title: Effects of pitavastatin on pressure overload-induced heart failure in mice.
abstract: BACKGROUND
  3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), which are widely used to lower plasma cholesterol levels, have been reported to have various pleiotropic effects such as protective effect of endothelial cells, angiogenic effect, antioxidant effect and anti-inflammatory effect. It is unclear, however, whether statins have any effects on the progression from left ventricular (LV) hypertrophy to heart failure in the established hypertrophied heart.
  
  
  RESULTS
  C57BL/6 mice were treated with pitavastatin (pitava) or vehicle (control) from 2 weeks (established hypertrophy stage) after transverse aortic constriction (TAC) and the treatment was continued for 4 weeks. Pitavastatin significantly inhibited the progression from LV hypertrophy to heart failure as assessed on echocardiography. The cardiomyocyte cross-sectional area was significantly increased in the control group compared to the sham-operated mice (sham group), but it was not significantly different between the control group and the pitava group at 6 weeks after TAC. Moreover, pitavastatin induced myocardial angiogenesis (ratio of number of endothelial cells to cardiomyocytes) and decreased the myocardial fibrosis and oxidative stress. The expression of angiopoietin-1 in the heart was significantly increased by pitavastatin at 6 weeks after TAC.
  
  
  CONCLUSIONS
  Pitavastatin has preventive effects on the progression of heart failure even in the hypertrophied heart.
authors.affiliation: Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, Chiba, Japan.
authors.forename: Yoshihito
authors.initials: Y
authors.lastname: Kameda
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Hasegawa
authors.forename: Akihiko
authors.initials: A
authors.lastname: Kubota
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Tadokoro
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Kobayashi
authors.forename: Issei
authors.initials: I
authors.lastname: Komuro
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Takano
mesh_terms: D042683:Angiopoietin-1 / Q000096:biosynthesis; D000818:Animals; D001794:Blood Pressure; D005355:Fibrosis / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D005786:Gene Expression Regulation / Q000187:drug effects; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology*; D017379:Hypertrophy, Left Ventricular / Q000150:complications / Q000378:metabolism / Q000473:pathology; D051379:Mice; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D018384:Oxidative Stress / Q000187:drug effects; D011804:Quinolines / Q000493:pharmacokinetics*; D013997:Time Factors
chemical_list: D042683:Angiopoietin-1; C467628:Angpt1 protein, mouse; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011804:Quinolines; C108475:pitavastatin