Current state of experimental imaging modalities for risk assessment of abdominal aortic aneurysm.

BACKGROUND: Abdominal aortic aneurysm (AAA) is a major cause of death in developed countries. Patients often lack clinical symptoms, most acute AAA patients do not survive rupture, and subsequent surgical repair has a significant postoperative mortality. Diagnostics for AAAs are currently centered on aneurysm diameter, but recent studies claim this method to be insufficiently accurate. More accurate diagnostic criteria need to be indentified to minimize the amount of unnecessary interventions and to provide earlier diagnosis of rupture-prone AAAs. METHODS: A literature study using the MEDLINE database followed by manual cross-referencing provided original studies concerning AAA diagnostics. RESULTS: The currently validated imaging modalities such as ultrasound, computed tomography, and magnetic resonance imaging allow AAA research to develop in several directions. Some studies investigate whether clinically visible entities like thrombus, calcification, and vascular anatomy could be implemented directly into clinical practice through use of ultrasound or computed tomography. Experimental studies on intravascular ultrasound, positron emission tomography-computed tomography, ultrasound particle image velocimetry and superparamagnetic particles in magnetic resonance imaging propose new methodologies to benefit AAA research. Other studies focus on available technology toward inflammation, metabolism, and the effects of hemodynamics on vascular integrity. CONCLUSIONS: Contradictory outcomes, low availability of experimental imaging modalities, and an often small population size hamper research in this field. Introducing new techniques and biomarkers in current or experimental modalities may prove to be the next step in the development of new diagnostic criteria for the risk assessment of AAA rupture. Until then, the AAA diameter remains the gold standard as a clinical risk factor.

Myeloperoxidase and serum amyloid A contribute to impaired in vivo reverse cholesterol transport during the acute phase response but not group IIA secretory phospholipase A(2).

Atherosclerosis is linked to inflammation. HDL protects against atherosclerotic cardiovascular disease, mainly by mediating cholesterol efflux and reverse cholesterol transport (RCT). The present study aimed to test the impact of acute inflammation as well as selected acute phase proteins on RCT with a macrophage-to-feces in vivo RCT assay using intraperitoneal administration of [(3)H]cholesterol-labeled macrophage foam cells. In patients with acute sepsis, cholesterol efflux toward plasma and HDL were significantly decreased (P < 0.001). In mice, acute inflammation (75 microg/mouse lipopolysaccharide) decreased [(3)H]cholesterol appearance in plasma (P < 0.05) and tracer excretion into feces both within bile acids (-84%) and neutral sterols (-79%, each P < 0.001). In the absence of systemic inflammation, overexpression of serum amyloid A (SAA, adenovirus) reduced overall RCT (P < 0.05), whereas secretory phospholipase A(2) (sPLA(2), transgenic mice) had no effect. Myeloperoxidase injection reduced tracer appearance in plasma (P < 0.05) as well as RCT (-36%, P < 0.05). Hepatic expression of bile acid synthesis genes (P < 0.01) and transporters mediating biliary sterol excretion (P < 0.01) was decreased by inflammation. In conclusion, our data demonstrate that acute inflammation impairs cholesterol efflux in patients and macrophage-to-feces RCT in vivo in mice. Myeloperoxidase and SAA contribute to a certain extent to reduced RCT during inflammation but not sPLA(2). However, reduced bile acid formation and decreased biliary sterol excretion might represent major contributing factors to decreased RCT in inflammation.