Abstract
Imaging is becoming increasingly important for the diagnosis of large vessel vasculitis (LVV). Atherosclerosis may be difficult to distinguish from LVV on imaging as both are inflammatory conditions of the arterial wall. Differentiating atherosclerosis from LVV is important to enable optimal diagnosis, risk assessment, and tailored treatment at a patient level. This paper reviews the current evidence of ultrasound (US), 2-deoxy-2-[18F]fluoro-D-glucose positron emission tomography (FDG-PET), computed tomography (CT), and magnetic resonance imaging (MRI) to distinguish LVV from atherosclerosis. In this review, we identified a total of eight studies comparing LVV patients to atherosclerosis patients using imaging—four US studies, two FDG-PET studies, and two CT studies. The included studies mostly applied different methodologies and outcome parameters to investigate vessel wall inflammation. This review reports the currently available evidence and provides recommendations on further methodological standardization methods and future directions for research.
Highlights
Large vessel vasculitis (LVV) is an inflammatory condition of the blood vessel wall affecting large- and medium-sized arteries
Eight imaging studies were included based on their inclusion of separate groups of LVV and atherosclerosis patients
One study included in this review showed that using a diffuse uptake pattern as a diagnostic criterium decreases the number of false positives, especially the number of false-positive atherosclerosis patients [23]
Summary
Large vessel vasculitis (LVV) is an inflammatory condition of the blood vessel wall affecting large- and medium-sized arteries. This may cause obstruction, ischemia, or aneurysm formation, resulting in vascular events, such as vision loss, cerebrovascular accidents, or aortic rupture [1]. The two major variants of LVV are giant cell arteritis (GCA) and Takayasu arteritis (TA). GCA and TA differ mainly in age of onset—older than 50 years and younger than. The aorta and its major branches are often affected in both variants. In GCA third-order branches of the aorta in the head and neck region, such as the temporal artery, are commonly involved [2]
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