Abstract Thu124: Coronary Plaque Inflammation in the Progression from Thin-cap Fibroatheroma to Plaque Rupture

Background: Inflammation plays a crucial role in the destabilization of coronary vulnerable plaques. However, pathological inflammation patterns and immune cell distribution in human vulnerable coronary plaques remain poorly described. Methods: We analyzed 58 coronary lesions (33 male, 25 female) from the CVPath autopsy registry, comprising 36 plaque ruptures and 22 thin-cap fibroatheromas (TCFAs). Analysis included pathological morphometry and immunohistochemical evaluation. Plaque inflammation was assessed at intimal-medial border, media, and adventitia, using a scoring system based on the severity and distribution, then combined into a total inflammation score ranging from 1 to 8. Results: Plaque rupture lesions demonstrated significantly higher inflammation scores at the intima-media border compared to TCFA (p=0.001), while scores in media (p=0.82) and adventitia (p=0.62) showed no significant differences. Inflammation score ≥ 5 was observed in 29% (17/58) of total lesions, 4.6 times more frequently in plaque rupture than in TCFA (82% [14/17] vs. 18% [3/17], respectively). Plaque rupture lesions exhibited more extensive internal elastic lamina (IEL) disruption (p=0.032). Inflammation scores at the intima-media border positively correlated with both necrotic core size (r 2 =0.41, p<0.001) and IEL disruption (r 2 =0.31, p<0.001). T cells, CD4 + , and CD8 + T cells, and macrophages were highest in IM border whereas CD20 + B cells and CD138 + plasma cells were dominant in the adventitia in plaque rupture. Conclusions: Inflammation at the intima-media border, with predominant T lymphocyte distribution, was significantly higher in plaque rupture compared to TCFA. Inflammation score at the intima-media border was associated with necrotic core size and IEL disruption, suggesting inflammatory cells at intima-media border may contribute to vessel vulnerable remodeling.