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

J Thromb Thrombolysis. 2015 Feb;39(2):186-95. doi: 10.1007/s11239-014-1142-x.


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.

Publication types

  • Randomized Controlled Trial
  • Research Support, N.I.H., Extramural

MeSH terms

  • Acute Coronary Syndrome* / blood
  • Acute Coronary Syndrome* / drug therapy
  • Acute Coronary Syndrome* / physiopathology
  • Adult
  • Aged
  • Biomarkers
  • Blood Platelets
  • CD40 Ligand / blood
  • Cell Communication / drug effects*
  • Creatine Kinase, MB Form / blood*
  • Dose-Response Relationship, Drug
  • Early Medical Intervention
  • Female
  • Humans
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / administration & dosage
  • Inflammation / blood
  • Male
  • Middle Aged
  • Monocytes
  • Neutrophils
  • P-Selectin / blood
  • Peroxidase / blood*
  • Platelet Factor 4 / blood
  • Rosuvastatin Calcium / administration & dosage*
  • Thrombosis / blood
  • Treatment Outcome
  • Troponin I / blood*


  • Biomarkers
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • P-Selectin
  • Troponin I
  • CD40 Ligand
  • Platelet Factor 4
  • Rosuvastatin Calcium
  • Peroxidase
  • Creatine Kinase, MB Form