DOI:10.2214/AJR.05.1176
AJR 2007; 188:W135-W137
© American Roentgen Ray Society
Assessment of Acute Reperfused Myocardial Infarction with Delayed Enhancement 64-MDCT
Timo Baks1,
Filippo Cademartiri,
Amber D. Moelker,
Willem J. van der Giessen,
Gabriel P. Krestin,
Dirk J. Duncker and
Pim J. de Feyter
1 All authors: Departments of Cardiology and Radiology, Erasmus Medical Center,
Dr. Molewaterplein 40, Rotterdam, The Netherlands.
Received July 8, 2005;
accepted after revision August 31, 2005.
Address correspondence to T. Baks
(t.baks{at}erasmusmc.nl).
WEB This is a Web exclusive article.
Abstract
OBJECTIVE. The purpose of this study was to evaluate the utility of
delayed enhancement 64-MDCT in the assessment of myocardial infarct size in a
porcine model of acute reperfused myocardial infarction. CT can be used for
noninvasive assessment of coronary artery stenosis, but to our knowledge,
evaluation of myocardial viability in the subacute phase of acute myocardial
infarction has not been validated. We performed delayed enhancement imaging on
six domestic swine 5 days after reperfused acute myocardial infarction and
assessed the relation between delayed enhancement patterns in vivo and the
extent of viable and nonviable myocardium at postmortem histochemical
analysis.
CONCLUSION. Delayed enhancement imaging with 64-MDCT can be used for
accurate assessment of the size of reperfused acute myocardial infarcts.
Keywords: cardiac imaging • cardiovascular imaging • CT • MDCT • myocardial infarction
Introduction
MDCT is used for the evaluation of coronary artery disease and has
high diagnostic accuracy in the detection of coronary artery stenosis
[1,
2]. The diagnostic value of
MDCT for assessment of myocardial viability in the subacute phase of acute
myocardial infarction is unclear. Studies
[3,
4] have shown that MDCT during
the first pass after administration of an iodinated contrast agent results in
low tissue contrast between infarcted and uninfarcted myocardium and that
total infarct size appears to be underestimated. A delayed enhancement imaging
protocol as used in MRI may be an alternative approach. Excellent tissue
contrast with MRI is obtained 10-30 minutes after administration of gadolinium
derivatives, because this type of contrast agent accumulates in the infarcted
tissue. The pharmacokinetic behavior of gadolinium chelates is somewhat
similar to that of iodinated contrast agents
[5]. We performed delayed
enhancement MDCT in a porcine model of reperfused acute myocardial infarction
to investigate whether reperfused infarct size can be assessed accurately with
delayed enhancement MDCT.
Materials and Methods
Animal Model
Six Yorkshire-Landrace pigs (age, 2-3 months; weight, 22 kg) were subjected
to coronary angiography followed by balloon occlusion of the left circumflex
coronary artery. Reperfusion was obtained by deflation of the balloon after 2
hours of ischemia. The study complied with the regulations of the animal care
committee of the Erasmus Medical Center and the "Guide for the Care and
Use of Laboratory Animals" (National Institutes of Health, 1996).
Animals were sedated (ketamine 20 mg/kg intramuscularly and midazolam 1 mg/kg
intramuscularly), anesthetized (thiopental, 12 mg/kg IV), intubated, and
mechanically ventilated (mixture of oxygen and nitrogen, 1:2). Anesthesia was
maintained with fentanyl (12.5 µg/kg/h).
CT
Five days after induction of myocardial infarction, all swine were
anesthetized as described earlier and subjected to MDCT. Mean heart rate
decreased from approximately 80 to 45 ± 9 beats per minute (BPM) after
administration of zatebradine (10 mg/kg IV). A 64-MDCT scanner (Sensation 64,
Siemens Medical Solutions) was used for imaging with the following
characteristics: number of detector rows, 32 x 2 (oversampling in the
z-axis obtained with flying focal spot); number of slices per
rotation, 64; individual detector width, 0.6 mm; gantry rotation time, 330
milliseconds; effective temporal resolution, 165 milliseconds. Delayed
enhancement imaging was performed 15 minutes after administration of 80 mL of
iodinated contrast agent (iomeprol 400 mg I/mL, Iomeron, Bracco) through an
ear vein. The following scan parameters were used: effective tube current, 900
mAs at kV 120; feed per rotation, 3.84 mm; scan direction, craniocaudal. The
estimated radiation dose if used for a human protocol would have been 15 mSv
for men and 21 mSv for women. Delayed enhancement MDCT data sets were
reconstructed at -300, -350, and -400 milliseconds before the next R wave
(end-diastolic phase of the cardiac cycle). From the data set with optimal
image quality, images with a slice thickness of 1 mm and an increment of 0.5
mm were reconstructed in the shortaxis view with a dedicated software platform
with multiplanar capabilities (Leonardo, Siemens).
