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The presence of fructosamine in human aortic valves is associated with valve stiffness

Abstract

Aims Human heart valves are prone to glycation, a fundamental process of ageing. The aim of this study was to establish the relationship between fructosamine formation and the mechanical properties of human aortic valves.

Methods 67 patients (age: 76±8 years) diagnosed with an aortic valve stenosis, who underwent an aortic valve replacement were enrolled. Fructosamine and calcium concentrations in aortic valves were determined. Using a transthoracic Doppler echocardiography, aortic valve orifice area and transvalvular pressure gradients were measured. In a subgroup of 32 patients, the aortic valve orifice area was sufficient to carry out mechanical testing on a LFPlus Universal material tester. An in vitro removal of fructosamine of the valve was initiated using ATP-dependent fructosamine 3-kinase (FN3K).

Results A significant correlation was found between the aortic valve fructosamine concentration and the calculated aortic valve orifice area: Y (aortic valve orifice area, mm2)=1.050−0.228X (aortic valve fructosamine concentration, µmol/g valve) (r=−0.38). A significantly higher calcium concentration was measured in the aortic valves of diabetics in comparison with those of non-diabetics. A multiple regression analysis revealed that the presence of diabetes mellitus and aortic valve fructosamine concentration were the main predictors of the extensibility of the aortic valves. In the in vitro deglycation study, a significant lower aortic valve fructosamine concentration was detected after treatment with FN3K. This resulted in an increased flexibility of the aortic valves.

Conclusions Although no direct causativeness is proven with the presented results, which just show an association between fructosamine, the effect of FN3K and aortic valve stiffness, the present study points for the first time towards a possible additional role of the Amadori products in the biomechanical properties of ageing aortic valves.

  • CARDIOTHORACIC PATHOLOGY
  • PROTEINS
  • fibrosis

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