We demonstrated that IPH, an important indicator of risk for future clinical events,6–9
can be reliably and accurately identified on source images from standard MRA sequences acquired at 3T, especially by using a CE-MRA technique. MRA is widely used to evaluate the severity of carotid luminal narrowing, and we have shown that it also provides information about IPH without additional imaging or dedicated sequences. Clinically relevant information can be disregarded if the interpreting radiologist does not know to look for it. Our results highlight the importance of MRA source images because this information is not readily identifiable on MIP images, which are often the only images reviewed when evaluating stenosis.
Detection of IPH on high-resolution carotid MR imaging has been previously reported at 1.5T by using T1-weighted techniques such as black-blood spin-echo,4
imaging. Moody et al13
reported 84% sensitivity and 84% specificity for identifying complicated plaques (presumptive IPH) by using the MRDTI technique. Our use of the mask sequence for IPH detection at 3T revealed similar sensitivity and higher specificity estimates compared with the studies reported at 1.5T by using dedicated sequences for IPH detection. Bitar et al21
used a high-resolution fat-suppressed T1-weighted SPGR sequence at 1.5T to identify IPH in patients scheduled for CEA and reported a slightly higher sensitivity (94%–100%) and lower specificity (80%–88%) compared with our results. However, these patients were first screened by MRDTI to select those suspected of having IPH, and this screening may have skewed the distribution of hemorrhage in this population and affected their estimates.
Only 1 other study reported IPH detection by MR imaging at 3T.25
Ota et al25
used a modified MPRAGE sequence similar to MRDTI and observed a higher sensitivity (80%) and specificity (97%) compared with TSE and TOF sequences based on histologic correlation, though they excluded cases with small IPH or heavy calcification that might interfere with IPH detection. Although our sensitivity was higher and specificity comparable by using a standard mask sequence, the difference could be attributed to the distribution or stage of hemorrhage within the samples. The MPRAGE sequence takes approximately 3–4 minutes to acquire. On the basis of our results and those of Ota et al, it seems that MR imaging at 3T may improve our ability to confirm IPH presence more than was previously achievable at 1.5T; this result is fortuitous, given the trend toward higher field imaging to measure carotid narrowing in routine practice.
Ulceration proved to be a frequent reason for false-positive identification of IPH on TOF images because the signal intensity of flowing blood within an ulcer is similar to that of IPH. Because the signal intensity of flowing blood is not enhanced on mask images, ulceration can be easily distinguished from IPH on this sequence, which is why mask images yielded far fewer false-positive results than corresponding TOF images for IPH detection. Mask images also resulted in fewer false-negatives because of the inherently greater CNR of IPH on these images compared with corresponding TOF images, likely because of the heavier T1-weighting achieved by the CE-MRA sequence. In addition, the TOF sequence was more prone to motion artifacts because of the longer acquisition time needed, which contributed to false-positive IPH detection.
The superior soft-tissue contrast offered by MR imaging compared with that offered by other imaging modalities can be extended to the in vivo detection of IPH. Sonography cannot discriminate IPH from the lipid core,26
and CT angiography is of limited utility because of the overlap of the distribution of densities between IPH and other plaque components.27
Limitations to our study include the following: 1) IPH signal intensity on T1WI may change as hematoma evolves from methemoglobin (hyperintense) to hemosiderin (hypointense),4
which could limit the utility of hyperintense signal intensity as a reliable feature for IPH detection. However, we and others5
have observed that hemorrhage in carotid plaque, unlike in the brain, may remain hyperintense for as long as 18 months, possibly because of the complex underlying core composition retarding its evolution. Furthermore, our high NPV indicates that relying on hyperintense signal intensity for IPH detection is reasonable. 2) False-negative results on both mask and TOF images can occur when blood is not present as methemoglobin, as described above, or when there is mixing of methemoglobin with tissues prone to susceptibility effects (eg, calcification or hemosiderin), as we observed in our study. This is a universal problem that would affect any of the other MR imaging sequences designed to detect IPH as well (eg, gradient-echo techniques such as MRDTI, T1-weighted TSE). Recent advances in susceptibility-weighted imaging may help to overcome this limitation by enabling the discrimination of calcification and IPH based on differences in susceptibility on filtered-phase images.28
False-positive results, as we have seen, can result from the misidentification of perivascular adipose tissue for IPH. This limitation can often be addressed by using the arterial phase CE-MRA image to verify the lumen boundary and confirm the location of the hyperintensity within the wall on the coregistered mask image. 3) All MRA sequences were acquired by using dedicated carotid coils, which are not widely used in routine evaluations for carotid stenosis. However, we have also observed hyperintense signal intensity corresponding with histologically confirmed IPH presence, even when using the body coil during routine clinical MRA evaluations for carotid stenosis in 2 patients, and IPH detection was also reported by Wintermark et al18
in 3 patients by using a standard coil.