Effects of statin therapy on inflammatory markers in chronic heart failure: a meta-analysis of randomized controlled trials

Arch Med Res. 2010 Aug;41(6):464-71. doi: 10.1016/j.arcmed.2010.08.009.

Abstract

Background and aims: Inflammation is thought to be important in mediating the progression of chronic heart failure (CHF). Whether beneficial effects on inflammation can be achieved by statins in patients with CHF remains uncertain. This meta-analysis was conducted to determine the role of statin therapy in inflammation markers in CHF patients.

Methods: Pubmed, MEDLINE, EMBASE, and EBM Reviews databases were searched for randomized controlled trials comparing statin treatment with non-statin treatment in CHF patients. Two reviews independently assessed studies and extracted data. Standardized mean differences (SMD) were calculated using random effects models.

Results: Ten studies with 6052 patients were included. Pooled analysis showed that statin therapy was associated with significant decrease in high-sensitivity C-reactive protein (SMD = -0.74, 95% CI -1.16 to -0.32; p = 0.0005) and soluble vascular cell adhesion molecule-1 (SMD = -0.49, 95% CI -0.91 to -0.08; p = 0.02). However, the beneficial effects of statin were not shown regarding interleukin-6 (SMD = -0.85, 95% CI -2.09 to 0.38; p = 0.18) and tumor necrosis factor-α (SMD = -0.13, 95% CI -0.50 to 0.25; p = 0.51). Sources of heterogeneity were not found by meta-regression analyses, whereas subgroup analyses showed that difference in age, etiology, baseline left ventricular ejection fraction, type of statins and follow-up duration might influence the effects of statins.

Conclusions: Statin may partially suppress inflammatory markers in patients with CHF; moreover, this beneficial effect may be associated with different types of statins, treatment intervals and characteristics of patients.

Publication types

  • Meta-Analysis
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biomarkers / metabolism
  • C-Reactive Protein / metabolism
  • Female
  • Heart Failure / drug therapy*
  • Heart Failure / metabolism*
  • Humans
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use*
  • Inflammation Mediators / metabolism*
  • Interleukin-6 / metabolism
  • Male
  • Tumor Necrosis Factor-alpha / metabolism
  • Vascular Cell Adhesion Molecule-1 / metabolism

Substances

  • Biomarkers
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • IL6 protein, human
  • Inflammation Mediators
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • C-Reactive Protein