Evidence suggests that the formation of the non-specific abdominal aorta aneurysm (AAA) is a local representation of a systemic disease of the vasculature1 and inflammation appears to play a role in the pathophysiological process . In addition to the histological verification of heightened proteolytic activity and lymphocytic abundance, there is also evidence of systemic elevation of C-reactive protein (CRP), a response to inflammation, and cytokines in patients with AAAs [2-8]. Various imaging techniques have been used to visualize inflammatory changes within the aortic aneurysmatic wall and thereby potentially facilitate estimate of prognosis and response to medical treatment. Positron emission tomography/computed tomography (PET/CT), for example, has been utilized to investigate the uptake of 18F-fluorodeoxyglucose as a marker of increased metabolic activity within the aneurysmatic aortic wall, suggesting inflammation [9, 10]. This approach has been hindered by the observation that at least half of all large arteries scanned show some degree of increased metabolic activity, despite no known vascular disease . Cardiovascular magnetic resonance (CMR) technology is another diagnostic option, and one recent study points to the feasibility of CMR in conjunction with ultrasmall superparamagnetic iron oxide infusion in assessing inflammatory activity .
The present study employs T2-weighted short tau inversion recovery CMR (T2-STIR CMR), which highlights hydrophilic tissue and reveals local edema, a marker of inflammation [13, 14]. Identifying edematous changes has been shown to be beneficial in differentiating between chronic and active inflammation in spinal cord injuries . It is sensitive enough to detect small vessel inflammation in the context of the acute coronary artery syndrome [16, 17]. Finally, its use in identifying active aortic inflammation in Takayasu’s arteritis has also recently been demonstrated .
Based on these strengths, it was hypothesized that T2-STIR CMR should identify edema in a larger vascular structure, such as the aorta, provided it is present. The null hypothesis is thus, no edematous changes are identified in the AAA wall in comparison to otherwise healthy aortic tissue. The ramifications of findings could therefore help to clarify the role of inflammation in the AAA and perhaps affect decisions regarding treatment and prognosis.
For full text: click here
(Author: Jacob Budtz-Lilly, Anders F. Mikkelsen, Samuel A. Thrysøe, William P. Paaske, Won Yong Kim