Markers of inflammation in men with small abdominal aortic aneurysm

BackgroundMarkers of inflammation and fibrin turnover are elevated in individuals with a large (>55 mm) abdominal aortic aneurysm (AAA). Fibrin degradation generates D-dimer, known to possess multiple proinflammatory effects, and levels are elevated during early AAA development. This study characterized the plasma inflammatory response during early AAA pathogenesis to determine the effect of D-dimer levels.MethodsThe study compared 75 men with a small AAA (range, 30–54 mm) with 90 age-, sex-, and race-matched controls. Plasma interleukin-6 (IL-6), complement C3, high-sensitivity C-reactive protein (hsCRP), fibrinogen, and D-dimer levels were measured.ResultsMean levels of fibrinogen (2.92 vs 2.59 g/L; P = .003), hsCRP (2.07 vs 1.29 ng/mL; P = .005), and D-dimer (346.7 vs 120.2 ng/mL; P < .001) were higher in men with a small AAA. These markers correlated with maximum aortic diameter determined by ultrasound imaging. On multivariate analysis, D-dimer levels were elevated in AAA individuals independent of smoking, cardiovascular disease (CVD), atherosclerotic risk factors, and inflammatory parameters. Fibrinogen and hsCRP levels remained elevated after adjustment for these covariates but lost significance when D-dimer was added to the model.ConclusionC-reactive protein and D-dimer levels are elevated during early AAA development. D-dimer levels are most tightly associated with AAA status, however, and may mediate the observed elevation in acute-phase reactants.

Clinical RelevancePlasma markers of inflammation and fibrin turnover are elevated in large (>55 mm) abdominal aortic aneurysms (AAAs). Fibrin degradation products include D-dimer, which has multiple proinflammatory effects. The interaction between inflammatory and coagulatory processes remains ill defined during early AAA development. This case-control study shows levels of C-reactive protein and fibrinogen are elevated in men with small AAAs (range, 30-54 mm). D-dimer levels were most tightly associated with AAA status, however, and may mediate the elevated levels of acute-phase reactants. Further studies are required to investigate this hypothesis and whether novel therapeutic strategies to inhibit fibrin turnover slow early AAA growth.