title: Does Vascular Calcification Accelerate Inflammation?: A Substudy of the dal-PLAQUE Trial.
abstract: BACKGROUND
  Atherosclerosis is an inflammatory condition with calcification apparent late in the disease process. The extent and progression of coronary calcification predict cardiovascular events. Relatively little is known about noncoronary vascular calcification.
  
  
  OBJECTIVE
  This study investigated noncoronary vascular calcification and its influence on changes in vascular inflammation.
  
  
  METHODS
  A total of 130 participants in the dal-PLAQUE (Safety and efficacy of dalcetrapib on atherosclerotic disease using novel non-invasive multimodality imaging) study underwent fluorodeoxyglucose positron emission tomography/computed tomography at entry and at 6 months. Calcification of the ascending aorta, arch, carotid, and coronary arteries was quantified. Cardiovascular risk factors were related to arterial calcification. The influences of baseline calcification and drug therapy (dalcetrapib vs. placebo) on progression of calcification were determined. Finally, baseline calcification was related to changes in vascular inflammation.
  
  
  RESULTS
  Age >65 years old was consistently associated with higher baseline calcium scores. Arch calcification trended to progress more in those with calcification at baseline (p = 0.055). There were no significant differences between progression of vascular calcification with dalcetrapib compared to that with placebo. Average carotid target-to-background ratio indexes declined over 6 months if carotid calcium was absent (single hottest slice [p = 0.037], mean of maximum target-to-background ratio [p = 0.010], and mean most diseased segment [p < 0.001]), but did not significantly change if calcification was present at baseline.
  
  
  CONCLUSIONS
  Across multiple arterial regions, higher age is consistently associated with higher calcium scores. The presence of vascular calcification at baseline is associated with progressive calcification; in the carotid arteries, calcification appears to influence vascular inflammation. Dalcetrapib therapy did not affect vascular calcification.
authors.affiliation: Division of Cardiovascular Medicine, University of Cambridge, Cambridge, United Kingdom.
authors.forename: Francis R
authors.initials: FR
authors.lastname: Joshi
authors.affiliation: Division of Cardiovascular Medicine, University of Cambridge, Cambridge, United Kingdom.
authors.forename: Nikil K
authors.initials: NK
authors.lastname: Rajani
authors.affiliation: Pharma Development, F. Hoffmann-La Roche AG, Basel, Switzerland.
authors.forename: Markus
authors.initials: M
authors.lastname: Abt
authors.affiliation: George Institute for Global Health, University of Sydney, Sydney, Australia; University of Oxford, Oxford, United Kingdom.
authors.forename: Mark
authors.initials: M
authors.lastname: Woodward
authors.affiliation: Translational and Molecular Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, New York; Department of Nuclear Medicine, and Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center, Maastricht, the Netherlands; Department of Nuclear Medicine, University Hospital RWTH Aachen, Aachen, Germany.
authors.forename: Jan
authors.initials: J
authors.lastname: Bucerius
authors.affiliation: Translational and Molecular Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, New York.
authors.forename: Venkatesh
authors.initials: V
authors.lastname: Mani
authors.affiliation: Massachusetts General Hospital, and Harvard Medical School, Boston, Massachusetts.
authors.forename: Ahmed
authors.initials: A
authors.lastname: Tawakol
authors.affiliation: Pharma Development, F. Hoffmann-La Roche AG, Basel, Switzerland.
authors.forename: David
authors.initials: D
authors.lastname: Kallend
authors.affiliation: Translational and Molecular Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, New York.
authors.forename: Zahi A
authors.initials: ZA
authors.lastname: Fayad
authors.affiliation: Division of Cardiovascular Medicine, University of Cambridge, Cambridge, United Kingdom. Electronic address: jhfr2@cam.ac.uk.
authors.forename: James H F
authors.initials: JH
authors.lastname: Rudd
mesh_terms: D000368:Aged; D000577:Amides; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D050197:Atherosclerosis / Q000150:complications* / Q000175:diagnosis / Q000188:drug therapy; D004952:Esters; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D064847:Multimodal Imaging; D049268:Positron-Emission Tomography; D012307:Risk Factors; D013438:Sulfhydryl Compounds / Q000627:therapeutic use; D014057:Tomography, X-Ray Computed; D061205:Vascular Calcification / Q000150:complications* / Q000175:diagnosis*; D014657:Vasculitis / Q000175:diagnosis* / Q000209:etiology*
chemical_list: D000577:Amides; D000924:Anticholesteremic Agents; D004952:Esters; D013438:Sulfhydryl Compounds; C411602:dalcetrapib
keywords: atherosclerosis; carotid arteries; cholesterol; dalcetrapib; fluorine-18; fluorodeoxyglucose; positron emission tomography