title: Atorvastatin improves left ventricular systolic function and serum markers of inflammation in nonischemic heart failure.
abstract: OBJECTIVE
  This study examined the effect of statin therapy on vascular markers of inflammation and echocardiographic findings in patients with nonischemic forms of cardiomyopathy.
  
  
  BACKGROUND
  Despite advances in therapy, morbidity and mortality from heart failure (HF) remain high. We wished to determine whether treatment with atorvastatin affects left ventricular (LV) systolic function and markers of inflammation in patients with nonischemic HF.
  
  
  METHODS
  A total of 108 patients with nonischemic HF and a left ventricular ejection fraction (LVEF) < or =35% were randomized to either atorvastatin 20 mg/day or placebo in a double-blinded fashion for a 12-month period. The LVEF and LV end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) were determined by echocardiography. Serum markers of inflammation and oxidation were also measured.
  
  
  RESULTS
  The LVEF increased from 0.33 +/- 0.05 to 0.37 +/- 0.04 (p = 0.01) in the atorvastatin group over the 12-month follow-up period, whereas those patients in the placebo group experienced a decline in ejection fraction during the same time period. In addition, LVEDD was reduced from 57.1 +/- 5.9 mm to 53.4 +/- 5.1 mm (p = 0.007) and LVESD was reduced from 42.4 +/- 3.8 mm to 39.1 +/- 3.8 mm (p = 0.02) in the cohort of patients treated with atorvastatin; these dimensions increased in the placebo group. There was an increase in erythrocyte superoxide dismutase (E-SOD) activity, and there were significant reductions in serum levels of high sensitivity C-reactive protein, interleukin-6 (IL-6), and tumor necrosis factor-alpha receptor II (TNF-alpha RII) in the atorvastatin group.
  
  
  CONCLUSIONS
  The use of atorvastatin in patients with nonischemic HF improves LVEF and attenuates adverse LV remodeling. The effects on soluble levels of several inflammatory markers with atorvastatin suggest, in part, mechanisms by which statins might exert their beneficial effects in nonischemic HF.
authors.affiliation: Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia 30303, USA.
authors.forename: Srikanth
authors.initials: S
authors.lastname: Sola
authors.forename: Muhammad Q S
authors.initials: MQ
authors.lastname: Mir
authors.forename: Stamatios
authors.initials: S
authors.lastname: Lerakis
authors.forename: Neeraj
authors.initials: N
authors.lastname: Tandon
authors.forename: Bobby V
authors.initials: BV
authors.lastname: Khan
mesh_terms: D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000032:analysis; D004311:Double-Blind Method; D004912:Erythrocytes / Q000201:enzymology; D005260:Female; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D006538:Heptanoic Acids / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D018836:Inflammation Mediators / Q000097:blood* / Q000502:physiology; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D011758:Pyrroles / Q000494:pharmacology* / Q000627:therapeutic use; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000097:blood; D013318:Stroke Volume / Q000187:drug effects; D013482:Superoxide Dismutase / Q000097:blood; D013599:Systole / Q000502:physiology; D014463:Ultrasonography; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D018836:Inflammation Mediators; D015850:Interleukin-6; D011758:Pyrroles; D047889:Receptors, Tumor Necrosis Factor, Type II; D002097:C-Reactive Protein; D000069059:Atorvastatin; D013482:Superoxide Dismutase