PMID- 24429804
OWN - NLM
STAT- MEDLINE
DCOM- 20150813
LR  - 20161026
IS  - 1827-191X (Electronic)
IS  - 0021-9509 (Linking)
VI  - 56
IP  - 3
DP  - 2015 Jun
TI  - Reduced visfatin levels in aortic stenosis increase after aortic valve 
      replacement and may contribute to reverse left ventricular remodelling.
PG  - 483-92
AB  - AIM: 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. CONCLUSION: 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.
FAU - Majak, P
AU  - Majak P
AD  - Department of Cardiothoracic Surgery, Oslo University Hospital, Ulleval, Oslo, 
      Norway - uxbjjb@ous-hf.no.
FAU - Lunde, I G
AU  - Lunde IG
FAU - Hasic, A K
AU  - Hasic AK
FAU - Husebye, T
AU  - Husebye T
FAU - Christensen, G
AU  - Christensen G
FAU - Tonnessen, T
AU  - Tonnessen T
FAU - Bjornstad, J L
AU  - Bjornstad JL
LA  - eng
PT  - Clinical Trial
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20140116
PL  - Italy
TA  - J Cardiovasc Surg (Torino)
JT  - The Journal of cardiovascular surgery
JID - 0066127
RN  - 0 (Biomarkers)
RN  - 0 (Cytokines)
RN  - EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase)
RN  - EC 2.4.2.12 (nicotinamide phosphoribosyltransferase, human)
RN  - EC 2.4.2.12 (nicotinamide phosphoribosyltransferase, mouse)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Animals
MH  - Aortic Valve/physiopathology/*surgery
MH  - Aortic Valve Stenosis/blood/complications/physiopathology/*surgery
MH  - Biomarkers/blood
MH  - Case-Control Studies
MH  - Cytokines/*blood
MH  - Disease Models, Animal
MH  - Female
MH  - *Heart Valve Prosthesis Implantation
MH  - Humans
MH  - Hypertrophy, Left Ventricular/blood/*etiology/physiopathology
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Myocardium/*metabolism
MH  - Nicotinamide Phosphoribosyltransferase/*blood
MH  - Prospective Studies
MH  - Time Factors
MH  - *Ventricular Function, Left
MH  - Ventricular Remodeling
EDAT- 2014/01/17 06:00
MHDA- 2015/08/14 06:00
CRDT- 2014/01/17 06:00
PHST- 2014/01/17 06:00 [entrez]
PHST- 2014/01/17 06:00 [pubmed]
PHST- 2015/08/14 06:00 [medline]
AID - R37Y9999N00A140153 [pii]
PST - ppublish
SO  - J Cardiovasc Surg (Torino). 2015 Jun;56(3):483-92. Epub 2014 Jan 16.