Multidetector computed tomography in reperfused acute myocardial infarction. Assessment of infarct size and no-reflow in comparison with cardiac magnetic resonance imaging.

Abstract

(1) To determine the accuracy of delayed enhancement multidetector computed tomography (MDCT) in measuring the extent of acute myocardial infarct and no-reflow areas using cardiac magnetic resonance imaging (MRI) as standard of reference and (2) to define the optimum timing between injection and MDCT image acquisition to characterize infarcted myocardium and no-reflow areas after reperfusion therapy.
Nineteen patients were prospectively included after acute myocardial infarction and revascularization. Each patient had an MDCT acquisition before and 5 and 10 minutes after injection of 1.5 mL/kg iodinated contrast medium, and a contrast-enhanced MRI at 5 and 10 minutes after injection of 0.2 mmol/kg gadolinium chelate. We assessed image quality and infarct extent using MDCT and MRI, and we measured parameters related to iodinated contrast media kinetics (DeltaHU and DeltaHU ratio).
The areas of hyperenhanced myocardium located on the MDCT corresponded to the occluded vessel located on the coronary angiogram (kappa = 0.9). There were strong correlations between the extent of hyperenhanced infarcted myocardium on MDCT and MRI at 5 minutes (20.4% +/- 2.7% of left ventricle (LV) and 20.9% +/- 2.4%, respectively, R = 0.85; P < 0.0001) and 10 minutes after injection (21.0% +/- 2.9% of LV and 19.4% +/- 2.5%, respectively, R = 0.80; P < 0.0001). However, the correlation between the area of hypoenhanced myocardium measured using MDCT and CMR 5 minutes after injection (R = 0.86; P < 0.0001) was better than the measurement obtained 10 minutes after injection (R = 0.64; P = 0.002). On contrast-enhanced MDCT, 5 minutes after injection, the signal-to-noise ratio was significantly higher than at 10 minutes after injection in LV blood (28 +/- 1 to 21 +/- 1, respectively; P = 0.0007), normal myocardium (18 +/- 1 to 15 +/- 1; P = 0.0009), and hyperenhanced infarcted myocardium (24 +/- 1 to 20 +/- 1; P = 0.004). MDCT image quality was significantly better at 5 minutes (3.2 +/- 0.1) than at 10 minutes (2.8 +/- 0.2, P = 0.01, kappa = 0.4). The DeltaHU ratio increased slightly but significantly between 5 minutes (0.83 +/- 0.01) and 10 minutes (0.93 +/- 0.01; P = 0.01), suggesting a slow wash-in and wash-out of contrast medium in infarcted myocardium.
In ST segment elevation myocardial infarction patients contrast-enhanced MDCT is an accurate method for characterizing and sizing myocardial infarct and no-reflow. Contrast-enhanced MDCT performed 5 minutes after injection yields a higher signal-to-noise ratio and image quality than the 10 minutes time point with no difference in the extent of infarct measurement.

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ORIGINAL ARTICLE
Multidetector Computed Tomography in Reperfused
Acute Myocardial Infarction
Assessment of Infarct Size and No-Reflow in Comparison With
Cardiac Magnetic Resonance Imaging
Alexis Jacquier, MD,* Loı ¨c Boussel, MD,† Nicolas Amabile, MD,‡ Jean Michel Bartoli, MD,*
Philipe Douek, MD,† Guy Moulin, MD,* Franck Paganelli, MD,‡ Maythem Saeed, PhD,§
Didier Revel, MD,† and Pierre Croisille, MD, PhD†
Objectives: (1) To determine the accuracy of delayed enhancement
multidetector computed tomography (MDCT) in measuring the
extent of acute myocardial infarct and no-reflow areas using cardiac
magnetic resonance imaging (MRI) as standard of reference and (2)
to define the optimum timing between injection and MDCT image
acquisition to characterize infarcted myocardium and no-reflow
areas after reperfusion therapy.
Materials and Methods: Nineteen patients were prospectively
included after acute myocardial infarction and revascularization.
Each patient had an MDCT acquisition before and 5 and 10 minutes
after injection of 1.5 mL/kg iodinated contrast medium, and a
contrast-enhanced MRI at 5 and 10 minutes after injection of 0.2
mmol/kg gadolinium chelate. We assessed image quality and infarct
extent using MDCT and MRI, and we measured parameters related
to iodinated contrast media kinetics (?HU and ?HU ratio).
