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Published on: November 10, 2017
Statins decrease thrombin generation in patients with hypercholesterolemia
Armando Tripodi1, Fabio Pellegatta2, Veena Chantarangkul1
1Angelo Bianchi Bonomi Hemophilia and Thrombosis Center, Department of Clinical Sciences and Community Health, Università degli Studi di Milano, IRCCS Cà Granda Ospedale Maggiore Foundation, Milano, Italy.
Insights
Statins significantly reduce thrombin generation in hypercholesterolemia patients, suggesting a direct link to coagulation beyond lipid lowering. This finding supports statins
Area of Science:
- Cardiovascular Medicine
- Hematology
- Pharmacology
Background:
- Statins are primarily known for cholesterol reduction.
- Emerging evidence suggests statins possess antithrombotic effects independent of lipid-lowering.
- Traditional coagulation tests have not adequately reflected statin-induced changes.
Purpose of the Study:
- To investigate the impact of statin therapy on thrombin generation in hypercholesterolemic patients.
- To assess if statins modify endogenous thrombin potential (ETP).
Main Methods:
- A study involving 51 hypercholesterolemic patients initiating statin treatment.
- Measurement of endogenous thrombin potential (ETP) before and two months after statin therapy.
Main Results:
- Statin treatment significantly reduced total cholesterol and increased HDL cholesterol.
- A significant decrease in median endogenous thrombin potential (ETP) was observed post-treatment (p<0.001).
Conclusions:
- Results support a direct association between statins and coagulation, specifically by lowering thrombin generation.
- The antithrombotic effects of statins may be partly mediated by reduced ETP.
- Further clinical trials are warranted to confirm this hypothesis.
Objective:
Statins are cholesterol-lowering agents with antithrombotic effect possibly unrelated to their lipid-lowering properties. Traditional global coagulation tests failed, however, to reveal clinically relevant change after treatment. We therefore sought to investigate whether statins were able to modify thrombin generation in hypercholesterolemia.
Methods:
Fifty-one patients who needed treatment with statins were enrolled in this study. Thrombin generation, assessed as endogenous thrombin potential (the amount of thrombin generated after triggering coagulation with small amount of tissue factor) was measured at pre- and two months post-treatment with statins.
Results:
The median (inter-quartile range) level of total cholesterol that was 325 mg/dL (278-405) decreased significantly [211 mg/dL (197-247)] at post-treatment (p<0.001); the median level of HDL cholesterol that was 49 mg/dL (43-56) increased significantly [55 mg/dL (47-66)] at post-treatment (p<0.001). The median endogenous thrombin potential (inter-quartile range) before treatment was 2372 nM·min (2008-2617) and decreased to 2,048 nM·min (1764-2375) (p<0.001) after treatment.
Conclusion:
The results support the hypothesis of a direct link between statins and coagulation through their capacity to lower thrombin generation in patients with hypercholesterolemia.
Practice Implications:
The antithrombotic properties of statins could be mediated (at least in part) by their endogenous thrombin potential lowering effect. This interesting hypothesis warrants evaluation by clinical trials.
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