Objective-Lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ) is a predictor for incident atherosclerotic disease. We investigated the effect of 3 hypolipidemic drugs that exert their action through different mechanisms on plasma and lipoprotein-associated Lp-PLA 2 activity and mass. Methods and Results-In 50 patients with Type IIA dyslipidemia were administered rosuvastatin (10 mg daily), whereas in 50 Type IIA dyslipidemic patients exhibiting intolerance to previous statin therapy were administered ezetimibe as monotherapy (10 mg daily). Fifty patients with Type IV dyslipidemia were given micronised fenofibrate (200 mg daily). Low-and high-density lipoprotein (LDL and HDL, respectively) subclass analysis was performed electrophoretically, whereas lipoprotein subfractions were isolated by ultracentrifugation. Ezetimibe reduced plasma Lp-PLA 2 activity and mass attributable to the reduction in plasma levels of all LDL subfractions. Rosuvastatin reduced enzyme activity and mass because of the decrease in plasma levels of all LDL subfractions and especially the Lp-PLA 2 on dense LDL subfraction (LDL-5 Key Words: hyperlipidemia Ⅲ lipoproteins Ⅲ PAF-acetylhydrolase Ⅲ Lp-PLA 2 Ⅲ ezetimibe Ⅲ fenofibrate Ⅲ rosuvastatin P latelet-activating factor (PAF) acetylhydrolase exhibits a Ca 2ϩ -independent phospholipase A 2 activity and degrades PAF and oxidized phospholipids by catalyzing the hydrolysis of the ester bond at the sn-2 position. 1 PAF-acetylhydrolase in plasma is complexed to lipoproteins 2 ; thus it is also referred as lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ). 3 Lp-PLA 2 is associated mainly with apolipoprotein B (apoB)-containing lipoproteins and primarily with low-density lipoprotein (LDL), whereas a small proportion of circulating enzyme activity is also associated with high-density lipoprotein (HDL). 1,2 ⌻he majority of the LDL-associated Lp-PLA 2 activity is bound to the atherogenic small-dense LDL (sdLDL) particles, 2,4,5 and we recently showed that the enzyme activity is a marker of sdLDL particles in plasma. 6 Lp-PLA 2 is principally produced by hematopoietic cells including monocytes-macrophages. 7,8 Lp-PLA 2 has been identified in atherosclerotic plaques 9 ; however, its role in atherosclerosis is still under investigation. In this regard, it is suggested that this enzyme might have an antiinflammatory role because it degrades and inactivates proinflammatory PAF and oxidized phospholipids 10,11 ; other studies showed that Lp-PLA 2 may have a proinflammatory and proatherogenic role 12 because it generates lysophosphatidylcholine (lysoPC) 3,13 and bioactive oxidized fatty residues. 3 Data from large White population studies demonstrated an independent association between plasma Lp-PLA 2 with cardiovascular disease (CVD) risk. In this regard a recent metaanalysis showed that Lp-PLA 2 is significantly associated with CVD, and the risk estimate appears to be relatively unaffected by adjustment for conventional CVD risk factors. 14 In contrast to total plasma enzyme, which mainly represents ...

The hypertriglyceridemic waist (HTGW) phenotype (hypertriglyceridemia and increased waist circumference) has been proposed as an inexpensive tool to monitor individuals with the atherogenic metabolic triad, hyperinsulinemia, hyperapobetalipoproteinemia, and increased levels of small, dense LDL (sdLDL) particles. We assessed the association of the HTGW phenotype with the metabolic syndrome (MetSyn) and the atherogenic metabolic triad in inhabitants (n = 260) of northwestern Greece attending the Outpatient Lipid Clinic of the University Hospital of Ioannina. The LDL subfractions were assessed using the Lipoprint LDL System. HTGW (+) individuals had a more adverse lipid and lipoprotein profile compared with HTGW (-) individuals. Moreover, HTGW (+) subjects had elevated levels of sdLDL-C, as well as decreased mean and peak LDL particle size compared with HTGW (-) subjects. To our knowledge, this is the first report documenting the sdLDL-C abnormality in HTGW (+) subjects. Among men (n = 105), 52.3% of the MetSyn (+) individuals and 66.7% of the HTGW (+) individuals had the metabolic triad. Among women (n = 155), the corresponding percentages were 42.3% and 50.0%. Only 22.2% and 10.6% of the MetSyn (-) subjects (men and women, respectively) and 19.6% and 15.2% of the HTGW (-) subjects (men and women, respectively) had the atherogenic metabolic triad. In conclusion, the HTGW (+) phenotype is associated with a hostile lipid profile that includes higher levels of sdLDL-C and decreased LDL particle size. The HTGW phenotype, compared with the MetSyn criteria, can provide an easy and inexpensive tool to monitor patients characterized by an adverse lipid and lipoprotein profile.

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Concerns have been raised because of observations of proteinuria associated with rosuvastatin treatment. In this open-label study, a potential dose-dependent effect was investigated of rosuvastatin on urinary protein excretion and renal function parameters in 90 hyperlipidemic patients randomly assigned to rosuvastatin 10 mg/day (n = 45) or 20 mg/day (n = 45). Urinary samples were collected from patients and 40 age- and gender-matched controls to determine electrolyte, uric acid, creatinine, and protein (total, albumin, IgG, and alpha1-microglobulin) levels at baseline and after 12 weeks. A dose-dependent increase in the excretion of alpha1-microglobulin (17.6% in rosuvastatin 10 vs 34.9% in rosuvastatin, 20 mg/day; P = .03 for the comparison between groups) was observed. A trend toward an increase in the estimated glomerular filtration rate was noted in only patients receiving 20 mg/day of rosuvastatin. These findings indicate that rosuvastatin treatment increases the urinary excretion of alpha1-microglobulin urinary excretion in a dose-dependent manner without adversely affecting renal function.

Background: The Friedewald formula (LDL-F) for the estimation of low-density lipoprotein (LDL) cholesterol concentrations is the most often used formula in clinical trials and clinical practice. However, much concern has been raised as to whether this formula is applicable in all patient populations such as the presence of chylomicronaemia and/or hypertriglyceridaemia. The aim of the present study was to evaluate various LDL cholesterol calculation formulas as well as LDL cholesterol levels provided by the Lipoprint LDL System (LDL-L) in patients with the metabolic syndrome (MetSyn).

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