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A large AAA screening program at the VA detects more aneurysms, but at smaller diameters than that published in clinical trials. Over time, the number of inappropriate AAA screenings has continued to decrease, demonstrating greater awareness and application of the AAA screening guidelines by primary care providers. Developing surveillance guidelines for small and medium aneurysms is a potential area for future research.

Objective Statin therapy is utilized in the medical management of patients with peripheral vascular disease (PVD) and abdominal aortic aneurysm (AAA) for the pleiotropic and anti-inflammatory benefits. We hypothesize that the inflammatory mechanisms of monocyte-endothelial cell interactions in endothelial barrier dysfunction is more significant in patients with PVD compared to AAA. The purpose of this study is to assess patient peripheral blood monocyte adhesion molecules by flow cytometry and monocyte-induced endothelial barrier dysfunction by using an in vitro endothelial cell layer and electric cell-substrate impedance sensing system (ECIS). Methods Peripheral blood was collected from patients with either PVD (ABI<0.9, toe-arm index <0.8, or required lower extremity vascular intervention) or AAA (aortic diameter >3.0 cm). Monocytes were isolated from fresh whole blood using an accuspin-histopaque technique. The separated monocytes underwent flow cytometry analysis to evaluate expression levels of the cell membrane adhesion molecules: CD18, CD11a/b/c, and VLA-4. Endothelial cell function was assessed by adding monocytes to an endothelial monolayer on ECIS arrays and co-culturing overnight. Peak changes in trans-endothelial resistance were measured and compared between patient groups. Results Twenty-eight monocyte samples were analyzed for adhesion molecules (PVD: 19, AAA: 9) via flow cytometry and 11 patients were evaluated for endothelial dysfunction (PVD: 7, AAA: 4) via ECIS. There was no significant difference between risk factors among PVD and AAA patients except for age, where AAA patients were significantly older than PVD patients in both flow cytometry and ECIS groups (P=0.02, 0.01 respectively). There were significantly higher levels of adhesion molecules CD11a, CD18, and CD11c (averaged MFI P-values: 0.047, 0.038, 0.014, respectively) in PVD patients compared to AAA patients. No significant difference was found for CD11b and VLA-4 expression (P=0.21, 0.15 respectively). There was significantly more monocyte-endothelial cell dysfunction as a result of monocytes obtained from patients with PVD than from AAA, with a maximal effect seen at 15 hours after monocyte addition (P=0.032). Conclusions Patients with PVD have increased expression levels of certain monocyte adhesion molecules and greater monocyte-induced endothelial layer dysfunction when compared to patients with AAA. This may lead to other methods of targeted therapy to improve outcomes of these vascular patients.

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