Data Analysis
One day after MDCT, all pigs were sacrificed and the hearts excised. The
myocardium of the left ventricle was cut in 8-mm consecutive slices in the
shortaxis view with a commercially available meat slicer. For viability
staining, the slices were embedded in a solution of 1% triphenyltetrazolium
chloride (TTC) and 0.2 mol/L Sörensen's buffer (pH, 7.4) at 37°C for
15 minutes and then fixed in 4% formalin. The slices were photographed with a
digital camera. The digitalized TTC-stained slices were loaded in a separate
workstation with a commercially available analysis package (SigmaScan Pro 5.0,
Systat). TTC-negative borders and endocardial and epicardial borders of the
left ventricle were traced manually in all consecutive slices. Infarct size
was defined as TTC-negative area as a percentage of total left ventricular
slice area.
Reconstructed MDCT images were exported and transferred to a separate
workstation with dedicated software (Cine Tool, GE Healthcare). The region
with delayed enhancement was selected manually on these images. Infarct size
per slice was calculated by dividing the delayed enhanced area by the total
slice area. CT attenuation values were measured by drawing three
10-mm2 regions of interest in delayed enhanced myocardium, remote
myocardium, and the left ventricular cavity in a short-axis slice located at
the center of the infarction of each pig
[3].
Statistical Analysis
Data were presented as mean ± SD. Univariate linear regression
analysis and Bland-Altman analysis were used to evaluate the relation between
infarct size measured with MDCT and infarct size measured with postmortem
histochemical analysis. One-way analysis of variance with repeated measures
was used for the comparison of CT attenuation values of delayed enhanced
myocardium, remote myocardium, and the left ventricular cavity. Posthoc
Bonferroni correction was applied to adjust for multiple comparisons.
Significance was accepted at p 
0.05 (two-tailed).
Results
All MDCT data sets were of good image quality. Delayed enhancement observed
in the lateral wall of the left ventricle corresponded to the perfusion
territory of the circumflex coronary artery (Figs.
1A,
1B and
2A, and
2B). No delayed enhancement was
seen in remote myocardium. Four of the 42 available histochemical slices had
to be excluded because postmortem shrinkage made measurement of infarct area
and slice area impossible. TTC-negative areas (infarcted myocardium) were
found in the lateral wall of the left ventricle but not in remote myocardium
(Figs. 1A,
1B and
2A,
2B).
Mean infarct size was 28% ± 13% on MDCT images and 26% ± 12%
on histochemical images. Infarct size measured with MDCT correlated well with
infarct size measured on histochemical images (R2 =0.92;
p <0.001) (Fig. 3A,
3B). The mean MDCT value of
delayed enhanced myocardium (141 ± 10 H) was significantly different
from that of remote myocardium (71 ± 8 H; p < 0.001) and
from that of the left ventricular cavity (115 ± 8 H; p <
0.001). The relative difference in MDCT value between infarcted and
uninfarcted myocardium was 206% ± 14%.
Discussion
MDCT technology has developed rapidly with a marked increase in temporal
and spatial resolution. Noninvasive evaluation of coronary artery disease is
feasible, and several studies have shown good diagnostic accuracy in the
detection of coronary artery stenosis. Evaluation of myocardial viability in
the subacute phase of acute myocardial infarction has been studied with MDCT,
but limited data are available. For example, Hoffmann et al.
[3] performed 4-MDCT coronary
angiography within 5 hours of acute nonreperfused myocardial infarction in
swine and found good correlation between the size of perfusion defects and the
size of infarcts estimated at postmortem histochemical analysis. Mahnken et
al. [6] performed 16-MDCT
coronary angiography followed by delayed enhancement CT and MRI in patients
within 14 days of reperfused acute myocardial infarction. Infarct size
measured on delayed enhancement CT and delayed enhancement MRI was comparable,
but infarct size measured on perfusion images remained underestimated.
In this study, we used an experimental model of reperfused acute myocardial
infarction because early aggressive reperfusion is currently the preferred
treatment in the clinical setting of acute myocardial infarction. Delayed
enhancement imaging was performed because the contrast agents used for MDCT
(iodinated contrast material) and MRI (gadolinium derivatives) accumulate in
infarcted myocardium 10-30 minutes after IV administration while they are
being washed out of remote myocardium
[7,
8]. We did not perform
perfusion imaging because MRI studies of reperfused myocardial infarction have
shown that total infarct size remains underestimated with perfusion imaging.
During the first pass of a contrast agent, infarcted myocardium with an intact
microvasculature becomes normally enhanced while infarcted myocardium with
microvascular obstruction appears as a perfusion defect
[9]. We found that infarct size
can be assessed accurately with delayed enhancement 64-MDCT if imaging is
performed 5 days after reperfused myocardial infarction.
A well-known concern about MDCT is the use of iodinated contrast agents and
radiation exposure to the patient. Our results encourage further research into
optimization of protocols that involve use of less radiation and less
iodinated contrast material and into optimal timing of delayed enhancement
imaging after contrast administration. Furthermore, image quality is heart
rate dependent, and images may be impaired at heart rates greater than 70 BPM
[10].
Measurement of infarct size in patients with acute myocardial infarction is
clinically relevant because infarct size is predictive of left ventricular
function and geometric configuration and, hence, long-term clinical outcome
[11,
12]. Information on infarct
size obtained with MDCT would enhance the diagnostic armamentarium of
physicians who lack access to cardiac MRI or encounter patients who have
contraindications to MRI.
Acknowledgments
We thank Wendy Kerver for her help in the logistics of this study.
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Abstract
Introduction
