Aortic Aneurysm, Abdominal Clinical Trial
Official title:
Inflammation and Risk Prediction in Patients With Abdominal Aortic Aneurysm
The purpose of this study is to better understand the role of inflammation in the pathophysiology of abdominal aortic aneurysm. In this study we hope to show better ways of predicting risk in this condition by using a combination of FDG-PET with CT.
Cumulative experimental and pathological evidence support the postulate that inflammation
may serve as the unifying concept in the pathogenesis of atherosclerosis and its
complications. Aneurysmal disease is associated with inflammatory cell infiltrate and
enzymatic degradation of the vessel wall. Although the risk of abdominal aortic aneurysm
(AAA) rupture relates to the maximum cross-sectional diameter, rapid expansion of the aortic
diameters preceding fissuration and rupture has been observed in AAA independently of their
initial size. However, current diagnostic modalities stratify risk of AAA rupture based
solely on the size of the aneurysm without factoring potentially useful information
derivable from the degree of aneurysmal wall inflammatory response.
We propose to utilize fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging
co-registered with structural computerized tomography (CT) images for the in vivo
localization and quantification of vascular inflammation in patients with AAA in order to
determine whether increased inflammation within the walls of the aneurysm correlates with
rapid enlargement of AAA (change in aneurysmal diameter within 6 months), symptoms,
thrombosis, or intervention for ruptured, leaking, rapidly expanding, or painful AAAs.
In patients with underlying abdominal aortic aneurysm (AAA), the progression of disease i.e.
expansion is associated with increased inflammation within the aneurysm wall as
characterized by FDG-PET/CT, and the degree of inflammation is a risk predictor for adverse
events.
Prior studies have demonstrated that FDG uptake is greater in inflamed tissues, such as
infectious foci and tumors. In chronic inflammatory lesions and malignancies, FDG uptake is
increased in macrophage-dense regions. The relatively high uptake of FDG by macrophages is
attributed to the relatively high metabolic rates of macrophages, and the inability of
macrophages to store glycogen, making them more reliant upon external glucose as a source of
fuel. Activation of macrophages can further increase their glucose consumption. Both in
animal models and humans, inflamed blood vessels have been shown to have an increased uptake
of FDG. Several investigators have shown that FDG-PET can reliably detect inflammation in
atherosclerosis. Thus detection of enhanced FDG uptake in the aneurysmal walls of patients
with AAA may have potential significance.
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