Abstract 2733: Short-Term Atorvastatin Treatment In Patients With Congestive Heart Failure: Evidence For Anti-Inflammatory And Antithrombotic Effects
Background: Congestive heart failure (CHF) is characterised by increased proinflammatory stimuli, endothelial dysfunction and increased thrombogenecity. We investigated the effect of low dose torvastatin-treatment on endothelial function inflammation and thrombosis/fibrinolysis system in patients with CHF.
Methods. Thirty-five patients with CHF (NYHA II-IV) were randomized to receive atorvastatin 10mg/day (n=17) or no statin (n=18) for 4 weeks. Endothelium dependent dilation (EDD) and endothelium independent dilation (EID) were determined by gauge-strain plethysmography.Plasma levels of interleukin-6 (IL-6), tumor necrosis factor α (TNF-α), vascular cell adhesion molecule (sVCAM-1), antithrombin III (ATIII), protein C, factor V, tissue plasminogen activator (tPA) and plasminogen activator inhibitor 1 (PAI-1) were determined by ELISA.
Results. Atorvastatin improved EDD (42.44±4.5 to 83.7±8.5%, p<0.01), decreased plasma levels of tPA (15.5±2.2 to 12.3±1.6 ng/ml p<0.05), ATIII (82±3 to 74±4%, p<0.05), prtC (88±6 to 64±6%, p<0.01), fV (126±8 to 95±7%, p<0.01) and PAI-1 (3.02±0.39 to 1.96±0.34 IU/L, p<0.05). In control group, no significant change was observed in levels of ATIII (85±4 to 88±3%,p=ns), prtC(84±6 to 84±5%,p=ns), fV(131±10 to 122±9%,p=ns), tPA(13.2±1.5 to 11±2 ng/ml, p=ns) and PAI-1(2.64±0.38 to 3.25±0.34, p=ns). Similarly, levels of sVCAM-1, IL-6 and TNF-a were significantly decreased in atorvastatin group (from 650.7±61.7, 7.69±0.69 and 3.8±0.35 to 471.6±44.5 ng/ml, 6.02±0.81 pg/ml and 2.8±0.22 pg/ml respectively, p<0.05 for all) but not in controls (from 656.2±70.0, 7.30±0.72 and 4.5±0.62 to 643.9±71.1 ng/ml, 6.31±0.81 pg/ml and 4.53±0.61 pg/ml respectively, p=NS for all). EID remained unchanged in both study groups.
Conclusions. Short-term treatment with low dose of atorvastatin improves endothelial function and decreases the expression of proinflammatory cytokines and adhesion molecules in patients with CHF. Similarly it affects the expression of both liver- and endothelium- derived components of thrombosis/fibrinolysis. These findings suggest that statins may be beneficial for patients with heart failure by depressing inflammatory response and affecting the thrombosis/fibrinolysis system.