23
group B (46%). In all but one case the thrombi were t 2- group C 22
found on the anterior wall or the apex; in the remaining 10 Anorma

EC]~~~~~~~~~~~~~~~~~~4 LJI
10 d o0035
P.

septal wall anterior wall postero-lateral wall

FIGURE 4. Left ventricular wall thickness in normal subjects and in

patients with myocardial infarction. Septal wall thickness, anterior wall
thickness, and posterolateral wall thickness were measured from con-
trast-enhanced cardiac CT images of the middle level of the left ventri-
cle. In groups A and B. septal and anterior wall thickness were markedly
decreased, but no wall thinning was evident in group C.
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patient the thrombus was on the high lateral wall. The

thrombi in 18 subjects were detected in a left ventricu-
lar aneurysm (figure 3).
Seventy-eight patients were studied with CT and left
ventriculography at approximately the same time. CT
revealed left ventricular thrombi in 15, but thrombi
were not detected in 62 subjects, and in one patient
B s_r _ s results were inconclusive. On the other hand, left ven-
triculography demonstrated thrombi in 13 patients, in
63 thrombi were not found, and in two patients results
were inconclusive. The results obtained with the two
methods agreed in 95% of the cases. Among the 15
subjects found to have evidence of thrombi with CT,
thrombi were also detected by left ventriculography in
12, the results were questionable in one, and no
thrombi were seen in two. On the other hand, in 12 of
the 13 patients with thrombi detected by left ventricu-
lography, thrombi were also detected by CT (table 4).
Eighty-one patients underwent two-dimensional echo-
Wall thlckneu

C ~~~~~~~~~~~~~~~~~~12-
10 01 ~~~~~~~~~ro-fl.543
~~~~~~~~~~n=41
8~~~~~
- o~~~~ CO o

6- -- 0

FIGURE 3. Cardiac CT images from a 52-year-old man with an exten-

sive anterior infarction 4 nmonths after the onset. A, CT image from the
middle level if the left ventricle 15 minutes after the first bolus injection 15 30 45 60 75 90 1^s
of contrast material. B, CT image fromii 10 nini lower than that in A. C. dap
CT image frorm 10m nim lower than that in B. An area of late enhanccment FIGURE 5. The anterior wall thickness in 41 subjects in groups A and
(arrow) of the infarcted myocardiumz and a mural thrombus (arrow head) B and timiie froni the onset of intarction to the CT study. The arrows
in a left ventricular aneurysm were observed. indicate the changes in wall thickness in the same patient.

Vol. 70, No. 2, August 1984 221

 MASUDA et al.

was also evident. Figure 8 illustrates an example of

FIGURE 6. A left venltricular aneurysmi (An) is showsn on the contrast-
enhanced CT image from the middle level of the left ventricle in a 66-
year-old man with rcmote extensive anterior infarction.
cardiographic examination within a week of CT scan-
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calcification at the site of old myocardial infarction
(CT value approximately 200 HU).
Discussion
Initial studies by Adams et al.' and Ter-Pogossian et
al.2 demonstrated that the edematous myocardium of
experimental infarction could be distinguished from
normal myocardium on the CT image without contrast
enhancement. However, in human patients infarcted
and normal myocardium cannot be clearly distin-
guished on conventional CT images except by the cal-
cification of the myocardium observed after infarction.
The main reasons for the failure to demonstrate the
reduction in CT values in the edematous myocardium
in patients appear to be the distorted images obtained
and the decreased contrast resolution due to the cardiac

ning. Left ventricular thrombi were found in 20 pa-

tients by CT and in 13 by two-dimensional echo- motion. Further studies for the evaluation of myocardi-
cardiography. Of the 20 patients with thrombi detected al infarction by CT were carried out in living dogs and
by CT, the echocardiographic study demonstrated a few patients by Carlsson et al.4 ' They demonstrated
thrombi clearly in 13, only uncertainly in two, and in that the infarcted myocardium was detected not only as
five thrombi could not be demonstrated. On the other a negative filling defect within the first few minutes
hand, thrombi detected by two-dimensional echo- after intravenous administration of contrast material,
cardiography in 13 subjects were all detected by CT but also as a region of late enhancement of myocardi-
(table 4). um from several minutes to 1 hr after the administra-
Other complications. Pericardial effusion and calciti- tion of contrast material.
