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PVSS18. Complement Activation Leads to Systemic Inflammation After Ruptured Abdominal Aortic Aneurysm

William S. Johnson, Barry B. Rubin, Thomas F. Lindsay.
Toronto General Hospital; Toronto, Ontario, Canada.

OBJECTIVES: Ruptured abdominal aortic aneurysm (RAAA) is associated with systemic inflammation that results in multi-organ injury, which contributes to the 40% mortality rate. We sought to determine 1) if there was differential complement activation between RAAA and Elective Abdominal Aortic Aneurysm (EAAA) repair in humans and 2) were there differences in which complement pathways were activated.

METHODS: 6 RAAA and 8 EAAA patients enrolled in a blood sampling protocol after ethics approval. Blood was drawn pre-incision (PI), pre-release of the aortic cross clamp (PR), 2 and 4 hours post-release (2PR, 4PR), and post-op days 1-2 (D1,D2). Classical, MBL, and alternative pathway complement activation was tested in plasma using ELISA. Whole blood was used to assess neutrophil oxidant burst in response to stimulation with un-opsonized zymosan and phorbal myristate acetate (PMA).

RESULTS: See Table 1.

CONCLUSIONS: This data provides the first human evidence of complement activation following RAAA. In the early phase of reperfusion, complement activation is both classical and MBL dependent, with a sustained response through the classical pathway in the post-op period. RAAA patients also have a primed neutrophil oxidant burst beginning at the pre-incision sample. These primed inflammatory cells have significant potential to generate an oxidant burst and tissue injury in response to a second stimulus such as aortic clamping. The mechanism defined by these data suggests that an anti-complement intervention aimed at both the classical and MBL pathways may hold promise for improved outcome following RAAA.