4.6 Article

Relationship of Serum Inflammatory Biomarkers With Plaque Inflammation Assessed by FDG PET/CT The dal-PLAQUE Study

期刊

JACC-CARDIOVASCULAR IMAGING
卷 6, 期 10, 页码 1087-1094

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jcmg.2013.03.009

关键词

atherosclerosis; fluorodeoxyglucose F 18 positron emission tomography; inflammatory biomarkers

资金

  1. F. Hoffmann-La Roche Ltd.
  2. Tursiop Inc.
  3. National Institute for Health Research Cambridge Biomedical Research Centre
  4. Merck
  5. Bristol-Myers Squibb
  6. Genentech
  7. GlaxoSmithKline
  8. VBL Therapeutics
  9. Roche
  10. Novartis
  11. Via Pharmaceuticals
  12. Academy of Medical Sciences (AMS) [AMS-SGCL1-Rudd] Funding Source: researchfish
  13. British Heart Foundation [PG/09/083/27667, FS/12/29/29463] Funding Source: researchfish

向作者/读者索取更多资源

OBJECTIVES This study sought to longitudinally investigate the relationship between a broad spectrum of serum inflammatory biomarkers and plaque inflammation assessed by F-18-fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT). BACKGROUND Both plaque inflammation and serum biomarkers of inflammation are associated with atherothrombotic events; however, the relationship between them is unclear. METHODS We conducted a post hoc analysis of the dal-PLAQUE (A Randomized Placebo-Controlled Study of the Effect of RO4607381 on Progression or Regression of Atherosclerotic Hague in Patients With Coronary Heart Disease [CHD] Including Patients With Other CHD Risk Factors), a randomized, placebo-controlled study of dalcetrapib, a cholesteryl ester transfer protein inhibitor, in 130 patients with coronary heart disease, or coronary heart disease risk equivalents on stable lipid-lowering therapy. Baseline and change after 3-month follow-up in inflammatory biomarker levels and baseline and change after 3-month follow-up in aorta and carotid F-18-FDG PET/CT (mean maximum target-to-background ratio of the most diseased segment [TBRmds]) were analyzed. RESULTS Baseline myeloperoxidase positively correlated with baseline carotid TBRmds (rho = 0.25, p = 0.02). This correlation remained at the 3-month follow-up and was independent of traditional cardiovascular disease risk factors. Baseline lipoprotein-associated phospholipase A(2) mass correlated with aorta TBRmds (rho = 0.21, p = 0.03). However, this correlation disappeared at the 3-month follow-up and was not independent of cardiovascular disease risk factors. There was no association between change from baseline in myeloperoxidase or lipoprotein-associated phospholipase A(2) mass and change from baseline in aorta and carotid TBRmds. Baseline and change from baseline in high sensitivity C-reactive protein, interleukin 6, soluble P-selectin, soluble E-selectin, soluble intracellular adhesion molecule 1, soluble vascular cell adhesion molecule 1, and matrix-metalloproteinase 3 and 9 did not correlate with baseline or change from baseline in carotid or aorta TBRmds. CONCLUSIONS Our data show that, in patients with coronary heart disease or at high risk of coronary heart disease on stable lipid-lowering therapy, circulating myeloperoxidase levels are associated with carotid plaque inflammation. (A Randomized, Placebo-controlled Study of the Effect of RO4607381 on Progression or Regression of Atherosclerotic Plaque in Patients With Coronary Heart Disease [CHD] Including Patients With Other CHD Risk Factors [dal-PLAQUE]; NCT00655473) (C) 2013 by the American College of Cardiology Foundation

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