cation of the infarcted myocardium were detected Based on their observations, in our study the initial
readily by conventional nonenhanced CT. Figure 7 filling defect and late enhancement after administra-
illustrates an example of pericardial effusion after tion of contrast material were considered direct evi-
myocardial infarction. Pericardial fluid was observed dence of infarction. It is obvious that the initial filling
around the heart, and calcification of the left anterior defect is due to decreased perfusion in the myocardi-
descending, circumflex, and right coronary arteries um. However, the mechanism by which contrast mate-
rial accumulates in damanged myocardium is unclear.
Microvascular damage at the infarcted area may allow
TABLE 3
leakage of contrast to the extravascular space, and the
CT and left ventriculographic (L,VG) findings with regard to left
ventricular (ILV) aneurysm damaged cell membrane may allow the entry of con-
l VG findings TABLE 4
Locai ized I)etection rate of the mural thrombi by CT, left ventriculography
I,V I ocilized hyp(okinesis (IVG), and two-dimensional echocardiography (2-DE)
CT litidings atneuirysimi atkinesis or norimal
CT
Grouip A (n - 43) ± + - Ttoa
I.V aneuirysmIin 19) 12 7 0
No aneurysmii (n 24) 4 10 10 INGC
Group B (n = 17) 4+ 1}2 13
Iv antieuirysmii (ii 14) 11 3 0 1 2
No aneury.smti In 3) 1 0 2 2 1 60 63
(Group C' (n 18) TItal 15 1 62 78
V aneurysimi (n 3) 2 0 2-DE
No anieurysmi (ni 15) 3 6 6 4- 13 0 0 13
Totail in 781 ± 2 0 3
l V aineurysmi I1 361) 25 Il 0 5 1 59 65
No ineurysmIn - 42) 8 16 18 Total 2) 1 60 81

222 CIRCULAT[ION
 DIAGNOSTIC METHODS COMPUTER-ASSISTED TOMOGRAPHY
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a#Si
. as:
a
FIGURE 7. Cardiac CT images from a 79-year-old man with inferior infarction 10 days after the onset. Pericardial effusion (PE)
separated from the myocardiuni by subepicardial fat (F) is seen around the left ventricle (LV) and right ventricle (RV).
Calcifications of the coronary arteries are also shown. AA Ascending aorta: RVOT right ventricular outflow tract; RAU
=

right auriculum; LCA =left coronary artery: LAD left anterior descending artery., LCF left circumflex artery; RCA
=

right coronary artery; RA = right atriuml.

trast medium into the cells. Poor removal of contrast
material due to decreased perfusion may also be in-
volved.7 8. 15. 16
In our studies recent anteroseptal, apical, and exten-
sive anterior transmural infarctions could almost al-
ways be identified by the filling defect in the myocar-
dium evident on CT scans. On the other hand, inferior
and posterior transmural infarctions were rarely visual-
ized because of the parallel orientation of the inferior
wall to the x-ray beam and the pronounced movement
of the inferoposterior wall of the left ventricle.
FIGURE 8. A CT scan from a 72-year-old man with a remote extensive
anterior infarction showing myocardial calcifications after infarction.
Vol. 70, No. 2, August 1984
The late enhancement of the myocardium in -dogs
with recent and remote infarctions is usually visualized
well on delayed CT scans. However, late enhancement
of the myocardium is visualized in only about half of
patients with myocardial infarction. This discrepancy
may be explained by the injected dose of contrast ma-
terial per kilogram of body weight, which in dogs is
three to four times that in patients, and by the fact that
experimental infarction in dogs differs from the infarc-
tion caused by coronary sclerosis in man in that in the
former there is much formation of collateral vessels in
the infarcted wall.
One of the indirect signs of myocardial infarction
detected by CT is ventricular wall thinning.'5 Two
mechanisms for wall thinning in myocardial infarction
have been postulated. One is wall stretching soon after
the occurrence of myocardial infarction, and the other
is the elimination of necrotic infarcted tissue in the
course of healing.
