TY - JOUR
T1 - The effect of BMS-582949, a P38 mitogen-activated protein kinase (P38 MAPK) inhibitor on arterial inflammation
T2 - A multicenter FDG-PET trial
AU - Emami, Hamed
AU - Vucic, Esad
AU - Subramanian, Sharath
AU - Abdelbaky, Amr
AU - Fayad, Zahi A.
AU - Du, Shuyan
AU - Roth, Eli
AU - Ballantyne, Christie M.
AU - Mohler, Emile R.
AU - Farkouh, Michael E.
AU - Kim, Joonyoung
AU - Farmer, Matthew
AU - Li, Li
AU - Ehlgen, Alexander
AU - Langenickel, Thomas H.
AU - Velasquez, Linda
AU - Hayes, Wendy
AU - Tawakol, Ahmed
N1 - Publisher Copyright:
© 2015 Elsevier Ireland Ltd.
PY - 2015/6/1
Y1 - 2015/6/1
N2 - Objectives: This study evaluated the effect of p38 mitogen-activated protein kinase (p38MAPK) inhibitor, BMS-582949, on atherosclerotic plaque inflammation, using 18FDG-PET imaging. p38MAPK is an important element of inflammatory pathways in atherothrombosis and its inhibition may lead to reduced inflammation within atherosclerotic plaques. Methods: Subjects with documented atherosclerosis (n=72) on stable low-dose statin therapy and having at least one lesion with active atherosclerotic plaque inflammation in either aorta or carotid arteries were randomized to BMS-582949 (100mg once daily), placebo, or atorvastatin (80mg once daily), for 12 weeks. Arterial inflammation was assessed using 18FDG-PET/CT imaging of the carotid arteries and aorta. Uptake of arterial 18FDG was assessed as target-to-background ratio (TBR): 1) as a mean of all slices of the index vessel, and 2) within active slices of all vessels (AS: which includes only slices with significant inflammation (TBR≥1.6) at the baseline). Results: Treatment with BMS-582949 did not reduce arterial inflammation relative to placebo, (δTBR index: 0.10 [95% CI: -0.11, 0.30], p=0.34; δTBR AS: -0.01 [-0.31, 0.28], p=0.93) or hs-CRP (median %δCRP [IQR]: 33.83% [153.91] vs. 16.71% [133.45], p=0.61). In contrast, relative to placebo, statin intensification was associated with significant reduction of hs-CRP (%δCRP [IQR]: -17.44% [54.68] vs. 16.71% [133.45], p=0.04) and arterial inflammation in active slices (δTBRAS=-0.24 [95% CI: -0.46, -0.01], p=0.04). Conclusions: The findings of this study demonstrates that in stable atherosclerosis, 12 weeks of treatment with BMS-582949 did not reduce arterial inflammation or hs-CRP compared to placebo, whereas intensification of statin therapy significantly decreased arterial inflammation. •We evaluated the effect of p38MAPK inhibitor, BMS-582949, on arterial inflammation.•Subjects with known ASCVD were randomized to BMS-582949, placebo, or atorvastatin.•We demonstrate that treatment with BMS-582949 did not reduce arterial inflammation.•Intensification of statin therapy (positive control) reduced arterial inflammation.
AB - Objectives: This study evaluated the effect of p38 mitogen-activated protein kinase (p38MAPK) inhibitor, BMS-582949, on atherosclerotic plaque inflammation, using 18FDG-PET imaging. p38MAPK is an important element of inflammatory pathways in atherothrombosis and its inhibition may lead to reduced inflammation within atherosclerotic plaques. Methods: Subjects with documented atherosclerosis (n=72) on stable low-dose statin therapy and having at least one lesion with active atherosclerotic plaque inflammation in either aorta or carotid arteries were randomized to BMS-582949 (100mg once daily), placebo, or atorvastatin (80mg once daily), for 12 weeks. Arterial inflammation was assessed using 18FDG-PET/CT imaging of the carotid arteries and aorta. Uptake of arterial 18FDG was assessed as target-to-background ratio (TBR): 1) as a mean of all slices of the index vessel, and 2) within active slices of all vessels (AS: which includes only slices with significant inflammation (TBR≥1.6) at the baseline). Results: Treatment with BMS-582949 did not reduce arterial inflammation relative to placebo, (δTBR index: 0.10 [95% CI: -0.11, 0.30], p=0.34; δTBR AS: -0.01 [-0.31, 0.28], p=0.93) or hs-CRP (median %δCRP [IQR]: 33.83% [153.91] vs. 16.71% [133.45], p=0.61). In contrast, relative to placebo, statin intensification was associated with significant reduction of hs-CRP (%δCRP [IQR]: -17.44% [54.68] vs. 16.71% [133.45], p=0.04) and arterial inflammation in active slices (δTBRAS=-0.24 [95% CI: -0.46, -0.01], p=0.04). Conclusions: The findings of this study demonstrates that in stable atherosclerosis, 12 weeks of treatment with BMS-582949 did not reduce arterial inflammation or hs-CRP compared to placebo, whereas intensification of statin therapy significantly decreased arterial inflammation. •We evaluated the effect of p38MAPK inhibitor, BMS-582949, on arterial inflammation.•Subjects with known ASCVD were randomized to BMS-582949, placebo, or atorvastatin.•We demonstrate that treatment with BMS-582949 did not reduce arterial inflammation.•Intensification of statin therapy (positive control) reduced arterial inflammation.
KW - Atherosclerosis
KW - FDG
KW - FDG
KW - Hs-CRP
KW - Imaging
KW - Inflammation
KW - MAPK
KW - MAPK
KW - PET
KW - ROI
KW - SUV
KW - TBR
UR - https://www.scopus.com/pages/publications/84928251706
U2 - 10.1016/j.atherosclerosis.2015.03.039
DO - 10.1016/j.atherosclerosis.2015.03.039
M3 - Article
C2 - 25913664
AN - SCOPUS:84928251706
SN - 0021-9150
VL - 240
SP - 490
EP - 496
JO - Atherosclerosis
JF - Atherosclerosis
IS - 2
ER -