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Articles by Ngoc-Anh Le
Total Records ( 3 ) for Ngoc-Anh Le
  Jonathan R. Murrow , Salman Sher , Sarfraz Ali , Irina Uphoff , Riyaz Patel , Marcus Porkert , Ngoc-Anh Le , Dean Jones and Arshed A. Quyyumi


Atherogenic risk in subjects with metabolic syndrome is partly mediated by increased oxidative stress and subsequent endothelial dysfunction. Clinical trials have demonstrated differences in outcomes between subjects receiving lipophilic statins (atorvastatin) compared with hydrophilic statins (pravastatin). However, whether these findings are attributable to differences in the doses administered or to nonlipid-lowering pleiotropic effects of statins on oxidative stress and vascular function remains unknown. We hypothesized that equipotent doses of these two statins will have divergent effects on markers of oxidative stress and endothelial function.


Thirty-six subjects with hyperlipidemia and metabolic syndrome and/or diabetes were randomized in a double-blind manner to either pravastatin 80 mg or atorvastatin 10 mg daily. Oxidative stress (dROMs assay that measures lipid hydroperoxides, plasma thiobarbituric acid reactive substances [TBARS], and aminothiol levels) and brachial artery flow-mediated dilation (FMD) were measured at baseline and after 12 weeks of statin therapy.


Statin therapy reduced serum low-density lipoprotein cholesterol levels equally in both groups. Atorvastatin therapy was associated with a significant reduction in TBARS (P = .006) and dROMs levels (P = .02), which was not observed in subjects treated with pravastatin. Endothelial function improved with statin therapy (P = .02), but there was no difference between the statin groups.


In hyperlipidemic subjects with metabolic syndrome, atorvastatin is associated with a greater reduction in lipid markers of oxidation compared with pravastatin. Whether these effects are responsible for the outcome differences in trials comparing these agents needs further investigation.

  Ngoc-Anh Le , Monica Farkas-Epperson , Ran Jin , Andrew M. Tershakovec , David R. Neff , Robert Wolfert , Joanne E. Tomassini and Peter Wilson
  High levels of lipoprotein-associated phospholipase A2 (LpPLA2) are associated with increased risk of cardiovascular disease. LpPLA2 is an inflammatory enzyme marker and is less prone to effects of systemic infection as are other inflammatory markers such as C-reactive protein (hsCRP). In a previously reported study, co-administration of ezetimibe/simvastatin (E/S) 10/20 mg with extended-release niacin up to 2 g/day (N) reduced low-density lipoprotein cholesterol and increased high-density lipoprotein cholesterol levels significantly more than E/S and N alone in patients with type IIa/IIb hyperlipidemia (T2HLP) during 24 weeks.
  Ngoc-Anh Le , Ran Jin , Andrew M. Tershakovec , David R. Neff , Joanne E. Tomassini , James Otvos and Peter Wilson
  Intervention with concomitant high-density lipoprotein cholesterol (HDL-C)−raising and low-density lipoprotein cholesterol (LDL-C)−lowering therapies may be beneficial in reducing cardiovascular disease risk. The effects of these therapies on lipoprotein particle numbers have not been well-studied in patients with type II hyperlipidemia (T2HLP). Niacin is currently the most effective agent available for increasing HDL-C and also modestly reduces TG, Lp(a), and LDL-C. In numerous studies, ezetimibe/simvastatin (E/S) was shown to enhance LDL-C lowering and improve other lipids and hsCRP compared with statin therapy in hypercholesterolemic patients.
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