Results: The areas of hyperenhanced myocardium located on the
MDCT corresponded to the occluded vessel located on the coronary
angiogram (? ? 0.9). There were strong correlations between the
extent of hyperenhanced infarcted myocardium on MDCT and MRI
at 5 minutes (20.4% ? 2.7% of left ventricle (LV) and 20.9% ?
2.4%, respectively, R ? 0.85; P ? 0.0001) and 10 minutes after
injection (21.0% ? 2.9% of LV and 19.4% ? 2.5%, respectively, R
? 0.80; P ? 0.0001). However, the correlation between the area of
hypoenhanced myocardium measured using MDCT and CMR 5
minutes after injection (R ? 0.86; P ? 0.0001) was better than the
measurement obtained 10 minutes after injection (R ? 0.64; P ?
0.002). On contrast-enhanced MDCT, 5 minutes after injection, the
signal-to-noise ratio was significantly higher than at 10 minutes after
injection in LV blood (28 ? 1 to 21 ? 1, respectively; P ? 0.0007),
normal myocardium (18 ? 1 to 15 ? 1; P ? 0.0009), and
hyperenhanced infarcted myocardium (24 ? 1 to 20 ? 1; P ?
0.004). MDCT image quality was significantly better at 5 minutes
(3.2 ? 0.1) than at 10 minutes (2.8 ? 0.2, P ? 0.01, ? ? 0.4). The
?HU ratio increased slightly but significantly between 5 minutes
(0.83 ? 0.01) and 10 minutes (0.93 ? 0.01; P ? 0.01), suggesting
a slow wash-in and wash-out of contrast medium in infarcted
myocardium.
Conclusion: In ST segment elevation myocardial infarction patients
contrast-enhanced MDCT is an accurate method for characterizing
and sizing myocardial infarct and no-reflow. Contrast-enhanced
MDCT performed 5 minutes after injection yields a higher signal-
to-noise ratio and image quality than the 10 minutes time point with
no difference in the extent of infarct measurement.
Key Words: contrast media, imaging, magnetic resonance
imaging, multigated computed tomography, myocardial infarction
(Invest Radiol 2008;43: 773–781)
A
more, the presence of a no-reflow area within the infarcted
myocardium is a predictor of poor outcome.3Contrast-en-
hanced magnetic resonance imaging (MRI) is a well estab-
lished, accurate imaging method for characterizing acute and
chronic myocardial infarction at 1.5 T4and 3.0 T.5,6The
ability of computed tomography (CT) to identify infarcted
myocardium as an enhanced territory after coronary occlu-
sion was described in late 1970s on excised animal hearts.7
This method found a second wind with the arrival of multi-
detector computed tomography (MDCT) technology that led
to its clinical application.8There is growing interest in using
MDCT infarct size measurements as an end point in clinical
trials.9–11However, no standardized protocol currently exists,
and there are limited data available concerning the accuracy
ssessment of acute myocardial infarct size is predictive of
long-term myocardial function improvement.1,2Further-
Received November 7, 2007, and accepted for publication, after revision,
May 31, 2008.
From the *Department of Radiology, University of Marseille Me ´diterrane ´e
CHU la Timone, Marseille cedex 05, France; †Department of Radiology,
University Claude Bernard Lyon 1, CHU Louis Pradel, Bron, France;
‡Department of Cardiology, University of Marseille Me ´diterrane ´e, CHU
Nord, Chemin des bourrely, Marseille cedex 20, France; and §Depart-
ment of Radiology, University of California San Francisco, San Fran-
cisco, California.
Reprints: Alexis Jacquier, MD, Department of Radiology, University of
Marseille Me ´diterrane ´e, 264 rue St Pierre, 13385 Marseille cedex 05,
France. E-mail: alexis.jacquier@ap-hm.fr.
Copyright © 2008 by Lippincott Williams & Wilkins
ISSN: 0020-9996/08/4311-0773
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of myocardial infarct and no-reflow sizing and the effects of
the delay between injection and image acquisition.
Dynamic contrast-enhanced MRI has been used to
derive quantitative parameters that reflect microcirculation
integrity and tissue perfusion12; it has also been used to
determine the kinetics of MR contrast agents in the blood and
myocardium by measuring the relaxation times and concen-
tration.13,14The same linear kinetic model has been used to
assess microcirculation characteristics using MDCT.15MDCT
has several advantages over MRI for this purpose, including a
direct proportional linear relationship between enhanced x-ray
absorption and the concentration of the contrast agent.15
The aims of this clinical study were to: (1) determine
the accuracy of delayed enhancement MDCT in measuring
the extent of acute myocardial infarct and no-reflow areas
using cardiac MRI as standard of reference and (2) define the
optimum timing between injection and MDCT image acqui-
sition to characterize infarcted myocardium and no-reflow
areas after reperfusion therapy.