From our observations of wall thinning, usually a
week after the onset of infarction, the latter appears to
be more likely. The site of wall thinning, as detected
by CT, was limited in most cases to the anterior or
apical wall; thinning of the inferior or posterior wall
was rarely observed. This was assumed to be due to the
slice angle of the CT examination, which was unsuit-
able for detecting inferior wall abnormalities.
223
 MASUDA et al.
Edwards24 defined a ventricular aneurysm patho-
logically as a protrusion of a localized portion of the
external aspect of the left ventricle beyond the remain-
der of the cardiac surface, with simultaneous protru-
sion of the cavity. This definition can be applied in
enhanced cardiac CT. There have been only a few
studies of ventricular aneurysm by CT. Lipton et al.25
reported a case of a ventricular aneurysm after anterior
infarction and Lackner and Thurn26 reported a case of
ventricular aneurysm after posterior wall infarction.
We observed 39 patients with ventricular aneurysms
out of 103 patients with myocardial infarction. The
results of our study indicated that the ventricular aneu-
rysm that develops after myocardial infarction usually
develops in the anterior wall or the apex, but rarely
occurs in the inferoposterior wall.
The incidence and location of left ventricular aneu-
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rysm after myocardial infarction based on CT scanning
results were in agreement with the pathologic results
reported by Edwards.24 However, the correlation be-
tween CT and left ventriculographic results in terms of
demonstrating ventricular aneurysm in this study was
somewhat poor. There are two explanations for this.
First, biplane right and left anterior oblique ventriculo-
grams may not be sufficient to visualize all parts of the
left ventricle. Second, the diagnostic criteria for the
left ventricular aneurysm on CT scans were based on
the anatomic definition, which differs from the angio-
graphic criteria. The former does not include wall
movement disturbance, while the latter includes both
anatomic protrusion of the left ventricle and functional
disturbance of the wall movement, but does not con-
sider localized wall thinning of the aneurysm. Further
studies using electrocardiographically gated CT could
possibly solve this problem.
Left ventricular thrombosis is one of the most sig-
nificant complications of myocardial infarction. Two-
dimensional echocardiography has been validated as a
reliable noninvasive method for the detection of
thrombi. However, there has been a significant num-
ber of reports of failure to detect left ventricular
thrombi by two-dimensional echocardiography.23, 27. 28
With left ventriculography the opacification of the left
ventricular cavity determines the surface area of
thrombi precisely, but the border between thrombi and
endocardium of the left ventricle cannot be identified
sufficiently. The contrast resolution of CT is much
superior to that of left ventriculography, so that very
subtle differences in attenuation of the x-ray between
cardiac structures can be identified.9 Godwin et al. 0
reported that enhanced CT scans distinguished mural
thrombi very clearly in three patients with recent myo-
224
cardial infarction and that CT offered some advantages
over left ventriculography and echocardiography in
detecting thrombosis. Nair et al.3'1 studied 16 patients
suspected of having left ventricular thrombi and found
that CT and two-dimensional echocardiography pre-
dicted thrombi in 10 and eight of the 16 patients, re-
spectively. Both CT and left ventriculography correct-
ly predicted the presence of thrombi in two patients
and their absence in three patients in whom the diagno-
sis was confirmed surgically. In the same patient
group, however, two-dimensional echocardiography
failed to predict the presence of a thrombus in one
patient. Our results also support the superiority of CT
in the detection of ventricular thrombi. Since the
search for ventricular thrombi is usually done by two-
dimensional echocardiography only, it is presumed
that thrombi could well be much more common in
patients with myocardial infarction than has been pre-
viously reported.
Although calcification of myocardium and pericard-
ial effusion are easily detected on CT images, these CT
findings have been never reported in patients with
myocardial infarction. Since calcification and effusion
are very significant complications, CT would be very
useful in the clinical evaluation of patients with myo-
cardial infarction. In terms of the other CT findings
that were regarded as indirect evidence of myocardial
infarction, we previously reported the disturbance of
wall motion at the infarcted area'7 and the increase in
CT values in the lung due to pulmonary congestion.18
As far as the possible risk involved in CT studies is
concerned, all our patients with recent myocardial in-
farction underwent CT scanning with intravenous drip
infusion and close electrocardiographic monitoring.
