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Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:259-265

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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:259.)
© 2000 American Heart Association, Inc.


Thrombosis

Effect of {omega}-3 Fatty Acids and Simvastatin on Hemostatic Risk Factors and Postprandial Hyperlipemia in Patients With Combined Hyperlipemia

Arne Nordøy; Kaare H. Bønaa; Per Morten Sandset; John-Bjarne Hansen; Hugo Nilsen

From the Department of Medicine (A.N., J.-B.H., H.N.), Institute of Clinical Medicine, and the Institute of Community Medicine (K.H.B.), University of Tromsø, Tromsø, Norway, and the Department of Medicine (P.M.S.), Ullevål Hospital, University of Oslo, Oslo, Norway.

Correspondence to Prof A. Nordøy, Department of Medicine, University Hospital, 9038 Tromsø, Norway. E-mail medan{at}rito.no

Abstract—Patients with combined hyperlipemia have lipid abnormalities associated with an increased tendency to develop atherosclerosis and thrombosis. This tendency may be accelerated during postprandial hyperlipemia. In the present double-blind parallel study, 41 patients with combined hyperlipemia and serum triacylglycerols between 2.0 and 15.0 mmol/L and serum total cholesterol >5.3 mmol/L at the end of a 3-month dietary run-in period were treated with simvastatin at 20 mg/d for at least 10 weeks; patients were then randomized into 2 groups receiving simvastatin+{omega}-3 fatty acids at 3.36 g/d or placebo (corn oil) for an additional 5 weeks. Hemostatic variables that have been associated with increased thrombotic tendency were evaluated with subjects in the fasting state and during postprandial hyperlipemia before and after combined treatment. Supplementation of {omega}-3 fatty acid reduced tissue factor pathway inhibitor antigen (P<0.05) in the fasting state, reduced the degree of postprandial hyperlipemia (P<0.005), and reduced activated factor VII concentration appearing during postprandial hyperlipemia. In conclusion, {omega}-3 fatty acids given in addition to simvastatin to patients with combined hyperlipemia reduced the free tissue factor pathway inhibitor fraction in the fasting state and inhibited the activation of factor VII occurring during postprandial lipemia, thus representing a potential beneficial effect on the hemostatic risk profile in this patient group.


Key Words: combined hyperlipemia • postprandial hyperlipemia • hemostatic risk factors




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