Abstract 294: Adventitial Inflammation Reflects Intimal Coronary Atherosclerotic Plaque Morphology
The role of adventitial inflammation in coronary atherosclerosis is not clear. The relationship between adventitial inflammation, plaque type and culprit plaque morphology has not been studied in depth. We studied semiserial sections of coronary arteries at autopsy from patients dying with severe coronary disease, 81 men (age 50 Â± 12 years) and 14 women (age 52 Â± 13 years). Lesions were classified at 3–5 mm segments according to modified AHA criteria. Culprit plaque morphology was assessed as acute plaque rupture (n=44), acute plaque erosion (n=12), and stable plaque (n=39). Inflammation was assessed at every 5 mm interval and graded semiquantiatively: 0 (no inflammation), 1+ (scattered lymphocytes without aggregates), 2+ aggregates of lymphocytes > 25 cells in 1 quadrant of the adventitia; 3+ aggregates in 2 quadrants; and 4+ aggregates in 3– 4 quadrants. By culprit plaque morphology, mean adventitial inflammation score was 0.53 Â ± .05 in plaque erosion, .50 Â± .22 in plaque rupture, and .28 Â± .01 stable plaque (p<. 0001 vs. rupture and erosion). By univariate analysis of individual plaques, inflammation was correlated with percent stenosis (p0.2). Mean adventitial inflammation score was 1.1 Â± 0.1 for acute ruptures, 1.1 Â± 0.2 for erosions, 0.9 Â± 0.3 for plaque fissures, 0.9 Â± 0.3 for thin cap atheroma, and 0.7 Â± .07 for fibroatheromas with hemorrhage, 0.6 Â ± .04 for fibroatheromas with late cores, and < 0.5 for fibrous plaques, pathologic intimal thickening, fatty streaks, and fibrocalcific plaques. Hemorrhage into late core, rupture, erosion, and thin caps all had greater adventitial inflammation independent of percent stenosis compared to plaques without these characteristics (p<.0001). Features associated with plaque instability are associated with significantly greater degrees of adventitial inflammation. Further study is required to determine the nature of the association between intimal and adventitial inflammation.