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Effects of simvastatin within two weeks on anti-inflammatory cytokine interleukin 10 in patients with unstable angina
  1. J-J Li1,
  2. Y-S Li1,
  3. C-H Fang2,
  4. R-T Hui1,
  5. Y-J Yang1,
  6. J-L Cheng1,
  7. R-L Gao1
  1. 1Department of Cardiology, Fu Wai Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, People’s Republic of China
  2. 2Renmin Hospital, Wuhan University School of Medicine, Wuhan, People’s Republic of China
  1. Correspondence to:
    Dr Jian-Jun Li
    Department of Cardiology, Fu Wai Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100037, P R China; lijnjn{at}

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Evidence has shown that the inflammatory process is involved in all stages of atherosclerosis in various clinical settings and that an imbalance between anti-inflammatory mechanisms and proinflammatory factors, in favour of the proinflammatory factors, results in rupture of atherosclerotic plaque.1–3 Previous data also showed that proinflammatory cytokines are important in acute coronary events and that decreased plasma concentrations of anti-inflammatory cytokine are associated with acute coronary syndromes.1

In addition to their cholesterol lowering activity, statins have been shown to have pleiotropic effects, including anti-inflammatory effects.2,3 Recent studies have shown that the anti-inflammatory cytokine interleukin 10 has a protective role in both atherosclerotic formation and stability.4–6 However, the potential effects of statins on anti-inflammatory cytokines in patients with acute coronary disease has not been investigated. In the present study, we investigated whether a statin would affect interleukin 10 concentration within two weeks in patients with unstable angina (UA).


Forty two patients with typical UA were enrolled and randomly assigned to either standard treatment plus 20 mg/day or 80 mg/day of simvastatin immediately after admission. The standard treatment comprised aspirin, β blocker, heparin or low molecular weight heparin, angiotensin converting enzyme inhibitors, and oral nitrates. Patients with evidence of myocardial infarction consisting of ST elevation, formation of Q waves, and increased entry concentration of troponin T or I, congestive heart failure, poorly controlled hypertension, statin treatment before hospitalisation, valvar heart disease, a history of dysphagia, swallowing and intestinal motility disorders, and untreated thyroid disease were excluded from the study.

Selective coronary angiography was performed with the standard Judkins technique. The severity of coronary stenosis was evaluated with the incremental score method as in …

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