Key result
Simvastatin 40 mg/day significantly shortened clot lysis time by 11.2% and increased clot permeability by 4.4% in subjects with LDL cholesterol below 3.4 mmol/l.
Why the study?
Does simvastatin improve ex vivo plasma fibrin clot permeability and clot lysis time in subjects with LDL cholesterol <3.4 mmol/l?
Does simvastatin improve ex vivo plasma fibrin clot permeability and clot lysis time in subjects with LDL cholesterol <3.4 mmol/l?
Mean Difference: 12.9 (95% CI 10.3–15.5)
Absolute Event Rate: 102.6% vs 115.5%
p-value: p=<0.001
Simvastatin improves fibrin clot permeability and susceptibility to lysis in low-risk patients with average LDL cholesterol, suggesting an antithrombotic pleiotropic effect linked to its anti-inflammatory properties.
Should not yet change practice in low-risk patients; leaves open whether pleiotropic effects on clot properties reduce clinical thrombosis risk.
INTRODUCTION: Statins produce additional beneficial effects, including attenuation of prothrombotic mechanisms. In patients at high cardiovascular risk, who have markedly elevated low-density lipoprotein (LDL) cholesterol levels, simvastatin can reduce thrombin generation. Moreover, we have described simvastatin-induced improvement of fibrin clot properties, the formation of which represents the final step of blood coagulation. OBJECTIVES: The aim of the present study was to assess the effect of simvastatin on fibrin features observed in subjects with LDL cholesterol <3.4 mmol/l. PATIENTS AND METHODS: Thirty subjects (24M, 6F) aged <70 years with LDL cholesterol <3.4 mmol/l with no history of cardiovascular events were enrolled in the study. Patients were excluded if they had diabetes mellitus, chronic inflammatory diseases and renal insufficiency. Prior to and following a 3-month treatment with simvastatin (40 mg/d), ex vivo plasma fibrin clot permeability and efficiency of clot lysis were measured. RESULTS: Simvastatin led to a significant decrease in total cholesterol, LDL cholesterol, triglycerides and C-reactive protein (CRP), while fibrinogen levels remained unaltered. There were posttreatment increase in clot permeability by 4.4% (p<0.001) and shortening of clot lysis by 11.2% (p<0.001) compared to pretreatment values. These changes were correlated with reduction in CRP following simvastatin. Simvastatin-induced increase in clot permeability was associated only with age and decrease in CRP levels (R2 for the model = 0.61), while shortening of clot lysis time observed following simvastatin use was predicted only by reduction of triglycerides and CRP (R2 for the model = 0.62). CONCLUSIONS: Simvastatin exerts unique properties involving enhanced fibrin clot lysis and increased clot permeability in subjects with LDL cholesterol <3.4 mmol/l, which is associated with its anti-inflammatory effects. Altered fibrin clot function might contribute to clinical benefits of statins.
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Undas et al. (2009) studied LDL cholesterol <3.4 mmol/l without cardiovascular events (n=30). Simvastatin vs. Baseline (pretreatment) was evaluated on Clot lysis time (minutes) (MD 12.9, 95% CI 10.3-15.5, p=<0.001). Simvastatin 40 mg/day significantly shortened clot lysis time by 11.2% and increased clot permeability by 4.4% in subjects with LDL cholesterol below 3.4 mmol/l.
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