title: Metabolic syndrome is associated with faster degeneration of bioprosthetic valves.
abstract: BACKGROUND
  Several studies have reported similarities between calcification of the native aortic valve and atherosclerosis. Recent studies also suggested that hypercholesterolemia may be a risk factor for calcific degeneration of bioprosthetic valves. The metabolic syndrome (MS) is associated with a higher risk of vascular atherosclerosis. We thus hypothesized that the atherogenic features of MS could accelerate bioprosthetic valve degeneration.
  
  
  RESULTS
  We included 217 patients who underwent aortic valve replacement with a bioprosthetic valve in the study. Of these patients, 71 patients (33%) had MS defined according to the modified criteria proposed by the National Cholesterol Education Program Adult Treatment Panel III. The annualized increase in mean transprosthetic gradient and the worsening of transprosthetic regurgitation measured by Doppler echocardiography were used to assess the deterioration of valve hemodynamic function. Patients with MS had higher progression of gradient (+4+/-5 mm Hg/year versus +2+/-2 mm Hg/year, P<0.001), higher proportion of > or = 1/3 degree worsening of regurgitation (25% versus 12%, P=0.02), and higher proportion of valve function deterioration defined as regurgitation worsening and/or > or = 3 mm Hg/year increase in gradient (41% versus 25%, P=0.02) when compared with patients without MS. On multivariate analysis, MS was an independent predictor of gradient progression (P=0.01), regurgitation worsening (P=0.02), and valve function deterioration (P=0.02). The other independent predictors were diabetes, renal insufficiency, and higher mean gradient at baseline.
  
  
  CONCLUSIONS
  This is the first study to report that the MS is independently associated with faster bioprosthetic valve degeneration. This study could pave the way for the development of a new medical therapy able to significantly reduce the structural valve deterioration of bioprostheses.
authors.affiliation: Laval Hospital Research Center/Québec Heart Institute, Laval University, 2725 Chemin Sainte-Foy, Sainte-Foy, Québec, Canada, G1V-4G5.
authors.forename: Martin
authors.initials: M
authors.lastname: Briand
authors.forename: Philippe
authors.initials: P
authors.lastname: Pibarot
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: Després
authors.forename: Pierre
authors.initials: P
authors.lastname: Voisine
authors.forename: Jean G
authors.initials: JG
authors.lastname: Dumesnil
authors.forename: François
authors.initials: F
authors.lastname: Dagenais
authors.forename: Patrick
authors.initials: P
authors.lastname: Mathieu
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001022:Aortic Valve Insufficiency / Q000000981:diagnostic imaging / Q000209:etiology; D001024:Aortic Valve Stenosis / Q000150:complications / Q000503:physiopathology* / Q000601:surgery; D050197:Atherosclerosis / Q000150:complications / Q000503:physiopathology*; D001705:Bioprosthesis; D002114:Calcinosis / Q000150:complications / Q000503:physiopathology* / Q000601:surgery; D004198:Disease Susceptibility; D005260:Female; D006350:Heart Valve Prosthesis; D006439:Hemodynamics; D006801:Humans; D006937:Hypercholesterolemia / Q000150:complications / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000150:complications / Q000503:physiopathology; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications / Q000503:physiopathology*; D008875:Middle Aged; D011475:Prosthesis Failure; D012008:Recurrence; D013997:Time Factors; D014463:Ultrasonography