Statins and blood coagulation.
The 3-hydroxy-3-methylglutaryl (HMG)-coenzyme A (CoA) reductase inhibitors (statins) have been shown to exhibit several vascular protective effects, including antithrombotic properties, that are not related to changes in lipid profile. There is growing evidence that treatment with statins can lead to a significant downregulation of the blood coagulation cascade, most probably as a result of decreased tissue factor expression, which leads to reduced thrombin generation. Accordingly, statin use has been associated with impairment of several coagulant reactions catalyzed by this enzyme. Moreover, evidence indicates that statins, via increased thrombomodulin expression on endothelial cells, may enhance the activity of the protein C anticoagulant pathway. Most of the antithrombotic effects of statins are attributed to the inhibition of isoprenylation of signaling proteins. These novel properties of statins, suggesting that these drugs might act as mild anticoagulants, may explain, at least in part, the therapeutic benefits observed in a wide spectrum of patients with varying cholesterol levels, including subjects with acute coronary events. The HMG-CoA reductase inhibitors (statins) have been shown to exhibit several vascular protective effects, including antithrombotic properties, that are not related to changes in lipid profile. Treatment with statins can lead to a significant downregulation of the blood coagulation cascade, most probably as a result of decreased tissue factor expression, which leads to reduced thrombin generation.
Undas
Anetta
A
Department of Medicine, Jagiellonian University School of Medicine, Krakow, Poland.
Brummel-Ziedins
Kathleen E
KE
Mann
Kenneth G
KG
D000818:Animals; D000924:Anticholesteremic Agents / Q000494:pharmacology / Q000627:therapeutic use; D000925:Anticoagulants / Q000494:pharmacology / Q000627:therapeutic use; D001161:Arteriosclerosis / Q000097:blood; D001777:Blood Coagulation / Q000187:drug effects*; D001779:Blood Coagulation Factors / Q000378:metabolism; D001798:Blood Proteins / Q000378:metabolism; D005167:Factor VII / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D008954:Models, Biological; D017368:Protein Prenylation / Q000187:drug effects; D011499:Protein Processing, Post-Translational / Q000187:drug effects*; D013205:Staphylococcal Protein A / Q000378:metabolism; D013917:Thrombin / Q000096:biosynthesis; D018180:Thrombomodulin / Q000096:biosynthesis; D019851:Thrombophilia / Q000188:drug therapy / Q000517:prevention & control*; D013925:Thromboplastin / Q000096:biosynthesis; D020246:Venous Thrombosis / Q000188:drug therapy / Q000517:prevention & control
D000924:Anticholesteremic Agents; D000925:Anticoagulants; D001779:Blood Coagulation Factors; D001798:Blood Proteins; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D013205:Staphylococcal Protein A; D018180:Thrombomodulin; D005167:Factor VII; D005340:Fibrinogen; D013925:Thromboplastin; D013917:Thrombin