The effect of rosuvastatin on thromboinflammation in the setting of acute coronary syndrome

Travis R. Sexton, Eric L. Wallace, Tracy E. Macaulay, Richard J. Charnigo, Virgilio Evangelista, Charles L. Campbell, Alison L. Bailey, Susan S. Smyth

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


In patients with acute coronary syndromes (ACS), early therapy with high-dose statins may reduce short-term adverse clinical outcomes. The mechanisms responsible are not known but could involve anti-inflammatory or anti-thrombotic effects. Compelling evidence from experimental models and clinical studies suggests that the interplay between inflammatory and thrombotic systems, typified by platelet–monocyte and platelet–neutrophil interactions, might be a key regulator of ischemic vascular events. The study sought to determine if early, high-dose administration of the HMG-CoA reductase inhibitor rosuvastatin in the setting of ACS exerts beneficial vascular effects by reducing, and inhibiting biomarkers of thromboinflammation, such as platelet-monocyte and platelet-neutrophil interactions, and biomarkers of myocardial necrosis. A total of 54 patients presenting with ACS within 8 h of symptom onset were randomized to rosuvastatin 40 mg or placebo. Rosuvastatin significantly reduced interactions between platelets and circulating neutrophils (P = 0.015) and monocytes (P = 0.009) within 24 h. No significant effects were observed on platelet aggregation or plasma levels of PF4, sP-selectin, or sCD40L, whereas significant reductions of RANTES occurred over time in both treatment groups. Plasma levels of myeloperoxidase (MPO) declined more rapidly with rosuvastatin therapy than placebo. In a subset of patients with normal cardiac necrosis biomarkers at randomization, rosuvastatin therapy was associated with less myocardial damage as measured by troponin-I or CK-MB. Early administration of high-dose statin therapy in patients with ACS appears to improve biomarkers of inflammation within 8 h, which may translate into fewer ischemic events.

Original languageEnglish
Pages (from-to)186-195
Number of pages10
JournalJournal of Thrombosis and Thrombolysis
Issue number2
StatePublished - Feb 2015

Bibliographical note

Funding Information:
This work was supported by an investigator-initiated Grant from AstraZeneca. TRS was supported in part by T32HL091812 from the Heart Lung and Blood Institute, National Institutes of Health. Additional support was provided by the National Center for Research Resources and the National Center for Advancing Translational Sciences, National Institutes of Health, through Grant UL1TR000117. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

Publisher Copyright:
© 2014, The Author(s).


  • Acute coronary syndrome
  • Acute myocardial infarction
  • Platelets
  • Statin
  • Thromboinflammation

ASJC Scopus subject areas

  • Hematology
  • Cardiology and Cardiovascular Medicine


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