Different effects of simvastatin and losartan on cytokine levels in coronary artery disease

Kenji Sadamatsu, Hiroaki Shimokawa, Hideki Tashiro, Taku Seto, Hiroshi Kakizoe, Kunihiko Yamamoto

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)


Background and objective: Use of HMG-CoA reductase inhibitors (statins) and angiotensin II type 1 (AT1) receptor antagonists reduces the incidence of cardiovascular events. The cytokines macrophage colony-stimulating factor (M-CSF) and transforming growth factor (TGF)-β may exert proatherogenic and antiatherogenic effects, respectively. In this study, we examined whether treatment with a statin or an AT1 receptor antagonist alters M-CSF and TGF-β levels in patients with coronary artery disease. Methods: Twenty-seven consecutive patients with coronary artery disease were randomly assigned to the following three treatment groups for 8 weeks: simvastatin 5 mg/day (n = 10); losartan 50 mg/day (n = 9); or control (usual treatment; n = 8). Blood samples were collected before and after treatment. Results: Clinical characteristics and baseline cytokine levels were comparable among the three groups. Serum levels of M-CSF were significantly decreased only in the simvastatin group (from 403 ± 71 to 303 ± 116 pg/mL; p = 0.009). Plasma levels of TGF-β were significantly increased only in the losartan group (from 5.01 ± 1.13 to 7.50 ± 3.83 ng/mL; p = 0.021). Simvastatin decreased serum M-CSF levels independently of changes in total cholesterol or low-density lipoprotein-cholesterol. Conclusions: The results of this study indicate that simvastatin decreases serum levels of M-CSF while losartan increases plasma levels of TGF-β, suggesting that the two drugs may have different antiatherosclerotic properties.

Original languageEnglish
Pages (from-to)169-175
Number of pages7
JournalAmerican Journal of Cardiovascular Drugs
Issue number3
Publication statusPublished - 2006
Externally publishedYes

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology (medical)


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