D. Russell
Oslo University Hospital, Department of Neurology – Oslo, Norway
Several non-invasive imaging modalities have shown their potential to identify unstable carotid artery plaques. Echolucent plaques are thought to be more unstable than echo-rich plaques. Images can be evaluated either visually or by computer-assisted gray-scale median (GSM) measurements. Visual evaluation of plaque echogenicity has only fair reproducibility, whereas objective characterization is more reliable and less observer dependent. Plaque irregularity on ultrasound has also been reported to be a risk factor for stroke in general but not for ipsilateral stroke alone.
Symptomatic patients with microembolic signals (MES), assessed by TCD, have been shown to be at high risk for developing ipsilateral stroke. Whether MES positive asymptomatic patients also are at increased risk has not been clarified. The use of ultrasound contrast agents may be helpful in determining plaque surface and plaque neovascularization.
Multisequence MRI is able to quantify carotid plaque components. The use of a contrast agent improves quantification of total plaque burden, and contrast between fibrous cap and lipid core. Dynamic contrast-enhanced MRI allows assessment of plaque neovascularization.
Currently, there are few in vivo human studies on functional imaging of carotid plaques. These initial studies have shown the potential of USPIO -enhanced MRI, 18F-FDG PET, IL2 scintigraphy, and low-density lipoprotein scintigraphy to identify inflammation, the potential of annexin A5 scintigraphy to identify cell death, and platelet scintigraphy to depict plaque thrombosis. Biomarkers have been shown to improve prediction independent of conventional risk factors. High sensitivity C-reactive protein (hs-CRP) and lipoprotein-phospholipase A2 (PLA2) are two such candidates
It is at present undecided whether one imaging modality or a multimodality approach is most effective. Prospective clinical trials are needed to demonstrate if imaging methods do indeed result in an improvement in defining unstable plaques and if they can predict patient outcomes, particularly in asymptomatic subjects.
Key words: atherosclerosis, inflammation, vulnerable plaque.