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  • Tardif, Jean-ClaudeMontreal Heart Institute, Canada; University of Montreal, Canada (author)

Genotype-Dependent Effects of Dalcetrapib on Cholesterol Efflux and Inflammation Concordance With Clinical Outcomes

  • Article/chapterEnglish2016

Publisher, publication year, extent ...

  • LIPPINCOTT WILLIAMS & WILKINS,2016
  • electronicrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:liu-131911
  • https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-131911URI
  • https://doi.org/10.1161/CIRCGENETICS.116.001405DOI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • Funding Agencies|F. Hoffmann-La Roche
  • Background-Dalcetrapib effects on cardiovascular outcomes are determined by adenylate cyclase 9 gene polymorphisms. Our aim was to determine whether these clinical end point results are also associated with changes in reverse cholesterol transport and inflammation. Methods and Results-Participants of the dal-OUTCOMES and dal-PLAQUE-2 trials were randomly assigned to receive dalcetrapib or placebo in addition to standard care. High-sensitivity C-reactive protein was measured at baseline and at end of study in 5243 patients from dal-OUTCOMES also genotyped for the rs1967309 polymorphism in adenylate cyclase 9. Cholesterol efflux capacity of high-density lipoproteins from J774 macrophages after cAMP stimulation was determined at baseline and 12 months in 171 genotyped patients from dal-PLAQUE-2. Treatment with dalcetrapib resulted in placebo-adjusted geometric mean percent increases in high-sensitivity C-reactive protein from baseline to end of trial of 18.1% (P=0.0009) and 18.7% (P=0.00001) in participants with the GG and AG genotypes, respectively, but the change was -1.0% (P=0.89) in those with the protective AA genotype. There was an interaction between the treatment arm and the genotype groups (P=0.02). Although the mean change in cholesterol efflux was similar among study arms in patients with GG genotype (mean: 7.8% and 7.4%), increases were 22.3% and 3.5% with dalcetrapib and placebo for those with AA genotype (P=0.005). There was a significant genetic effect for change in efflux for dalcetrapib (P=0.02), but not with placebo. Conclusions-Genotype-dependent effects on C-reactive protein and cholesterol efflux are supportive of dalcetrapib benefits on atherosclerotic cardiovascular outcomes in patients with the AA genotype at polymorphism rs1967309.

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Added entries (persons, corporate bodies, meetings, titles ...)

  • Rhainds, DavidMontreal Heart Institute, Canada (author)
  • Brodeur, MathieuMontreal Heart Institute, Canada (author)
  • Feroz Zada, YassaminUniversity of Montreal, Canada (author)
  • Fouodjio, ReneUniversity of Montreal, Canada (author)
  • Provost, SylvieUniversity of Montreal, Canada (author)
  • Boule, MarieMontreal Heart Institute, Canada (author)
  • Alem, SoniaMontreal Heart Institute, Canada (author)
  • Gregoire, Jean C.Montreal Heart Institute, Canada; University of Montreal, Canada (author)
  • LAllier, Philippe L.Montreal Heart Institute, Canada; University of Montreal, Canada (author)
  • Ibrahim, RedaMontreal Heart Institute, Canada; University of Montreal, Canada (author)
  • Guertin, Marie-ClaudeMontreal Health Innovat Coordinating Centre, Canada (author)
  • Mongrain, IanUniversity of Montreal, Canada (author)
  • Olsson, AndersLinköpings universitet,Medicinska fakulteten,Avdelningen för kardiovaskulär medicin,Region Östergötland, Endokrinmedicinska kliniken(Swepub:liu)andol21 (author)
  • Schwartz, Gregory G.Vet Affairs Medical Centre, CO USA; University of Colorado, CO USA (author)
  • Rheaume, EricMontreal Heart Institute, Canada; University of Montreal, Canada (author)
  • Dube, Marie-PierreMontreal Heart Institute, Canada; University of Montreal, Canada; University of Montreal, Canada (author)
  • Montreal Heart Institute, Canada; University of Montreal, CanadaMontreal Heart Institute, Canada (creator_code:org_t)

Related titles

  • In:Circulation: LIPPINCOTT WILLIAMS & WILKINS9:4, s. 340-3481942-325X1942-3268

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