Effects of statin therapy on inflammatory markers in chronic heart failure: a meta-analysis of randomized controlled trials.
OBJECTIVE
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.
Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Shanghai Medical College of Fudan University, Shanghai, China.
Lei
L
Zhang
Shuning
S
Zhang
Hong
H
Jiang
Aijun
A
Sun
Yunkai
Y
Wang
Yunzeng
Y
Zou
Junbo
J
Ge
Haozhu
H
Chen
D015415:Biomarkers / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D005260:Female; D006333:Heart Failure / Q000188:drug therapy* / Q000378:metabolism*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D018836:Inflammation Mediators / Q000378:metabolism*; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
D015415:Biomarkers; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D002097:C-Reactive Protein