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Persistent endothelial dysfunction in calcified aortic stenosis beyond valve replacement surgery
  1. R Chenevard,
  2. M Bechir*,
  3. D Hurlimann*,
  4. F Ruschitzka,
  5. J Turina,
  6. T F Luscher,
  7. G Noll
  1. Cardiovascular Centre, Department of Cardiology, University Hospital Zurich, Switzerland
  1. Correspondence to:
    G Noll
    Department of Cardiology, University Hospital, CH-8091 Zurich, Switzerland; georg.noll{at}

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The leading cause of aortic valve morbidity in industrialised nations is degenerative calcified aortic stenosis. A convincing body of evidence suggests the concept that degenerative aortic stenosis represents a form of atherosclerotic vascular disease.1 Endothelial dysfunction promoting abnormal vasomotion, increased leucocyte adhesion, platelet dysfunction and vascular inflammation, which have been shown extensively in atherosclerosis, was recently found in degenerative aortic valve disease.2 Decreased nitric oxide (NO) bioavailability has a pivotal role in this process, and is largely determined by the expression of endothelial nitric oxide synthase (eNOS). Interestingly, eNOS expression is markedly influenced by haemodynamic factors, as shear stress is the main physiological trigger to enhance eNOS expression and activity.3 In the study by Poggianti et al,2 the effects of haemodynamic parameters have not been discussed as only patients with aortic valve sclerosis but without relevant haemodynamic stenosis were studied. We hypothesised that altered haemodynamics in aortic stenosis may at least partly be responsible for endothelial dysfunction and thus potentially normalise after aortic-valve replacement. Increased low-grade systemic inflammation has also been shown in aortic stenosis4 and consequently would be expected to influence vascular function similar to that described in coronary artery disease. Thus, we investigated endothelial dysfunction and signs of inflammation in haemodynamically relevant degenerative aortic stenosis before and after valve replacement.


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  • * Both authors contributed equally.

  • The study was supported by the Swiss National Foundation grant number 3200-065447.01, the Swiss Heart Foundation and the Foundation for Cardiovascular Research Zurich.

  • Competing interests: None.