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Background  Despite systemic exposure to risk factors, the circulatory system develops varying patterns of atherosclerosis for unclear reasons. In a porcine model, we investigated the relationship between site‐specific lesion development and inflammatory pathways involved in the coronary arteries ( COR s) and distal abdominal aortas ( AA s).    Methods and Results  Diabetes mellitus ( DM ) and hypercholesterolemia ( HC ) were induced in 37 pigs with 3 healthy controls. Site‐specific plaque development was studied by comparing plaque severity, macrophage infiltration, and inflammatory gene expression between  COR s and  AA s of 17  DM / HC  pigs. To assess the role of lipoprotein‐associated phospholipase A 2  (Lp‐ PLA  2 ) in plaque development, 20  DM / HC  pigs were treated with the Lp‐ PLA  2  inhibitor darapladib and compared with the 17  DM / HC  untreated pigs.  DM / HC  caused site‐specific differences in plaque severity. In the  AA s, normalized plaque area was 4.4‐fold higher ( P <0.001) and there were more fibroatheromas (9 of the 17 animals had a fibroatheroma in the  AA  and not the  COR ,  P =0.004), while normalized macrophage staining area was 1.5‐fold higher ( P =0.011) compared with  COR s.  DM / HC  caused differential expression of 8 of 87 atherosclerotic genes studied, including 3 important in inflammation with higher expression in the  COR s. Darapladib‐induced attenuation of normalized plaque area was site‐specific, as  COR s responded 2.9‐fold more than  AA s ( P =0.045).    Conclusions  While plaque severity was worse in the  AA s, inflammatory genes and inflammatory pathways that use Lp‐ PLA  2  were more important in the  COR s. Our results suggest fundamental differences in inflammation between vascular sites, an important finding for the development of novel anti‐inflammatory therapeutics.

journal of the american heart association

Atherosclerotic Plaque Inflammation Varies Between Vascular Sites and Correlates With Response to Inhibition of Lipoprotein‐Associated Phospholipase A 2