> Detailanzeige

Wallentin, Lars; Held, Claes; Armstrong, Paul W.; Cannon, Christopher P.; Davies, Richard Y.; Granger, Christopher B.; Hagström, Emil; Harrington, Robert A.; Hochman, Judith S.; Koenig, Wolfgang; Krug‐Gourley, Sue; Mohler, Emile R.; Siegbahn, Agneta; Tarka, Elizabeth; Steg, Philippe Gabriel; Stewart, Ralph A. H.; Weiss, Robert; Östlund, Ollie; White, Harvey D.; Budaj, Andrzej; Ardissino, Diego; Avezum, Alvaro; Aylward, Philip E.; Bryce, Alfonso; [...]

Lipoprotein‐Associated Phospholipase A 2 Activity Is a Marker of Risk But Not a Useful Target for Treatment in Patients With Stable Coronary Heart Disease

Literatur-
verwaltung

Zur
Merkliste

Lösche von
Merkliste

Per Whatsapp teilen

Schließen

Merkliste



Sie können Bookmarks mittels Listen verwalten, loggen Sie sich dafür bitte in Ihr SLUB Benutzerkonto ein.
  • Medientyp: E-Artikel
  • Titel: Lipoprotein‐Associated Phospholipase A 2 Activity Is a Marker of Risk But Not a Useful Target for Treatment in Patients With Stable Coronary Heart Disease
  • Beteiligte: Wallentin, Lars; Held, Claes; Armstrong, Paul W.; Cannon, Christopher P.; Davies, Richard Y.; Granger, Christopher B.; Hagström, Emil; Harrington, Robert A.; Hochman, Judith S.; Koenig, Wolfgang; Krug‐Gourley, Sue; Mohler, Emile R.; Siegbahn, Agneta; Tarka, Elizabeth; Steg, Philippe Gabriel; Stewart, Ralph A. H.; Weiss, Robert; Östlund, Ollie; White, Harvey D.; Budaj, Andrzej; Ardissino, Diego; Avezum, Alvaro; Aylward, Philip E.; Bryce, Alfonso; [...]
  • Erschienen: Ovid Technologies (Wolters Kluwer Health), 2016
  • Erschienen in: Journal of the American Heart Association
  • Sprache: Englisch
  • DOI: 10.1161/jaha.116.003407
  • ISSN: 2047-9980
  • Schlagwörter: Cardiology and Cardiovascular Medicine
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <jats:sec xml:lang="en"> <jats:title>Background</jats:title> <jats:p xml:lang="en"> We evaluated lipoprotein‐associated phospholipase A <jats:sub>2</jats:sub> (Lp‐ <jats:styled-content style="fixed-case">PLA</jats:styled-content> <jats:sub>2</jats:sub> ) activity in patients with stable coronary heart disease before and during treatment with darapladib, a selective Lp‐ <jats:styled-content style="fixed-case">PLA</jats:styled-content> <jats:sub>2</jats:sub> inhibitor, in relation to outcomes and the effects of darapladib in the <jats:styled-content style="fixed-case">STABILITY</jats:styled-content> trial. </jats:p> </jats:sec> <jats:sec xml:lang="en"> <jats:title>Methods and Results</jats:title> <jats:p xml:lang="en"> Plasma Lp‐ <jats:styled-content style="fixed-case">PLA</jats:styled-content> <jats:sub>2</jats:sub> activity was determined at baseline (n=14 500); at 1 month (n=13 709); serially (n=100) at 3, 6, and 18 months; and at the end of treatment. Adjusted Cox regression models evaluated associations between Lp‐ <jats:styled-content style="fixed-case">PLA</jats:styled-content> <jats:sub>2</jats:sub> activity levels and outcomes. At baseline, the median Lp‐ <jats:styled-content style="fixed-case">PLA</jats:styled-content> <jats:sub>2</jats:sub> level was 172.4 μmol/min per liter (interquartile range 143.1–204.2 μmol/min per liter). Comparing the highest and lowest Lp‐ <jats:styled-content style="fixed-case">PLA</jats:styled-content> <jats:sub>2</jats:sub> quartile groups, the hazard ratios were 1.50 (95% CI 1.23–1.82) for the primary composite end point (cardiovascular death, myocardial infarction, or stroke), 1.95 (95% CI 1.29–2.93) for hospitalization for heart failure, 1.42 (1.07–1.89) for cardiovascular death, and 1.37 (1.03–1.81) for myocardial infarction after adjustment for baseline characteristics, standard laboratory variables, and other prognostic biomarkers. Treatment with darapladib led to a ≈65% persistent reduction in median Lp‐ <jats:styled-content style="fixed-case">PLA</jats:styled-content> <jats:sub>2</jats:sub> activity. There were no associations between on‐treatment Lp‐ <jats:styled-content style="fixed-case">PLA</jats:styled-content> <jats:sub>2</jats:sub> activity or changes of Lp‐ <jats:styled-content style="fixed-case">PLA</jats:styled-content> <jats:sub>2</jats:sub> activity and outcomes, and there were no significant interactions between baseline and on‐treatment Lp‐ <jats:styled-content style="fixed-case">PLA</jats:styled-content> <jats:sub>2</jats:sub> activity or changes in Lp‐ <jats:styled-content style="fixed-case">PLA</jats:styled-content> <jats:sub>2</jats:sub> activity levels and the effects of darapladib on outcomes. </jats:p> </jats:sec> <jats:sec xml:lang="en"> <jats:title>Conclusions</jats:title> <jats:p xml:lang="en"> Although high Lp‐ <jats:styled-content style="fixed-case">PLA</jats:styled-content> <jats:sub>2</jats:sub> activity was associated with increased risk of cardiovascular events, pharmacological lowering of Lp‐ <jats:styled-content style="fixed-case">PLA</jats:styled-content> <jats:sub>2</jats:sub> activity by ≈65% did not significantly reduce cardiovascular events in patients with stable coronary heart disease, regardless of the baseline level or the magnitude of change of Lp‐ <jats:styled-content style="fixed-case">PLA</jats:styled-content> <jats:sub>2</jats:sub> activity. </jats:p> </jats:sec> <jats:sec xml:lang="en"> <jats:title>Clinical Trial Registration</jats:title> <jats:p xml:lang="en"> <jats:styled-content style="fixed-case">URL</jats:styled-content> : <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="https://www.clinicaltrials.gov">https://www.clinicaltrials.gov</jats:ext-link> . Unique identifier: <jats:styled-content style="fixed-case">NCT</jats:styled-content> 00799903. </jats:p> </jats:sec>
  • Zugangsstatus: Freier Zugang