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Fluvastatin and low-density lipoprotein oxidation in hypercholar disease in these patients [1, 2]. Genetic predisposition, lesterolemic renal transplant patients.immunosuppression with azathioprine, steroids, cyclospo-Background. Hyperlipidemia contributes to the development

To assess the antioxidative effect of the non-alcoholic components of wine, human low-density lipoprotein (LDL) was oxidized in vitro by copper ions in the presence of polyphenolic extracts from three wines:  standard red wine (R), standard white wine (W1), and white wine the must of which had been in contact with grape solids during 8 h before fermentation (W2). Lipoprotein peroxidation was monitored as the formation of conjugated dienes, of thiobarbituric acid reactive substances (TBARS), and fluorescent substances. At equal volume-of-extract additions to LDL, the lag phase of diene production increased proportionally with the polyphenol concentration of each extract. By the addition of equal phenolic substance concentration (8 μmol of gallic acid equiv/L) the timing of lag phase was 410 ± 8, 442 ± 11, and 516 ± 37 min for W1, R, and W2 respectively compared to 78 ± 6 min for control LDL without added extract. At 9 h of incubation, TBARS and fluorescence production were drastically inhibited by W1 but completely inhibited by R and W2. At 24 h of oxidation only fluorescence was still inhibited. The results indicate that the polyphenols contained in wines could inhibit protein derivatization but only delay lipid peroxidation and that the type, as well as the concentrations, of polyphenols of the different wines have varying protective effects. The wine-making process that includes the pre-incubation of the must with the grape skin prior to and during fermentation (red and certain white wines) was the most effective in preventing LDL oxidation in vitro. Keywords: Wine extracts; polyphenols; lipoprotein peroxidation; atherosclerosis

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Isolated low high-density lipoprotein cholesterol (HDLc) is a well-known risk factor for cardiovascular disease and is associated with arterial endothelium dysfunction. Several studies have shown that cholesterol lowering in patients with hypercholesterolemia improves endothelial function, but the effect of treating low HDLc levels remains unknown. We studied the effect of increasing HDLc on endothelial function in patients with coronary artery disease (CAD) and isolated low HDLc (HDLc) <0.91 mM, low-density lipoprotein cholesterol (LDLc) <4.1 mM, and triglycerides <2.8 mM. Flow-mediated endothelium-dependent dilatation (FMD) in response to reactive hyperemia was measured by brachial ultrasound, before and after bezafibrate treatment (400 mg daily for 6 months) in 16 patients with CAD and impaired FMD (<10%). After bezafibrate therapy, HDLc increased from 0.79-1.0 mM (p = 0.0008) at the expense of both HDL2 and HDL3 subfractions, apolipoprotein A-I increased from 1.04-1.19 g/l (p = 0.0012), and fibrinogen decreased from 4.45-3.39 g/l (p = 0.0007). The impaired FMD increased after bezafibrate treatment from a median of 2.5-12.3% (p = 0.0004). Endothelial function was normalized in eight patients (50%), improved in four (25%), and did not change in four (25%). These observations indicate that in patients with isolated low HDLc and CAD, bezafibrate treatment improves endothelial function of brachial arteries, increases HDLc and apolipoprotein A-I, and lowers fibrinogen concentrations.