title: Statin treatment decreased serum asymmetric dimethylarginine (ADMA) levels in ischemic stroke patients.
abstract: OBJECTIVE
  It remains unclear whether the decrease in the ADMA level associated with statin treatment results from the LDL-C-lowering effect or the pleiotropic effects of statins. A prospective, controlled study was conducted to examine whether statin treatment affects serum ADMA concentrations in ischemic stroke patients.
  
  
  METHODS
  Consecutive outpatients with non-cardiogenic ischemic stroke who had never been treated with statins and whose LDL-cholesterol level was higher than 140 mg/dL were enrolled and compared with control patients whose LDL-cholesterol level was lower than 140 mg/dL. Overall, 114 patients were enrolled in the study (56 and 58 in statin-treated and non-statin-treated groups, respectively). Patients in the statin group were treated with pravastatin 10 mg/day (n=15), fluvastatin 20 mg/day (n=14), pitavastatin 1 mg/day (n=14), or atorvastatin 10 mg/day (n=13).
  
  
  RESULTS
  The serum ADMA concentration and LDL-C level were significantly decreased by statin treatment (p=0.003 and p< 0.001, respectively), and the ADMA concentration in subjects treated with statins was significantly lower than that of the control (p=0.028). Multiple linear regression analysis showed that age (β=0.26, p< 0.05) and statin use (β=-0.20, p< 0.05) were independently associated with the ADMA level.
  
  
  CONCLUSIONS
  A significant relation between statin treatment and decreased levels of ADMA was demonstrated in ischemic stroke patients with an adequately controlled lipid profile, suggesting the statin treatment might prevent atherosclerotic disease in ischemic stroke patients through suppression of ADMA concentration.
authors.affiliation: Division of Neurology, Nephrology and Rheumatology, Department of Internal Medicine, Nippon Medical School, Bunkyo-ku, Tokyo, Japan. nomo@nms.ac.jp
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Nishiyama
authors.forename: Masayuki
authors.initials: M
authors.lastname: Ueda
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Otsuka
authors.forename: Ken-ichiro
authors.initials: K
authors.lastname: Katsura
authors.forename: Arata
authors.initials: A
authors.lastname: Abe
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nagayama
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Katayama
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood; D050197:Atherosclerosis / Q000517:prevention & control; D000069059:Atorvastatin; D002545:Brain Ischemia / Q000097:blood* / Q000188:drug therapy*; D008078:Cholesterol, LDL / Q000097:blood; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology; D005260:Female; D000077340:Fluvastatin; D006538:Heptanoic Acids / Q000494:pharmacology; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology*; D007211:Indoles / Q000494:pharmacology; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D017035:Pravastatin / Q000494:pharmacology; D011446:Prospective Studies; D011758:Pyrroles / Q000494:pharmacology; D011804:Quinolines / Q000494:pharmacology; D020521:Stroke / Q000097:blood* / Q000188:drug therapy*
chemical_list: D008078:Cholesterol, LDL; D005229:Fatty Acids, Monounsaturated; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D011758:Pyrroles; D011804:Quinolines; D000077340:Fluvastatin; C018524:N,N-dimethylarginine; D001120:Arginine; D000069059:Atorvastatin; D017035:Pravastatin; C108475:pitavastatin