Total time required for one examination was, on the
average, about 30 min. Although rapid bolus injec-
tions of contrast provide enhanced CT images of better
quality than do drip infusions, injections could pro-
duce more undesirable side effects than infusions. The
amount of contrast material used for the study should
be minimized. We injected 15 to 20 ml of 76% meglu-
mine diatrizoate for each CT scan until the total dose
was 60 to 120 ml. Using this method we observed no
significant side effects and the minor effects observed
in a few patients were those such as nausea, urticaria,
and pain at injection site.
Thus, CT scanning is considered to be a safe nonin-
vasive method to evaluate patients with iiyocardial
infarction, even in the acute phase, anid it can provide
information that is useful for the diagnosis of mnyocar-
dial infarction and for the evaluation of the hemody-
namic status of the patient. Although there are still a
CIRCIU LATION
 DIAGNOSTIC METHODS-COMPUTER-ASSISTED TOMOGRAPHY
few technical problems, such as the rather limited ca-
pability to evaluate the status of the inferior wall,
which could hopefully be solved in the future with the
development of more efficient equipment, CT scan-
ning should be more widely used in the evaluation of
patients with myocardial infarction.
References
1. Adams DF, Hessel SJ, Judy PF, Stein JA, Abrams HL: Computed
tomography of the normal and infarcted myocardium. Am J Radiol
126: 786, 1976
2. Ter-Pogossian MM, Weiss ES, Coleman RE, Sobel BE: Computed
tomography of the heart. Am J Radiol 127: 79, 1976
3. Powell WJ, Wittenberg J, Maturi RA, Robert BA, Dinsmore RE,
Miller SW: Detection of edema associated with myocardial isch-
emia by computerized tomography in isolated, arrested canine
hearts. Circulation 55: 99, 1977
4. Carlsson E, Lipton MJ, Berninger WH, Doherty P, Redington
RW: Selective left coronary myocardiography by computed
tomography in living dogs. Invest Radiol 12: 559, 1977
5. Carlsson E, Lipton MJ, Brundage B, Doherty P, Beminger WH,
Downloaded from http://circ.ahajournals.org/ by guest on November 1, 2017
Redington RW: Diagnostic potential of cardiac CT. Appl Radiol 7:
105, 1978
6. Gray WR, Buja LM, Hagler HK, Parkey RW, Willerson JT: Com-
puted tomography for localization and sizing of experimental acute
myocardial infarcts. Circulation 58: 497, 1978
7. Higgins CB, Sovak M, Schmidt W, Siemer PT: Differential accu-
mulation of radiopaque contrast material in acute myocardial in-
farction. Am J Cardiol 43: 47, 1979
8. Higgins CB, Siemers PT, Schmidt W, Newell JD: Evaluation of
myocardial ischemic damage of various ages by computerized
transmission tomography, Time dependent effects of contrast ma-
terial. Circulation 60: 284, 1979
9. Powell WJ, Wittenberg J, Miller SW, Maturi RA, Dinsmore R:
Assessment of drug intervention on the ischemic myocardium,
serial imaging and measurement with computerized tomography.
Am J Cardiol 44: 46, 1979
10. Lipton MJ, Higgins CB: Evaluation of ischemic heart disease by
computerized transmission tomography. Radiol Clin North Am 18:
557, 1980
11. Doherty PW, Lipton MJ, Berninger WH, Skioldebrand CG, Carls-
son E, Redington RW: Detection and quantitation of myocardial
infarction in vivo using transmission computed tomography. Cir-
culation 63: 597, 1981
12. Huber DJ, Lapray JF, Hessel SJ: In vivo evaluation of experimen-
tal myocardial infarcts by ungated computed tomography. Am J
Radiol 136: 469, 1981
13. Cipriano PR, Nassi M, Ricci M, Reitz BA, Brody WR: Acute
myocardial ischemia detected in vivo by computed tomography.
