Statin and fibrate treatment of combined hyperlipidemia: the effects on some novel risk factors

Miran Šebeštjen; Irena Keber; Branka Žegura; Saša Simčič; Mojca Božič; Martine Migaud Fressart; Mojca Stegnar

doi:10.1160/TH03-04-0250

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 2004; 92(05): 1129-1135
DOI: 10.1160/TH03-04-0250

Cell Signalling and Vessel Remodelling

Schattauer GmbH

Statin and fibrate treatment of combined hyperlipidemia: the effects on some novel risk factors

Miran Šebeštjen

¹University Clinical Centre, Department of Angiology, Ljubljana, Slovenia

,

Irena Keber

¹University Clinical Centre, Department of Angiology, Ljubljana, Slovenia

,

Branka Žegura

¹University Clinical Centre, Department of Angiology, Ljubljana, Slovenia

,

Saša Simčič

²Institute of Microbiology and Immunology, Medical Faculty, Ljubljana, Slovenia

,

Mojca Božič

¹University Clinical Centre, Department of Angiology, Ljubljana, Slovenia

,

Martine Migaud Fressart

³Diagnostica Stago, Asnières, France

,

Mojca Stegnar

¹University Clinical Centre, Department of Angiology, Ljubljana, Slovenia

› Author Affiliations

Abstract

Summary

The effects of cerivastatin and fenofibrate on proteins involved in haemostasis and on markers of inflammation were investigated in otherwise healthy middle-aged males with combined hyperlipidemia. Besides classical risk factors, other so-called novel risk factors for coronary artery disease are seen to be playing an increasingly important role in the development and progression of atherosclerosis. Thirty-eight males, aged 49 ± 5 years were randomised to 12 weeks treatment either with cerivastatin at a daily dose of 0.2 mg to 0.4 mg to achieve the LDL cholesterol goal of <3.0 mM, or with fenofibrate 250 mg daily. Fasting serum lipids, homocysteine, total and free tissue factor pathway inhibitor (TFPI), plasminogen activator inhibitor (PAI-1) and tissue plasminogen activator (t-PA) antigen and activity, C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured. No change in homocysteine level was observed in the cerivastatin group, while after fenofibrate administration it increased (p <0.0001).Total TFPI decreased significantly after cerivastatin (p = 0.002), but not after fenofibrate. Free TFPI did not decrease after either drug. Neither drug affected (t-PA) antigen and activity, while fenofibrate increased PAI-1 antigen (p <0.05) and activity (p <0.05). Cerivastatin decreased serum CRP values by 49.5% (p = 0.001), and fenofibrate by 29.8% (p = 0.03). The decreases of CRP in the two groups differed significantly (p = 0.04). IL-6 levels decreased significantly in the fenofibrate group (39%; p <0.0001), but not in the cerivastatin group (15%; p = 0.24) No significant decreases were observed for TNF-α. Cerivastatin had neutral effects on fibrinolysis, homocysteine or coagulation. On the other hand, fenofibrate increased PAI-1 antigen and activity and homocysteine, and did not affect coagulation. Both cerivastatin and fenofibrate reduced CRP levels, the decrease being significantly greater after cerivastatin. Fenofibrate also significantly decreased IL-6.

Keywords

Novel risk factors - fenofibrate - cerivastatin

Full Text

References

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