MATERIALS AND METHODS
Patients
This prospective, monocentric, trial was performed
after approval of the institution’s review board and written,
informed consent was obtained from all 19 patients who
enrolled in this study. The inclusion criteria were: acute
coronary syndrome with ST elevation ?ST segment elevation
myocardial infarction (STEMI)? treated with successful per-
cutaneous coronary intervention (PCI) within the first 12
hours after the onset of pain, thrombolysis in myocardial
infarction (TIMI) score 2 or 3 after reperfusion. The exclu-
sion criteria were MRI contraindication, congestive heart
failure, persistent chest pain, renal failure, or allergy to
iodine-based contrast media. All patients were given a MDCT
and MRI in the course of the same week between 72 hours and
15 days after coronary reperfusion therapy. The 2 examinations
were performed at an interval of 24 hours to 7 days.
Imaging Modalities
Multidetector Computed Tomography
MDCT studies were performed on a 64-slice scanner
(Sensation 64, Siemens, Erlangen, Germany). The patient was
placed in the dorsal decubitus position. The first acquisition was
made before injection under retrospective cardiac synchroniza-
tion with the following parameters: detector collimation ? 1.5
mm, keV ? 80, mAs ? 500. We used a bolus of 1.5 mL/kg
iodinated contrast media (95–152 mL) (Iomeprol 350, Bracco-
BYK, Le Me ´e sur Seine, France) injected at a rate of 2 mL/s.
Two MDCT acquisitions, 5 and 10 minutes after injection of the
contrast agent were performed at end-inspiration breath-hold
and under retrospective cardiac gating. The following param-
eters were used: detector collimation ? 1.5 mm, keV ? 80,
mAs ? 500, temporal resolution ? 175 milliseconds, recon-
structed slice thickness ? 5 mm with no gap between the
slices in the short axis, 2-chamber and 4-chamber views. For
both acquisitions, the reconstruction window was selected
between 60% and 75% of the R-to-R interval. No additional
beta-blocker injection was given before MDCT.
Magnetic Resonance Imaging
MRI studies were performed on a 1.5-T whole-body MR
scanner (Symphony, Siemens, Erlangen, Germany) using dedi-
cated synergy coil array with the patient placed in a supine
position. Images were acquired at end-inspiration breath-hold
under cardiac gating. Two MR sequences were used
Global Function. Cine SSFP sequences were acquired
in the short axis for global function analysis with the following
parameters: TR/TE ? 40/1.8 milliseconds, slice thickness ?
6 mm, spacing ? 6 mm, flip angle ? 20 degrees, field of view ?
350 ? 350 mm, matrix ? 148 ? 256, and phases ? 25
depending on the heart rate.
Delayed Contrast Enhancement. Inversion recovery
gradient echo sequences were acquired 5 minutes and 10
minutes after intravenous administration of 0.2 mmol/kg of
Gd-DOTA encompassing the left ventricles in the short axis,
4 and 2-chamber view. The sequences parameters were:
TR/TE ? 780/1.56 milliseconds, slice thickness ? 5 mm,
spacing ? 0, flip angle ? 10 degrees, field of view ? 350 ?
400 cm, and matrix ? 152 ? 134. The inversion time equal
to 270 to 325 milliseconds, set to null normal myocardium at
end-diastolic phase.
Image Analysis
Using MRI cine sequences, the segments of myocardial
dysfunction (ie, hypokinetic, akinetic) were allocated using a
17-segment model.16For the purposes of analysis, myocar-
dial dysfunction was assigned to the 3 major coronary arteries
and reported as lateral (territory of the circumflex coronary
artery including segments 5, 6, 11, 12, and 16), inferior
(territory of the right coronary artery including segments 3, 4,
9, 10, and 15), or anterior (territory of the left anterior
coronary artery including segments 1, 2, 7, 8, 13, 14, and
17).16Anatomic landmarks such as right ventricular insertion
and papillary muscle insertion were used to coregister con-
trast-enhanced MDCT and MRI images acquired 5 and 10
minutes after injection and MDCT images acquired before
injection. Based on the delayed enhancement on MRI, we
defined the slice passing through the core of the infarct on the
short and long axis images. The investigators selected the
corresponding MDCT and MRI slices at each time point and
made measurements on these selected images. The images
were selected on the basis of a consensus between 2 observers
(A.J, L.B.). The series of selected images was then anony-
mized and randomized using DicomWorks software (www.
