title: In patients with aortic stenosis increased flow-mediated dilation is independently associated with higher peak jet velocity and lower asymmetric dimethylarginine levels.
abstract: BACKGROUND
  Recently, it has been shown that endothelial dysfunction and aortic stenosis (AS) share several risk factors. Endothelial function represents a crucial factor for the regulation of vascular tonus and its malfunction influences the formation of thrombosis and inflammation. However, the role of endothelial dysfunction in AS remains unclear.
  
  
  METHODS
  Echocardiographic, clinical, and laboratory data of 34 patients (age 74.5 ± 7.9 years, 20 men) with at least moderate AS (peak jet velocity 3.8 ± 0.8 m/s) were collected. In all patients, endothelial function was determined by brachial artery flow-mediated dilation (FMD). Patients with rheumatic or endocarditic valve disease, bicuspid valves, a left ventricular ejection fraction of ≤40%, and coronary artery disease were excluded. Sixteen volunteers (age 69.3 ± 9.4 years, 10 men) without valve disease served as controls.
  
  
  RESULTS
  Patients with AS had a trend toward a lower FMD than controls with a comparable risk profile (5.4% ± 3.6% vs 7.4% ± 4.1%, P = .1). Univariate correlates of FMD in patients with AS were peak jet velocity, medication with angiotensin-converting enzyme inhibitor, diabetes, diastolic blood pressure, and asymmetric dimethylarginine. Backward elimination identified peak jet velocity (β = 0.51, P = .001), and asymmetric dimethylarginine (β = -0.45, P = .003) as independent predictors of FMD in multivariate analysis.
  
  
  CONCLUSIONS
  In patients with AS, we found a strong positive relation between the peak jet velocity and a higher FMD. This effect might be mediated by nitric oxide release due to turbulent poststenotic blood flow or the rising transvalvular gradient, and the increasing pulse pressure may be counteracted by a parallel increase in FMD.
authors.affiliation: Department of Internal Medicine I, Friedrich-Schiller-University, Jena, Germany. julia.schumm@med.uni-jena.de
authors.forename: Julia
authors.initials: J
authors.lastname: Schumm
authors.forename: Stephanie
authors.initials: S
authors.lastname: Luetzkendorf
authors.forename: Wilma
authors.initials: W
authors.lastname: Rademacher
authors.forename: Marcus
authors.initials: M
authors.lastname: Franz
authors.forename: Christiane
authors.initials: C
authors.lastname: Schmidt-Winter
authors.forename: Michael
authors.initials: M
authors.lastname: Kiehntopf
authors.forename: Hans R
authors.initials: HR
authors.lastname: Figulla
authors.forename: Bernhard R
authors.initials: BR
authors.lastname: Brehm
mesh_terms: D000368:Aged; D001024:Aortic Valve Stenosis / Q000097:blood / Q000000981:diagnostic imaging / Q000503:physiopathology*; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood; D001783:Blood Flow Velocity / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology*; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D004108:Dilatation, Pathologic / Q000000981:diagnostic imaging / Q000503:physiopathology; D004452:Echocardiography; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D012307:Risk Factors; D012720:Severity of Illness Index; D013318:Stroke Volume / Q000502:physiology*; D018608:Ultrasonography, Doppler
chemical_list: C018524:N,N-dimethylarginine; D001120:Arginine; D019001:Nitric Oxide Synthase