title: Age-related differences in the pathogenesis of calcific aortic stenosis: the potential role of resistin.
abstract: BACKGROUND
  Aortic stenosis (AS) is considered as an atherosclerotic related process. However, there are uncertainties whether AS in the elderly is associated with the same pathophysiological processes as in younger patients. We hypothesized that the metabolic determinants of the valvular inflammatory and calcifying processes occurring in elderly patients are different from those observed earlier in life.
  
  
  METHODS
  Among 114 patients operated for a severe AS, a complete plasma lipid blood profile and plasma levels of adipokines (resistin, leptin) were determined. The calcium content of the aortic valve was measured and valvular inflammation was quantified.
  
  
  RESULTS
  Elderly patients (>or=70 years) had significantly lower LDL-C (p=0.02), lower LDL-C associated with small size particles (LDL-C <255 A) (p=0.003), and higher HDL peak particle size than younger patients (p=0.03). In addition, elderly patients had increased plasma leptin (p=0.04) and resistin (p=0.0004) levels compared to the middle-aged group (<70 years). In the elderly patients, higher plasma resistin blood levels were associated with increased valve calcium content and inflammation.
  
  
  CONCLUSIONS
  The lipid profile of elderly patients was found less atherogenic than that of middle-aged patients. On the other hand, older patients with AS had higher plasma level of resistin which was associated with the degree of valvular calcification and inflammation. These results suggest that, beyond lipid model of atherosclerosis, age-related processes affecting resistin blood levels may also be involved in the late development of AS.
authors.affiliation: Laboratoire d'Etudes Moléculaires des Valvulopathies, Groupe de Recherche en Valvulopathies, Quebec Heart Institute/Hôpital Laval Research Center, Department of Surgery, Laval University, Quebec, Canada.
authors.forename: Dania
authors.initials: D
authors.lastname: Mohty
authors.forename: Philippe
authors.initials: P
authors.lastname: Pibarot
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: Després
authors.forename: Amélie
authors.initials: A
authors.lastname: Cartier
authors.forename: Benoit
authors.initials: B
authors.lastname: Arsenault
authors.forename: Frédéric
authors.initials: F
authors.lastname: Picard
authors.forename: Patrick
authors.initials: P
authors.lastname: Mathieu
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000097:blood / Q000502:physiology*; D001021:Aortic Valve / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D001024:Aortic Valve Stenosis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*; D015415:Biomarkers / Q000097:blood; D002114:Calcinosis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*; D009202:Cardiomyopathies / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D015331:Cohort Studies; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood / Q000502:physiology; D008297:Male; D008875:Middle Aged; D052243:Resistin / Q000097:blood / Q000502:physiology*; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D052243:Resistin