dicomworks.com). A Leonardo workstation (Siemens, Erlan-
gen, Germany) was used to analyze the image set. To avoid
the readers recognizing the images, they were not read until
6 weeks after the selection session. Areas of late hyperen-
hanced (infarcted myocardium) late hypoenhanced myocar-
dium (no-reflow area), and normal myocardium were traced
by 2 observers. The percentage of infarcted hyperenhanced
myocardium and no-reflow areas was calculated for the
whole LV following the methods described previously.11
Infarct extent was calculated by dividing the infarct area
measured on the whole LV by the total slice area of LV and
was then expressed as a percentage of LV demonstrating
Jacquier et al
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delayed hyperenhancement. The readers used a 4-step scale to
assess image quality: (1: nondiagnostic images, 2: poor quality
images, 3: good quality images, 4: excellent images) on the
complete series of images. A region of interest (ROI) (0.4 cm2)
was placed to measure the regional signal intensity in LV blood,
normal, and hyperenhanced myocardium on the MDCT
and MRI images performed 5 and 10 minutes after injec-
tion and on the MDCT images performed before injection.
On each MDCT or MRI image, an ROI was placed in the
air around the patient to assess image noise (air standard
deviation). For 5 and 10 minutes images on both MDCT
and MRI, the signal-to-noise ratio (SNR) was calculated as
follows: SNR ? signal intensity (SI)/noise, for LV blood,
normal, and hyperenhanced myocardium. Contrast-to-
noise ratio (CNR) was calculated as follows: CNR ?
(SIhyperenhanced myocardium? SInormal myocardium)/image noise.
The enhancement was calculated in Hounsfield units
(?HU) on the MDCT images at 5 minutes and 10 minutes by
subtracting the measured precontrast density values from the
postcontrast values in LV blood, normal, and hyperenhanced
myocardium. The ?HU was taken to be proportionate to the
concentration of the contrast medium either in the blood, nor-
mal, or hyperenhanced myocardium. The ?HU values obtained
from blood and tissue were used for kinetic analysis and to
calculate the ?HU ratio: (?HUmyocardium/?HUblood).14,15,17The
data expressed as a ?HU ratio and the changes it underwent in
time provided information on contrast distribution in viable and
nonviable myocardium. The ?HU ratio was proportionate to the
fractional distribution volume of the contrast agent, defined as
fractionaldistributionvolume??HUratio?(1-hct),wherehct
is hematocrit level.14,15,17
Statistical Analysis
All values are given as mean ? standard error of the mean
(SEM). The statistical analysis was performed using Medcalc
7.3 (Meriakerke, Belgium) and GraphPad Prism 5.01 (San
Diego, CA). Discordant readings were resolved by consensus
between the 2 readers. The average of the measurements of both
readers was used for further analysis. Two-tailed paired Student
t tests were used to compare the continuous variable values. We
measured the correlation between the continuous variables using
Pearson’s correlation coefficient. The agreement between meth-
ods of semiquantitative measurement was compared with ?
statistics and two-tailed paired Student t test. A P value below
0.05 was considered significant.
RESULTS
Patients
All patients successfully underwent MDCT and MRI
with no adverse reaction to the contrast agent. There was no
significant difference in heart rate (72 ? 6 bpm) between the
MRI and MDCT studies. In absolute terms the iodine contrast
medium used ranged between 95 and 152 mL. The patients’
clinical characteristics are shown in Table 1.
Contrast-Enhanced Pattern on the MDCT
Images
All 19 patients had areas of hyperenhanced myocar-
dium 5 and 10 minutes after contrast injection on the MDCT
(Figs. 1 and 2). In all patients this hyperenhanced area of
myocardium fitted the anatomic distribution of the infarct-
related area determined by both ECG and coronary angiog-
raphy. There was a good agreement between the hyperen-
hanced regions located on MDCT and the previously
occluded vessel as defined on the angiograms (? ? 0.9).
