title: Long-term effect of atorvastatin on neurohumoral activation and cardiac function in patients with chronic heart failure: a prospective randomized controlled study.
abstract: BACKGROUND
  Statins have pleiotropic effects, such as improvement in endothelial function and antiinflammatory, antiproliferative, and antioxidative effects, that should be beneficial for patients with chronic heart failure (CHF). The aim of this study was to investigate the long-term effect of statins on neurohumoral activation and cardiac function in patients with CHF.
  
  
  METHODS
  We enrolled 38 outpatients with mild to moderate CHF and radionuclide left ventricular ejection fraction (LVEF) <40%. These patients were randomly assigned to receive atorvastatin (10 mg/d) or conventional treatment for heart failure and were prospectively followed up for at least 3 years. At entry, we measured plasma concentrations of brain natriuretic peptides (BNPs) and left ventricular end-diastolic dimension and LVEF by echocardiography; thereafter, these measurements were repeated at least every 6 months. The primary end point was defined as the improvement in cardiac function and BNP.
  
  
  RESULTS
  There were no significant differences in age, sex, New York Heart Association class, left ventricular end-diastolic dimension, LVEF, and serum cholesterol level at entry between patients with (n = 19) and without atorvastatin (control, n = 19). After a follow-up period of 31 +/- 14 months, BNP (median [25th, 75th percentile]) significantly decreased in the atorvastatin group (84 [36, 186] to 55 [37, 91] pg/mL, P = .02) but not in the control group. Left ventricular end-diastolic dimension significantly decreased (67.1 [59.9, 70.8] to 61.1 [58, 63.9] mm, P = .02), and LVEF also significantly increased in the atorvastatin group (33.3% +/- 7.4% to 39.1% +/- 12.1%, P = .01) but not in the control group.
  
  
  CONCLUSIONS
  Long-term atorvastatin therapy decreases neurohumoral activation and improves cardiac function in patients with mild to moderate CHF.
authors.affiliation: Division of Cardiology, Osaka General Medical Center, Sumiyoshi-ku, Osaka, Japan. takaymda@nike.eonet.ne.jp
authors.forename: Takahisa
authors.initials: T
authors.lastname: Yamada
authors.forename: Koichi
authors.initials: K
authors.lastname: Node
authors.forename: Takanao
authors.initials: T
authors.lastname: Mine
authors.forename: Takashi
authors.initials: T
authors.lastname: Morita
authors.forename: Hidetaka
authors.initials: H
authors.lastname: Kioka
authors.forename: Yasumasa
authors.initials: Y
authors.lastname: Tsukamoto
authors.forename: Shunsuke
authors.initials: S
authors.lastname: Tamaki
authors.forename: Masaharu
authors.initials: M
authors.lastname: Masuda
authors.forename: Keiji
authors.initials: K
authors.lastname: Okuda
authors.forename: Masatake
authors.initials: M
authors.lastname: Fukunami
mesh_terms: D000368:Aged; D000069059:Atorvastatin; D009320:Atrial Natriuretic Factor / Q000378:metabolism; D018572:Disease-Free Survival; D004452:Echocardiography; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology*; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000378:metabolism*; D011446:Prospective Studies; D011758:Pyrroles / Q000627:therapeutic use*; D013318:Stroke Volume; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*
chemical_list: D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D011758:Pyrroles; D020097:Natriuretic Peptide, Brain; D009320:Atrial Natriuretic Factor; D000069059:Atorvastatin