Author/Authors :
Kato، نويسنده , , Masahiko and Hisatome، نويسنده , , Ichiro and Tomikura، نويسنده , , Yoko and Kotani، نويسنده , , Kazuhiko and Kinugawa، نويسنده , , Toru and Ogino، نويسنده , , Kazuhide and Ishida، نويسنده , , Katsunori and Igawa، نويسنده , , Osamu and Shigemasa، نويسنده , , Chiaki and Somers، نويسنده , , Virend K.، نويسنده ,
Abstract :
Hyperuricemia has been associated with an increased risk for cardiovascular disease and increased mortality. However, the biologic mechanisms that link elevated serum uric acid to cardiovascular disease are uncertain. This study tested the hypothesis that elevated serum uric acid is associated with impaired endothelial function in hyperuricemic patients without any overt cardiovascular disease. Seventeen male patients with hyperuricemia (mean age 42 ± 4 years) and 9 control subjects (mean age 45 ± 5 years) were studied. All subjects were nonsmokers. All patients had never been treated for hyperuricemia, were on no medications, and were free of any other known diseases. Endothelial function was evaluated by flow-mediated dilation measured by ultrasound. Flow-mediated dilation was significantly impaired in patients with hyperuricemia (4.0 ± 0.7%) compared with control subjects (6.4 ± 0.8%) (p = 0.044). Flow-mediated dilation correlated inversely with uric acid levels (r = −0.4, p = 0.05). Nitrate-induced dilation was 12.3 ± 1.0% in patients with hyperuricemia and 11.8 ± 2.3% in control subjects (p = 0.82). Impaired endothelial-dependent vasodilation is present in hyperuricemic patients even in the absence of any overt cardiovascular disease. The elevated serum uric acid, per se, may constitute a novel risk factor for endothelial dysfunction.