Furthermore, in each patient the hyperenhanced region on
MDCT showed segmental dysfunction on cine MRI and
delayed hyperenhancement on MRI. The mean density of the
hyperenhanced myocardium (134 ? 6 HU) was significantly
greater than normal myocardium 5 minutes after contrast
injection (96 ? 3 HU; P ? 0.0001). This difference was also
significant 10 minutes after injection (118 ? 5 HU for
hyperenhanced vs. 81 ? 3 HU for normal; P ? 0.0001,
respectively). The mean density values of LV blood, normal,
and hyperenhanced myocardium were significantly higher 5
minutes after injection (156 ? 6 HU, 96 ? 3 HU, 134 ? 6
HU, respectively) compared with the values measured 10
minutes after injection (126 ? 4 HU, 81 ? 3 HU, 118 ? 5
HU, P ? 0.0001–0.1) (Fig. 3).
Hypoenhanced myocardium (no-reflow subregion) was
detected in the core of the hyperenhanced myocardium in 7
patients at 5 and 10 minutes after injection on the MDCT.
Good agreement (? ? 0.8) was found between the areas of
hypoenhanced myocardium picked up on MDCT and MRI.
The mean density of the hypoenhanced myocardium 5 min-
utes after contrast injection was significantly lower (68 ? 7
HU) compared with hyperenhanced myocardium (134 ? 6
HU; P ? 0.0001); this difference persisted for 10 minutes
after contrast injection (64 ? 4 HU vs. 118 ? 5 HU; P ?
0.0001, respectively).
Assessment of the Extent of Enhancement and
Hypoenhanced Area Using MDCT Compared
With MRI
On MDCT, there was no significant difference between
the mean area of hyperenhanced myocardium measured 5
minutes (20.4% ? 2.7% of LV) and 10 minutes after contrast
TABLE 1.
Patients’ Clinical Characteristics (N ? 19)
Male/female ratio
Age
Heart rate
Weight
Systolic blood pressure at admission
Time to therapy ?3 h
Risk factor
Hypertension
Diabetes
Active smoking
Dyslipidemia
Hereditary
Location of myocardial infarction (using
angiography)
Anterior (left anterior descending territory)
Lateral (circumflex artery territory)
Inferior (right coronary artery territory)
16/3
57 ? 2 (33–73 yr old)
72 ? 6 bpm
84 ? 3 kg
126 ? 6 mm Hg
3/19
7/19
5/19
17/19
7/19
3/19
10/19
6/19
3/19
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injection (21.0% ? 2.9% of LV; P ? NS) (Fig. 4). The mean
area of hyperenhanced myocardium measured on MDCT was
not significantly different compared with the measurements
obtained on MRI at 5 minutes (20.9% ? 2.4%) and 10
minutes (19.4% ? 2.4%; P ? NS) after injection. The
regression analysis showed a strong correlation between the
FIGURE 1. Contrast-enhanced MDCT images ac-
quired at 5 minutes (A) and 10 minutes (B) (slice
thickness 1.5 mm, kV: 80, mAs: 500, temporal reso-
lution: 175 milliseconds, reconstructed slice thick-
ness: 5 mm, W ? 174, L ? 141) and corresponding
contrast-enhanced MRI acquired at 5 minutes (C)
and 10 minutes (D) (IR-GRE, TR/TE ? 780/1.56 mil-
liseconds, thickness ? 5 mm, ?alpha? ? 10 degrees,
matrix ? 152 ? 134) in a 51-year-old man 5 days
after reperfusion of the circumflex coronary artery.
Infarcted myocardium at 5 minutes and 10 minutes
appears as a hyperenhanced region on MDCT. The
hyperenhanced region matched that on contrast-
enhanced MRI (white arrow: C, D). IR-GRE, inver-
sion recovery gradient echo.
FIGURE 2. Contrast-enhanced MDCT images 5
minutes (A) and 10 minutes (B) (slices thickness
1.5 mm, kV: 80, mAs: 500, temporal resolution:
175 milliseconds, reconstructed slice thickness: 5
mm, W ? 94, L ? 104) and corresponding con-
trast-enhanced MRI 5 minutes (C) and 10 minutes
(D) (IR-GRE, TR/TE ? 780/1.56 milliseconds, thick-
ness ? 5 mm, ?alpha? ? 10 degrees, matrix ?
