title: Reduced visfatin levels in aortic stenosis increase after aortic valve replacement and may contribute to reverse left ventricular remodelling.
abstract: OBJECTIVE
  Visfatin may play a part in reverse left ventricular remodelling. Using a mouse model of reversible left ventricle pressure overload, we examined if visfatin was altered in the myocardium. Furthermore, we addressed this issue in patients with aortic stenosis (AS) and examined whether visfatin levels are related to reverse remodelling following aortic valve replacement (AVR).
  
  
  METHODS
  Myocardial visfatin was analysed after aortic banding (AB) and debanding (DB) in mice and compared to sham operated animals. Myocardial visfatin was measured in biopsies from patients undergoing AVR and compared to controls. Serum visfatin was measured before and after AVR in patients with AS and correlated with echocardiographic measurments of cardiac morphology and function.
  
  
  RESULTS
  Four weeks after AB, myocardial visfatin protein was reduced by 50% compared to sham. Three days after DB, myocardial protein levels increased significantly. Myocardial visfatin and serum visfatin levels were reduced by 23% and 64%, respectively, in patients with AS compared to controls. Twelve months after AVR, serum visfatin levels increased compared to preoperative values and correlated negatively with degree of left ventricular hypertrophy.
  
  
  CONCLUSIONS
  Myocardial visfatin and serum visfatin levels are reduced by cardiac pressure overload. Visfatin levels increase after correction of pressure overload and may play a part in postoperative reverse remodelling.
authors.affiliation: Department of Cardiothoracic Surgery, Oslo University Hospital, Ullevål, Oslo, Norway - uxbjjb@ous-hf.no.
authors.forename: P
authors.initials: P
authors.lastname: Majak
authors.forename: I G
authors.initials: IG
authors.lastname: Lunde
authors.forename: A K
authors.initials: AK
authors.lastname: Hasic
authors.forename: T
authors.initials: T
authors.lastname: Husebye
authors.forename: G
authors.initials: G
authors.lastname: Christensen
authors.forename: T
authors.initials: T
authors.lastname: Tønnessen
authors.forename: J L
authors.initials: JL
authors.lastname: Bjørnstad
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D001021:Aortic Valve / Q000503:physiopathology / Q000601:surgery*; D001024:Aortic Valve Stenosis / Q000097:blood / Q000150:complications / Q000503:physiopathology / Q000601:surgery*; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D016207:Cytokines / Q000097:blood*; D004195:Disease Models, Animal; D005260:Female; D019918:Heart Valve Prosthesis Implantation; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000378:metabolism*; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood*; D011446:Prospective Studies; D013997:Time Factors; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
chemical_list: D015415:Biomarkers; D016207:Cytokines; D054409:Nicotinamide Phosphoribosyltransferase; C085455:nicotinamide phosphoribosyltransferase, human; C495867:nicotinamide phosphoribosyltransferase, mouse