Adventitial lymphocytic inflammation in human coronary arteries with intimal atherosclerosis.

Background: The relationship between adventitial inflammation, plaque type, and culprit plaque morphology in the epicardial arterial circulation has not been studied in detail.

Methods: We studied semiserial sections of coronary arteries at autopsy from patients dying with severe coronary disease, 81 men (age 50 + or - 12 years) and 13 women (age 52 + or - 13 years). Lesions were classified at 3- to 5-mm segments according to modified AHA criteria. Adventitial lymphocyte aggregates were assessed at every 5-mm interval and graded semiquantitatively. Macrophage density in the adventitial fat and intima was assessed with anti-CD68 staining.

Results: Adventitial lymphocytic inflammation increased with percent stenosis (P<.0001) and not calcification (P>.2). Hemorrhage into late core, rupture, erosion, and thin caps all had greater adventitial lymphocytic inflammation independent of percent stenosis (P<.0001). Peri-adventitial adipose macrophage density was increased in plaques with atheromas (206 + or - 22 mm(2) vs. 121 + or - 15 mm(2) in fibrous plaques; P=.02) and correlated positively with adventitial lymphocytes (P<.0001) and intimal macrophage content (P<.0001).

Conclusions: Features associated with plaque instability are associated with significantly greater degrees of adventitial lymphocytic inflammation, both as lymphocyte aggregates and as adipocyte-derived macrophages. Further study is required to determine the nature of the association between intimal and adventitial lymphocytic inflammation.