title: Pitavastatin, an HMG-CoA reductase inhibitor, ameliorates endothelial function in chronic smokers.
abstract: BACKGROUND
  Smoking is a major cardiovascular risk factor, leading to endothelial dysfunction. The present study investigated the hypothesis that pitavastatin, an HMG-CoA reductase inhibitor, may improve endothelial function in chronic smokers via its antioxidant properties.
  
  
  RESULTS
  The 30 male chronic smokers who exhibited mild hypercholesterolemia at the time of physical check-up were enrolled and randomized to the pitavastatin group (2 mg/day, n=15) or the untreated control group (n=15). Before and after the 4-week treatment period, endothelium-dependent flow-mediated dilation (FMD) and endothelium-independent dilation by glyceryl trinitrate (GTD) were examined, and the FMD/GTD ratio was calculated. The pitavastatin group showed a significant restoration of endothelial function (percent change in FMD: +49.6% vs +1.4%; percent change in FMD/GTD ratio: +26.6% vs 4.5%, P<0.05 respectively), and a significant reduction in oxidative stress levels (malondialdehyde-low-density lipoprotein-cholesterol: 16.6% vs +7.5%; free radical activity: 1.8% vs +9.7%, P<0.05 respectively) compared with the control group. Pitavastatin had no effect on the number of circulating CD34(+)CD133(+) progenitor cells, endothelial progenitor cells, or the MMP-2, MMP-9 and VEGF levels. In vitro oxidative stress monitoring assay revealed that pitavastatin protected endothelial cells against oxidative stress.
  
  
  CONCLUSIONS
  Pitavastatin restores endothelial function, even in chronic smokers, possibly through its antioxidative properties. (Circ J 2010; 74: 195 - 202).
authors.affiliation: Department of Cardiology, Nagoya University Graduate School of Medicine, Japan.
authors.forename: Osamu
authors.initials: O
authors.lastname: Yoshida
authors.forename: Takahisa
authors.initials: T
authors.lastname: Kondo
authors.forename: Yasuko
authors.initials: Y
authors.lastname: Kureishi-Bando
authors.forename: Tomonori
authors.initials: T
authors.lastname: Sugiura
authors.forename: Kengo
authors.initials: K
authors.lastname: Maeda
authors.forename: Kenji
authors.initials: K
authors.lastname: Okumura
authors.forename: Toyoaki
authors.initials: T
authors.lastname: Murohara
mesh_terms: D000328:Adult; D002465:Cell Movement / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002784:Cholesterol / Q000097:blood; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology*; D005609:Free Radicals / Q000097:blood; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology*; D008297:Male; D019255:NADPH Oxidases / Q000037:antagonists & inhibitors; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D011804:Quinolines / Q000494:pharmacology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D012907:Smoking / Q000097:blood / Q000503:physiopathology*; D013234:Stem Cells / Q000166:cytology / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D005609:Free Radicals; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011804:Quinolines; D017382:Reactive Oxygen Species; D002784:Cholesterol; D052250:Nitric Oxide Synthase Type III; D019255:NADPH Oxidases; C108475:pitavastatin