Radiology 140: 727, 1981
14. Cipriano PR, Nassi M, Brody WR: Dynamic of Myocardial con-
trast enhancement, An in vivo computed tomographic study. Radi-
ology 140: 823, 1981
Vol. 70, No. 2, August 1984
15. Palmer RG, Masuda Y, Carlsson E: Washout curves from myocar-
dial infarctions in dogs, studied by contrast-enhanced computed
tomography. Cardiovasc Intervent Radiol 5: 221, 1982
16. Slutsky RA, Mattrey RE, Long SA, Higgins CB: In vivo estima-
tion of myocardial infarct size and left ventricular function by
prospectively gated computerized transmission tomography. Cir-
culation 67: 759, 1983
17. Masuda Y, Yoshida H, Morooka N, Takahashi 0, Watanabe S,
Inagaki Y, Uchiyama G, Tateno Y: ECG-synchronized computed
tomography in clinical evaluation of total and regional cardiac
motion, Comparison of post-myocardial infarction to normal hearts
by rapid sequential imaging. Am Heart J 103: 230, 1982
18. Morooka N, Watanabe S, Masuda Y, Inagaki Y: Estimation of
pulmonary water distribution and pulmonary congestion by com-
puted tomography. Jpn Heart J 23: 697,1982
19. The criteria committee of the New York Heart Association: No-
menclature and criteria for diagnosis of diseases of the heart and
great vessels, ed 8. Boston, 1979, Little Brown and Company
20. Gorlin R, Klein MD, Sullivan JM: Prospective correlative study of
ventricular aneurysm. Mechanistic concept and clinical recogni-
tion. Am J Med 42: 512, 1967
21. Cheng TO: Incidence of ventricular aneurysm in coronary artery
disease. An angiographic appraisal. Am J Med 50: 340, 1971
22. Hamby RI, Wisoff BG, Davidson ET, Hartstein ML: Coronary
artery disease and left ventricular mural thrombi; clinical, hemody-
namic, and angiographic aspects. Chest 66: 488, 1974
23. Stratton JR, Lighty GW, Pearlman AS, Ritchie JL: Detection of
left ventricular thrombus by two-dimensional echocardiography:
sensitivity, specificity, and causes of uncertainty. Circulation 66:
156, 1982
24. Edwards JE: An atlas of acquired diseases of the heart and great
vessels. Philadelphia, 1961, W.B. Sauders Co., vol II
25. Lipton MJ, Brundage BH, Doherty PW, Herfkens R, Berninger
WH, Redington RW, Chatterjee K, Carlsson E: Contrast medium-
enhanced computed tomography for evaluation ischemic heart dis-
ease. Cardiovasc Med 4: 1219, 1979
26. Lackner K, Thurn P: Computed tomography of the heart, ECG-
gated and continuous scans. Radiology 140: 413, 1981
27. Come PC, Markis JE, Vine HS, Sacks B, Mcardle C, Ramirez A:
Echocardiographic diagnosis of left ventricular thrombi. Am Heart
J 100: 523, 1980
28. Asinger RW, Mikell FL, Sharma B, Hoges M, Michaud L, El-
sperger J, Bass D, Karlson K: Observations on detecting left ven-
tricular thrombus with two-dimensional echocardiography: empha-
sis on avoidance of false positive diagnosis. Am J Cardiol 47: 145,
1981
29. Masuda Y, Morooka N, Yoshida H, Watanabe S, Inagaki Y: Non-
invasive diagnosis of thrombus in the heart and large vessels.
Usefulness of two-dimensional echocardiography and X-ray CT.
Jpn Circ J 48: 83, 1984
30. Godwin JD, Herfkens RJ, Skioldebland CG, Brundage BH, Schil-
ler NB, Lipton MJ: Detection of intraventricular thrombi by com-
puted tomography. Radiology 138: 717, 1981
31. Nair CK, Sketch MH, Mahoney PD, Lynch JD, Nooss AN, Ken-
ney NP: Detection of left ventricular thrombi by computerized
tomography; a preliminary report. Br Heart J 45: 535, 1981
225
 The usefulness of x-ray computed tomography for the diagnosis of myocardial infarction.
Y Masuda, H Yoshida, N Morooka, S Watanabe and Y Inagaki

Circulation. 1984;70:217-225
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doi: 10.1161/01.CIR.70.2.217
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