152 ? 134) in a 42-year-old man 7 days after
reperfusion of circumflex coronary artery. On
MDCT infarcted myocardium appears as hyperen-
hanced region (white arrow) with a dark suben-
docardial core (black arrow head). The same pat-
tern is shown on the MRI where infarcted
myocardium appears as hyperenhanced region
(white arrow) surrounding dark hypoenhanced
core. IR-GRE, Inversion recovery gradient echo.
Jacquier et al
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hyperenhanced infarcted region on MDCT and MRI 5 min-
utes after injection (R ? 0.85; P ? 0.0001) and 10 minutes
after injection (R ? 0.80; P ? 0.0001) (Fig. 5).
On MDCT, the extent of hypoenhanced subregion was
0.7% ? 0.3% LV at 5 minutes after injection and showed a
tendency to decrease at 10 minutes (0.5% ? 0.2%, P ? NS).
There was no significant difference between the extent of
hypoenhanced subregion measured on MDCT and MRI at 5
and 10 minutes after contrast injection. However, a better
correlation was detected between the extent of hypoenhanced
subregion measured on MDCT and MRI at 5 minutes (R ?
0.86; P ? 0.0001) than 10 minutes after injection (R ? 0.64;
P ? 0.002) (Fig. 6).
SNR, CNR, and Qualitative Images Analysis
On the contrast-enhanced MDCT images, the SNR
value of hyperenhanced myocardium was higher at 5 minutes
(24 ? 1) and 10 minutes (20 ? 1) compared with normal
myocardium (17 ? 1 and 14 ? 1; P ? 0.0001, respectively)
(Fig. 7). On the other hand, the SNR value of LV blood was
only significantly higher than in the hyperenhanced myocar-
dium at the 5 minutes time point (28 ? 1 vs. 24 ? 1; P ?
0.03, respectively). On contrast-enhanced MDCT, 5 minutes
after injection the SNR was significantly greater than the 10
minutes measurement in normal myocardium (18 ? 1 at 5
minutes to 15 ? 1 at 10 minutes; P ? 0.0009), LV blood (28 ?
1 to 21 ? 1; P ? 0.0007), and hyperenhanced myocardium
(24 ? 1 to 20 ? 1; P ? 0.004). On contrast-enhanced MRI,
there was no significant difference between SNR measured at
5 minutes and 10 minutes in LV blood, normal myocardium,
and hyperenhanced myocardium.
On MDCT 5 and 10 minutes after injection, CNR
((SIhyperenhanced myocardium? SInormal myocardium)/noise) values
were measured at 6.5 ? 0.7 and 5.6 ? 0.6, respectively (P ?
NS). These values were significantly lower compared with
the CNR values assessed by MRI at 5 minutes (16.6 ? 1.5;
P ? 0.0001) and 10 minutes (17.6 ? 1.2; P ? 0.0001) (Fig.
8). MDCT image quality was significantly better 5 minutes
after injection compared with 10 minutes (3.2 ? 0.1 at 5
minutes vs. 2.8 ? 0.2, P ? 0.01, ? ? 0.4).
FIGURE 4. Extent of hyperenhanced myocardium assessed
by MDCT (white bars) and MRI (black bars). There was no
significant difference in the extent of hyperenhanced myo-
cardium measured at 5 and 10 minutes after contrast injec-
tion using MDCT and MRI.
FIGURE 3. Contrast-enhanced MDCT images
(slice thickness 1.5 mm, kV: 80, mAs: 500, tem-
poral resolution: 175 milliseconds, reconstructed
slice thickness: 5 mm) acquired at 5 minutes (A,
C) and 10 minutes (B, D) displayed with the same
window level (W ? 93, L ? 108) showed the de-
crease in image quality from 5 to 10 minutes after
injection. Infarcted myocardium appears as hyper-
enhanced region (arrow) and no-reflow appears
as hypoenhanced subregion.
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Regional Changes in ?HU and ?HU Ratio
At 5 minutes, iomeprol induced a greater increase in
?HU in LV blood (110 ? 6 HU) than in infarcted myocar-
dium (93 ? 6 HU, P ? 0.0001) (Fig. 9). At 10 minutes, there
was no significant difference in the ?HU between LV blood
and hyperenhanced infarcted region. There was a significant
difference in the ?HU values measured for hyperenhanced
myocardium at 5 (93 ? 6 HU) and 10 minutes (76 ? 5 HU)
and normal myocardium at the same time points (51 ? 3 HU
and 36 ? 3 HU; P ? 0.0001, respectively). A significant
decline in ?HU was measured between 5 and 10 minutes in
both blood and normal myocardium, indicating gradual elim-
ination of iomeprol from the blood.
