Atorvastatin reduces plasma MCP-1 in patients with acute coronary syndrome

Clin Chim Acta. 2003 Dec;338(1-2):17-24. doi: 10.1016/s0009-8981(03)00321-8.


Background: The monocyte chemoattractant protein-1 (MCP-1) is a chemokine responsible for the recruitment of monocytes to sites of inflammation. MCP-1 may play critical roles in plaque instability. Anti-inflammation may be one benefit of statin drugs in acute coronary syndrome (ACS). We investigated the effects of atorvastatin therapy on plasma MCP-1 concentrations and production of MCP-1 released by peripheral blood monocytes from ACS patients.

Methods: Forty patients with ACS were randomly separated into two groups, those receiving conventional therapy (Group A, n=20), and conventional therapy+atorvastatin (10 mg/day, Group B, n=20). The study the effects of atorvastatin on secretion and expression of MCP-1, human peripheral blood monocytes from healthy donors were incubated with atorvastatin (0.1-10 micromol/l) for up to 24 h in vitro. MCP-1 concentrations in plasma and monocytes culture supernatants were measured by enzyme-linked immunosorbent assays (ELISA). MCP-1 expression was measured by RT-PCR.

Results: Plasma concentrations of MCP-1 were significantly lower after 4 weeks therapy in both groups of patients [Group A from 97.4 (50.1-164) to 72.6 (36.3-156) pg/ml, Group B from 101 (60-178) to 45 (29-91) pg/ml, (P<0.05, respectively)]. Compared with conventional therapy alone, atorvastatin significantly further reduced plasma MCP-1 concentrations. There was no significant correlation between the degree of changes in plasma MCP-1 and LDL-C. In vitro, atorvastatin inhibits production of MCP-1 up to 73%, in a concentration-dependent manner, and suppressed MCP-1 expression in peripheral blood monocytes.

Conclusions: Atorvastatin reduced plasma MCP-1 concentrations in patients with ACS. These effects may explain some clinical benefits of statins in the treatment of these patients.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial

MeSH terms

  • Atorvastatin
  • Cells, Cultured
  • Chemokine CCL2 / analysis
  • Chemokine CCL2 / blood*
  • Chemokine CCL2 / genetics
  • Chemokine CCL2 / metabolism
  • Coronary Disease / blood*
  • Coronary Disease / drug therapy
  • Coronary Disease / genetics
  • Coronary Disease / metabolism
  • Culture Media, Conditioned / chemistry
  • Female
  • Heptanoic Acids / pharmacology*
  • Heptanoic Acids / therapeutic use
  • Humans
  • Lipids / blood
  • Male
  • Middle Aged
  • Monocytes / drug effects
  • Monocytes / metabolism
  • Pyrroles / pharmacology*
  • Pyrroles / therapeutic use
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism


  • Chemokine CCL2
  • Culture Media, Conditioned
  • Heptanoic Acids
  • Lipids
  • Pyrroles
  • RNA, Messenger
  • Atorvastatin