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.

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.

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.

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.