No significant difference was found between the
?HU ratio (?HUnormal
myocardium at 5 (0.46 ? 0.01) and 10 minutes (0.50 ?
0.01; P ? NS), suggesting fast exchange of iomeprol
between the blood and interstitial fluid. On the contrary,
the ?HU ratio (?HUhyperenhanced myocardium/?HUblood) of
infarcted myocardium increased from 5 (0.83 ? 0.01) to
10 minutes (0.93 ? 0.01; P ? 0.01), suggesting a slow
wash-in and wash-out of iomeprol in infarcted myocar-
dium (Fig. 10).
myocardium/?HUblood) of normal
DISCUSSION
The main findings of this study among STEMI patients
were:
1. On contrast-enhanced MDCT, the infarct area appears as
hyperenhanced myocardium and no-reflow myocardium
appears as hypoenhanced myocardium within the bound-
aries of the infarct area. There was a good agreement
between the myocardial infarct area and the extent of
no-reflow area measured using MDCT and MRI at 5 and
10 minutes after injection in STEMI patients.
2. The changes in myocardial signal intensity on MDCT
reflect the concentration of iodinated contrast media. Con-
trast-enhanced MDCT performed 5 minutes after injection
provided a higher SNR and image quality than the 10
minutes time point with no difference in the extent of
infarct.
3. Temporal changes in the ?HU ratio suggest a slow wash-in
and wash-out of iomeprol in infarcted myocardium.
Myocardial viability assessment using the contrast-
enhanced MDCT method is based on the same principle as
MRI late enhancement.7The pharmacokinetics of intrave-
nously administered iodinated contrast medium are similar to
those of extracellular MR contrast medium.18This class of
agents escapes rapidly from the intravascular compartment to
the extracellular compartment, but cannot enter the intracel-
lular compartment.18Discrimination between viable and non-
viable myocardium depends on the regional concentration
and kinetics of contrast medium. Myocardial infarction
causes interstitial edema, loss of cellular membrane integrity,
and microvascular injury. On the MR and MDCT imaging,
the magnitude of enhancement of infarcted myocardium de-
pends on 2 factors: (1) myocardial perfusion19and vascular
patency and (2) distribution volume of the contrast agent.14,20
The relaxivity of MR contrast agent is an additional factor in
FIGURE 5. Correlation between hyperenhanced
infarcted myocardium measured on contrast-en-
hanced MDCT and MRI at 5 minutes (left graph)
and 10 minutes (right graph) after contrast injec-
tion. Note the high correlation between the mea-
surements.
FIGURE 6. Correlation between no-reflow subre-
gion measured on contrast-enhanced MDCT and
MRI 5 minutes (left graph) and 10 minutes (right
graph) after contrast injection. Good correlation
was observed between the 2 measurements.
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MRI. The first 2 factors explain why infarcted myocardium
appeared hyperenhanced on the MDCT images compared
with normal myocardium at 5 and 10 minutes. The current
results are in line with a previous report by Gerber et al.11The
investigators showed a good correlation between contrast-
enhanced MDCT and contrast-enhanced MRI in assessing
myocardial infarction in both animal models and humans.
Inversion recovery gradient echo is considered the gold
standard method for assessing infarct size in the acute and
chronic phases.4,21In another study, Wagner et al22did not
find any significant difference in the size of infarction mea-
sured at 5 or 30 minutes after injection of MR contrast
medium. Our result for both contrast-enhanced MRI and
FIGURE 7. Temporal evolution in signal-to-noise ratio (SNR)
assessed in normal myocardium, infarcted myocardium, and LV
blood at 5 minutes and 10 minutes after injection of 1.5 mL/kg
iomeprol 350 (top graphs) using MDCT and 5 minutes and 10
minutes after injection of 0.2 mmol/kg of Gd-DOTA (bottom
graph) using MRI. On MDCT, but not on MRI, the SNR value
was significantly lower 10 minutes after injection compared
with 5 minutes. *P ? 0.05 in comparison with values obtained
at 5 minutes using paired Student t test.
FIGURE 8. Contrast-to-noise ratio (CNR) between infarcted
and normal myocardium assessed by MRI (white bars) and
MDCT (black bars) 5 and 10 minutes after Gd-DOTA and
iomeprol 350 injection, respectively. There was no signifi-
cant difference between CNR assessed using MDCT at 5
minutes and 10 minutes after contrast injection. *P ?
