The effect of BMS-582949, a P38 mitogen-activated protein kinase (P38 MAPK) inhibitor on arterial inflammation: A multicenter FDG-PET trial

  • Hamed Emami
  • , Esad Vucic
  • , Sharath Subramanian
  • , Amr Abdelbaky
  • , Zahi A. Fayad
  • , Shuyan Du
  • , Eli Roth
  • , Christie M. Ballantyne
  • , Emile R. Mohler
  • , Michael E. Farkouh
  • , Joonyoung Kim
  • , Matthew Farmer
  • , Li Li
  • , Alexander Ehlgen
  • , Thomas H. Langenickel
  • , Linda Velasquez
  • , Wendy Hayes
  • , Ahmed Tawakol

Research output: Contribution to journalArticlepeer-review

70 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)490-496
Number of pages7
JournalAtherosclerosis
Volume240
Issue number2
DOIs
StatePublished - 1 Jun 2015

Keywords

  • Atherosclerosis
  • FDG
  • FDG
  • Hs-CRP
  • Imaging
  • Inflammation
  • MAPK
  • MAPK
  • PET
  • ROI
  • SUV
  • TBR

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