Relationship between aortic stiffness and serum uric acid in essential hypertension

Abstract

In last years hyperuricemia has been associated with an increased incidence of renal and cardiovascular events in general population, as well as in patients with diabetes and hypertension. However, the role of serum uric acid (SUA) as independent cardiovascular risk factor is still controversial. It is well known that increased aortic stiffness is a powerful independent predictor of cardiovascular events. Little is known about the influence of uric acid on aortic distensibility in subjects with arterial hypertension. The aim of our study was to evaluate the relationships between SUA and aortic stiffness in a group of essential hypertensive patients, attending our Hypertension Centre. We enrolled 222 untreated hypertensive patients (mean age: 44 ± 10 years; 60 % males), without cardiovascular complications and without severe renal insufficiency. In all subjects routine blood chemistry, including SUA determination (by uricase/peroxidase method) and albumin excretion rate (AER) assay were obtained. Moreover, measurement of carotid-femoral pulse wave velocity (c-f PWV), by an automatic computerised method (Complior) and 24-h ambulatory blood pressure (BP) monitoring were performed Patients with c-f PWV > 12 m/sec (n = 44) showed SUA levels significantly higher than those wiyh lower values of PWV (5.9 ± 1.2 vs 5.3 ± 1.1 m/sec; p = 0.002). This difference held after correction by ANCOVA for age, gender, mean arterial pressure (MAP), body mass index, and serum creatinine (p = 0.02), but not after further adjustment for AER. Univariate analysis of correlation disclosed a significant association of SUA with c-f PWV (r = 0.23; p = 0.001). This correlation lost statistical significance when AER was added in a multiple regression model including, as covariates, age, gender, MAP, serum creatinine, metabolic syndrome and SUA The results of our study show that, in essential hypertensive subJects, a positive relationship between SUA and aortic stiffness exists. This association may be mediated by endothelial dysfunction, as suggested by the loss of its statistical significance, after adjustment for albumin excretion rate.