0.0001 in comparison with values obtained with MDCT us-
ing paired Student t test.
FIGURE 9. The kinetics of iomeprol 350 are reflected in the
regional changes in ?HU value (density postcontrast-density
precontrast) of LV blood (E), normal myocardium (?) hy-
perenhanced myocardium (?). Data were obtained at 5 and
10 minutes after administration of 1.5 mL/kg iomeprol. A
decrease in ?HU value of the LV blood between 5 and 10
minutes reflects the fast clearance of the contrast media.
FIGURE 10. Changes in ?HU ratio (?HU myocardium/?HU
blood) of hyperenhanced infarcted myocardium (?) and
normal myocardium (?) measured at 5 and 10 minutes af-
ter administration of 1.5 mL/kg iomeprol. The significant
increase in ?HU ratio in infarcted myocardium suggests a
slow wash-in and wash-out of the iodine contrast media in
the no-reflow subregion. *P ? 0.01 in comparison with values
obtained at 5 minutes using 2-tailed paired Student t test.
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contrast-enhanced MDCT agrees with this report. The delay
between injection and MDCT image acquisition has not been
adequately defined in humans, for example, investigators rec-
ommend 5 minutes,107 minutes,9,2310 minutes,11and even 15
minutes after injection.24In our study, the MDCT images
acquired 5 minutes after contrast medium injection provide
higher SNR and image quality compared with 10 minutes late
images without any difference in terms of the measurement of
infarct extent. This could be explained by the greater con-
centration of iodine contrast medium in blood, myocardial
infarct, and normal myocardium measured 5 minutes after
injection. This result is in line with those of an animal study
in which Lardo et al25assessed the kinetics of iodine contrast
media in a pig model of infarct in vivo. Investigators showed
that the infarct area was well delineated and reached peak
enhancement 5 minutes after injection and then washed out
because of the progressive renal clearance of the contrast
medium. This was confirmed later by Gerber et al11who
found that the infarct area reached peak enhancement be-
tween 2 and 6 minutes after iodine injection, and then
decreased. Furthermore, Gerber et al11also showed that the
CNR of infarcted and normal myocardium are significantly
higher on contrast-enhanced MRI compared with contrast-
enhanced MDCT, suggesting that the sensitivity of MRI is
better than that of MDCT in detecting myocardial infarction.
However, the relationship between contrast medium concen-
tration and signal intensity measured on MRI is not linear,
and specific sequences and calculations are required to mea-
sure contrast medium concentration on MRI.13,14On the
other hand, the relationship between contrast medium con-
centration and signal intensity (measured in Hounsfield units)
is linear on MDCT images,26providing an accurate measure-
ment of myocardial viability. In this article we did not assess
the ability of MDCT to detect and measure subendocardial
infarcts and wall motion abnormalities accurately.
The significant increase in the HU ratio in infarcted
myocardium showed a lack of equilibrium between the iodine
concentrations in the blood and infarcted myocardium. This
finding indicates a slow wash-in and wash-out of the extra-
cellular contrast medium in infarcted myocardium. Similar
findings were reported in dog and rabbit models of acute
infarct.20,27Kim et al20showed that the differential image
intensity in reperfused myocardial infarcts was primarily due
to regional differences in wash-in and wash-out dynamics.
Unlike infarcted myocardium, normal myocardium showed a
stable ?HU ratio, suggesting a fast exchange of the contrast
medium in this compartment. Saeed et al14showed that a
steady state is reached in normal myocardium within 5
minutes after contrast injection. The exposure to radiation
and potentially toxic contrast agent restricts the repeated use
of MDCT. Because of radiation exposure, CT should not be
used as a first line test for viability if MRI is available.
In conclusion, contrast-enhanced MDCT is capable of
demonstrating regions of infarct and no-reflow in STEMI
patient. The extent of myocardial infarct and no-reflow on
contrast-enhanced MDCT was comparable with contrast-
enhanced MRI. Contrast-enhanced MDCT performed 5 min-
utes after injection yields a higher SNR and image quality
than the 10 minutes time point with no difference in the
extent of infarct measurement. The kinetics of iodinated
contrast medium in infarcted myocardium is similar to MR
contrast media. This study has confirmed the potential for
MDCT to serve as an alternative imaging modality to MRI
for myocardial viability assessment. It would also be suitable
for patients who are not candidates for MRI because of severe
claustrophobia or implantable cardiac devices.
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