Table 1 M.R.I. Signal Intensity
Lipid rich Hematoma
Imaging sequence Calcification
Dense fibrocellular High
PDW Intermediate
Intermediate Nil
Intermediate High
High Nil
T1W Low
T2W Low
High Nil
atherosclerotic plaque area was calculated by tracing the inner surface of the media readily identifiable on
both MR and histopathology, and subtracting the luminal area. Separate investigators, blinded to the
results of others, performed each analysis.
The data were then analyzed mean wall thickness for coronary artery and aortic specimens, plaque area for
aortic specimens by simple linear regression with 95 CIs Statview, Abacus Corp.
To facilitate the analysis by MR imaging of atherosclerotic plaque components, we formulated
criteria based on a visual assessment of the signal intensity of the different areas of the atherosclerotic
lesion for each of the imaging sequences used i.e. T1W, T2W and PDW-see Table 1. This table extends the
information gained from previous work in this field. One investigator, blinded to the results of the histo-
pathology and the number of atherosclerotic plaque components present, analyzed all MR images of com-
plex plaques with three or greater components using this table in order to validate its diagnostic accuracy.
3. Results
The MR images of the coronary artery specimens that were matched with histopathology n = 54 in-
cluded segments from all three coronary arteries. Both atherosclerotic and non-atherosclerotic segments were
included in the analysis. The MR images from the aortic specimens that were histopathology matched
n = 43 included sections from the renal arteries to the iliac trifurcation. Some of these had no significant
plaque while others had extensive complex atheroscle- rotic disease.
On the cholesterol enriched diet, there was an eleva- tion of the total serum cholesterol serum total choles-
terol 466.5 9 17.5 mgdl.
3
.
1
. Coronary atherosclerosis Of the 54 matched coronary segments, there were 22
sections from the left anterior descending LAD, 10 from the left circumflex LCx and 22 from the right
coronary artery RCA. In order to maximize the num- ber of segments from the proximal LAD, some seg-
ments from the origin of the LCx were sacrificed. The correlation between the measurements of mean artery
wall thickness by MR and histopathology r = 0.94, slope: 0.81 was highly significant P B 0.0001 Fig.
1a. This correlation P B 0.0001 was independent of vessel site including the LAD interventricular course:
r = 0.94, slope: 0.87 and the RCALCx collectively atrio-ventricular course: r = 0.94, slope: 0.77.
Fig. 1. Linear regression analyses showing excellent correlation of the mean wall thickness as measured by MR and matched histopathology
in the a coronary arteries; and b aortas.
Fig. 2. MR image PDW of the LAD showing an inferior crescentic atherosclerotic plaque with bright signal white arrow indicative of fibrocellular composition. The accompanying histopathology section confirms this with the fibrous structures staining green on the Masson’s
trichome and elastin stain.
Fig. 3. MR image T2W of the RCA showing no obvious atherosclerotic plaque but defining the media high signal; white with a black arrow from the dense adventitia low signal; black with a white arrow. The corresponding histopathology section confirms the accurate identification
of the vessel wall. Surrounding the vessel wall is another high signal structure on the T2W image representing connective tissue.
Coronary atherosclerotic lesions were well defined by all MR imaging sequences and appeared as a homoge-
neous bright high signal structure consistent with a fibrocellular composition Fig. 2. This was confirmed
with histopathology. With T2W imaging the normal components of the vessel wall could be readily distin-
guished. The dense adventitia appeared dark and the media appeared bright Fig. 3 as previously described
[10].
3
.
2
. Aortic atherosclerosis There was a highly significant correlation P B
0.0001 between mean wall thickness of the MR images
Fig. 4. Series of three different MR imaging sequences of the same abdominal aortic section and the corresponding histopathology section, highlighting the various signal intensities for each atherosclerotic plaque component with the different MR imaging sequences.
Fig. 5. A higher magnification of the T2W image from Fig. 4 with the corresponding histopathology section stained with both combined Masson’s trichome and elastin and Hematoxylin and Eosin techniques. The decalcification process removes mineral calcium only, leaving behind the
characteristic matrix, which is basophilic and thus appears bluish on the Hematoxylin and Eosin section. This allows the accurate identification of calcified white arrows, dense fibrocellular black arrowheads, lipid rich black arrows and hemorrhagic white arrowheads regions.
and matched histopathological sections r = 0.94, slope: 0.81 for the aortic specimens Fig. 1b. Total athero-
sclerotic plaque area per section was measured and was also significantly correlated P B 0.0001 between
MR imaging and matched histopathology r = 0.97, slope: 0.90.
The experimental model of atherosclerosis used in- duced complex atherosclerotic lesions characterized by
lipid rich, dense fibrocellular, calcified and hemorrhagic regions. These regions were accurately identified with
the imaging sequences performed Figs. 4 and 5. With T1W imaging, the calcifications were well defined by
signal loss, due to the low mobile proton density within the calcified area, but there was less contrast between
the other regions within the atherosclerotic plaque. The calcifications were also well visualized with T2W and
PDW imaging. The dense fibrocellular cap was well distinguished from the less dense body of the plaque
containing regions of extracellular lipid deposition on T2W imaging as previously reported [10,16] but also
on PDW imaging. Plaque hematoma was also well visualized with both T2W and PDW imaging. How-
ever, there was less tissue contrast between the lipid rich areas and the hematoma with the PDW and T2W
images, than for either of these two atherosclerotic plaque components and the dense fibrocellular regions.
Of the complex atherosclerotic lesions with three or more plaque components n = 13, using the criteria in
Table 1 we were able to accurately identify dense fibrocellular 13 of 13, lipid rich 13 of 13 and calcifi-
cation 13 of 13. Hematoma was accurately identified in two of three cases 66 sensitivity, and one speci-
men was falsely characterized as having hematoma 92 specificity.
4. Discussion