Bruce Wasserman

High-resolution contrast-enhanced MRI has been shown to reliably and accurately depict features of atherosclerotic plaque that are considered risk markers for stroke. In fact, we now recognize that these features seem to be as important as angiographic measures of stenosis for determining stroke risk.¹ Intraplaque hemorrhage (IPH) is one such feature and the target of several investigations that have established MRI’s ability to detect its presence; however, this is just one part of a complex profile of plaque vulnerability. Histopathologic specimen studies have shown that inflammation, in particular, neovascularity, is another important feature that might serve as a meaningful indicator of stroke risk. The ability to reliably identify and grade neovascularity on anatomic MRI of plaque could be an important clinical tool. In our study we used high-resolution contrast-enhanced black-blood (BB) MRI, which can be acquired as part of a routine clinical MRI exam, to provide this information. We gained insight into the implications of identifying this feature, namely, that it is associated with prior cerebrovascular events independent of other factors, including IPH presence.

We routinely implement high-resolution BB MRI exams to characterize carotid plaque morphology for determining stroke risk. IPH is a key target to identify on these exams; having been shown in prospective studies to correlate with future events, it carries an important implication when detected, especially when ipsilateral to a stroke or TIA.^2,3 Degree of neovascularity is also routinely assessed on these MRI studies based on the extent of adventitial enhancement determined where the plaque is thickest. However, we are more cautious to place much weight on neovascularity degree given the lack of prospective data on the clinical consequence of this feature. For example, how can we be sure we are not detecting the result of rather than a predictor of plaque rupture? Nevertheless, we expect that it has some clinical value, based on our knowledge that the risk of stroke in the territory of a plaque that has previously ruptured is increased,⁴ and at the very least, this feature suggests the plaque previously ruptured. In fact, the combined presence of

high neovascularity grade and IPH correlates even more strongly with prior rupture. Furthermore, there is prospective evidence that carotid plaque inflammation detected in vivo by combined [¹⁸F] fluorodeoxyglucose positron-emission tomography (FDG-PET)/CT is associated with early stroke recurrence,⁵ and we have good reason to believe that we are detecting inflammation.⁶ So, as we await prospective validation, the identification of these features in carotid plaque by MRI might at least trigger more aggressive medical management or contribute to the consideration of surgery when other risk markers are identified.

Our lab has been following populations imaged using carotid plaque MRI in order to validate this and other features of carotid plaque as predictors of stroke risk. Once established, these features can be integrated to create a risk profile for each individual. This will enable us to more accurately stratify risk and prepare us for the next step: a surgical trial to define the parameters for managing carotid plaque using this new paradigm.

References

1. Wasserman BA, Wityk RJ, Trout HH 3rd, et al. Low-grade carotid stenosis: looking beyond the lumen with MRI. Stroke 2005;36:2504–13. doi: 10.1161/​01.STR.0000185726.83152.00
2. Altaf N, Daniels L, Morgan PS, et al. Detection of intraplaque hemorrhage by magnetic resonance imaging in symptomatic patients with mild to moderate carotid stenosis predicts recurrent neurological events. J Vasc Surg 2008;47:337–42. doi: 10.1016/j.jvs.2007.09.064
3. Takaya N, Yuan C, Chu B, et al. Association between carotid plaque characteristics and subsequent ischemic cerebrovascular events: a prospective assessment with MRI—initial results. Stroke 2006 Mar;37:818–23. doi: 10.1161/​01.STR.0000204638.91099.91
4. Inzitari D, Eliasziw M, Gates P, et al. The causes and risk of stroke in patients with asymptomatic internal-carotid-artery stenosis: North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med 2000;342: 1693–700. doi: 10.1056/NEJM200006083422302
5. Marnane M, Merwick A, Sheehan OC, et al. Carotid plaque inflammation on 18F-fluorodeoxyglucose positron emission tomography predicts early stroke recurrence. Ann Neurol 2012;71:709–18. doi: 10.1002/ana.23553
6. Kerwin W, Hooker A, Spilker M, et al. Quantitative magnetic resonance imaging analysis of neovasculature volume in carotid atherosclerotic plaque. Circulation 2003;107:851–56. doi: 10.1161/​01.CIR.0000048145.52309.31

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