Serum Uric Acid, Hypertriglyceridemia, and Carotid Plaques: A Sub-Analysis of the URic Acid Right for Heart Health (URRAH) Study.
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Agabiti Rosei Claudia, Paini Anna, Buso Giacomo, Maloberti Alessandro, Giannattasio Cristina, Salvetti Massimo, Casiglia Edoardo, Tikhonoff Valerie, Angeli Fabio, Barbagallo Carlo Maria, Bombelli Michele, Cappelli Federica, Cianci Rosario, Ciccarelli Michele, Cicero Arrigo Francesco Giuseppe, Cirillo Massimo, Cirillo Pietro, Dell'Oro Raffaella, D'Elia Lanfranco, Desideri Giovambattista, Ferri Claudio, Galletti Ferruccio, Gesualdo Loreto, Grassi Guido, Iaccarino Guido, Lippa Luciano, Mallamaci Francesca, Masi Stefano, Masulli Maria, Mazza Alberto, Mengozzi Alessandro, Nazzaro Pietro, Palatini Paolo, Parati Gianfranco, Pontremoli Roberto, Quarti-Trevano Fosca, Rattazzi Marcello, Reboldi Gianpaolo, Rivasi Giulia, Russo Elisa, Tocci Giuliano, Ungar Andrea, Verdecchia Paolo, Viazzi Francesca, Volpe Massimo, Virdis Agostino, Muiesan Maria Lorenza, Borghi Claudio, Working Group on Uric Acid and Cardiovascular Risk of the Italian Society of Hypertension
Аннотация
High levels of serum uric acid (SUA) and triglycerides (TG) might promote high-cardiovascular-risk phenotypes, including subclinical atherosclerosis. An interaction between plaques xanthine oxidase (XO) expression, SUA, and HDL-C has been recently postulated. Subjects from the URic acid Right for heArt Health (URRAH) study with carotid ultrasound and without previous cardiovascular diseases (CVD) (n = 6209), followed over 20 years, were included in the analysis. Hypertriglyceridemia (hTG) was defined as TG ≥ 150 mg/dL. Higher levels of SUA (hSUA) were defined as ≥5.6 mg/dL in men and 5.1 mg/dL in women. A carotid plaque was identified in 1742 subjects (28%). SUA and TG predicted carotid plaque (HR 1.09 [1.04-1.27], p < 0.001 and HR 1.25 [1.09-1.45], p < 0.001) in the whole population, independently of age, sex, diabetes, systolic blood pressure, HDL and LDL cholesterol and treatment. Four different groups were identified (normal SUA and TG, hSUA and normal TG, normal SUA and hTG, hSUA and hTG). The prevalence of plaque was progressively greater in subjects with normal SUA and TG (23%), hSUA and normal TG (31%), normal SUA and hTG (34%), and hSUA and hTG (38%) (Chi-square, 0.0001). Logistic regression analysis showed that hSUA and normal TG [HR 1.159 (1.002 to 1.341); p = 0.001], normal SUA and hTG [HR 1.305 (1.057 to 1.611); p = 0.001], and the combination of hUA and hTG [HR 1.539 (1.274 to 1.859); p = 0.001] were associated with a higher risk of plaque. Our findings demonstrate that SUA is independently associated with the presence of carotid plaque and suggest that the combination of hyperuricemia and hypertriglyceridemia is a stronger determinant of carotid plaque than hSUA or hTG taken as single risk factors. The association between SUA and CVD events may be explained in part by a direct association of UA with carotid plaques.