Combining Rosuvastatin with Sartans of Different Peroxisome Proliferator-Activated Receptor-gamma Activating Capacity Is Not Associated with Different Changes in Low-Density Lipoprotein Subfractions and Plasma Lipoprotein-Associated Phospholipase A(2)

 
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Combining Rosuvastatin with Sartans of Different Peroxisome Proliferator-Activated Receptor-gamma Activating Capacity Is Not Associated with Different Changes in Low-Density Lipoprotein Subfractions and Plasma Lipoprotein-Associated Phospholipase A(2) (EN)

Rizos, C. V. (EN)

Πανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Χημείας (EL)
Rizos, C. V. (EN)

Background: Rosuvastatin reduces low-density lipoprotein cholesterol (LDL-C) and plasma lipoprotein-associated phospholipase A(2) (Lp-PLA(2)). Some sartans partially activate peroxisome proliferator-activated receptor-g (PPAR gamma), possibly having a favorable effect on metabolic parameters. Telmisartan is the most potent partial PPAR gamma activator, followed by irbesartan, whereas olmesartan does not hold such capacity. In an open-label randomized study, we assessed the effects of combining sartans of different PPAR gamma-activating capacity with rosuvastatin on LDL subfractions and plasma Lp-PLA(2) in patients with mixed dyslipidemia, hypertension, and prediabetes. Methods: Following dietary intervention, patients were allocated randomly to rosuvastatin (10 mg/day) plus telmisartan 80 mg/day (RT group, n - 52) or irbesartan 300 mg/day (RI group, n - 48) or olmesartan 20 mg/day (RO group, n - 51). After 6 months of treatment, changes in LDL subfraction cholesterol and plasma Lp-PLA(2) activity and mass were evaluated blindly. Results: A total of 151 patients (73 male; mean age 60 years) were included. Large LDL-C decreased in the RT (-36%), RI (-39%), and RO (-41%) groups (P<0.001 for all vs. baseline). Small dense LDL-C decreased in the RT (-67%), RI (-58%), and RO (-61%) groups (P<0.001 for all vs. baseline). All regimens increased LDL particle size versus baseline (RT+1.4%, P = 0.002; RI+1.0%, P = 0.04; and RO+1.4%, P = 0.001). No difference for the change of LDL subfractions and LDL size was noticed among groups. Plasma Lp-PLA(2) activity decreased equally in all groups (RT -38%, RI -38%, RO -43%) (P<0.001 for all vs. baseline). Plasma Lp-PLA(2) mass decreased similarly in all groups versus baseline (RT -28%, P = 0.001; RI -32%, P = 0.01; and RO -27%, P = 0.001). No difference for the change of Lp-PLA(2) mass or activity was noticed among groups. Conclusions: The combination of rosuvastatin with sartans of different PPAR gamma-activating capacity did not differentiate alterations of LDL subfraction cholesterol and plasma Lp-PLA(2) activity and mass. (EN)

coronary-heart-disease (EN)

Πανεπιστήμιο Ιωαννίνων (EL)
University of Ioannina (EN)

Metabolic Syndrome and Related Disorders (EN)

2011

<Go to ISI>://000291001200009



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