Arteriosclerosis, thrombosis, and vascular biology
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Arterioscler. Thromb. Vasc. Biol. · Nov 2010
Genetic variants influencing circulating lipid levels and risk of coronary artery disease.
Genetic studies might provide new insights into the biological mechanisms underlying lipid metabolism and risk of CAD. We therefore conducted a genome-wide association study to identify novel genetic determinants of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides. ⋯ We have identified 4 novel loci associated with circulating lipids. We also show that in addition to those that are largely associated with LDL-C, genetic loci mainly associated with circulating triglycerides and HDL-C are also associated with risk of CAD. These findings potentially provide new insights into the biological mechanisms underlying lipid metabolism and CAD risk.
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Arterioscler. Thromb. Vasc. Biol. · Nov 2010
The risk of deep venous thrombosis associated with injectable depot-medroxyprogesterone acetate contraceptives or a levonorgestrel intrauterine device.
To assess the risk of venous thrombosis associated with nonoral contraceptives (ie, injectable depot-medroxyprogesterone acetate contraceptives, hormone [levonorgestrel]-releasing intrauterine devices, a contraceptive patch, or a contraceptive implant). ⋯ The risk of venous thrombosis was increased for injectable depot-medroxyprogesterone acetate contraceptive users, while we were able to reliably exclude an increased risk associated with levonorgestrel intrauterine device use. Therefore, the latter seems to be the safest option regarding the risk of venous thrombosis.
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Arterioscler. Thromb. Vasc. Biol. · Nov 2010
SCH 602539, a protease-activated receptor-1 antagonist, inhibits thrombosis alone and in combination with cangrelor in a Folts model of arterial thrombosis in cynomolgus monkeys.
To determine the antithrombotic effects of SCH 602539, an analog of the selective protease-activated receptor (PAR)-1 antagonist vorapaxar (formerly SCH 530348) currently in advanced clinical development, and the P2Y(12) ADP receptor antagonist cangrelor, alone and in combination. ⋯ The combined inhibition of the PAR-1 and the P2Y(12) ADP platelet activation pathways had synergistic antithrombotic and antiplatelet effects. The addition of a PAR-1 antagonist to a P2Y(12) ADP receptor antagonist may provide incremental clinical benefits in patients with atherothrombotic disease, both in short- and long-term settings. These hypotheses need to be tested clinically.