Highlights
- •It is already known that SUA is a predictor of incident hypertension
- •Our data add information on the role of SUA as a factor associated with poor BP control despite antihypertensive therapy
- •This could be related to the negative effect of SUA on arterial stiffness
Abstract
Introduction
Serum uric acid (SUA) has been associated to incident hypertension and increased risk
of cardiovascular diseases.
Materials and methods
Among the 2191 subjects enrolled during the last population survey of the Brisighella
Heart Study, we identified 146 new cases of arterial hypertension and 394 treated
but uncontrolled hypertensive patients with different levels of SUA. Their hemodynamic
characteristics have been compared with those of age- and sex-matched normotensive
(N. 324) and controlled hypertensive (N. 470) subjects. Then, by logistic regression
analysis, we evaluated which factors were associated with a worse BP control under
pharmacological treatment.
Results
SUA levels were significantly higher in untreated hypertensive and uncontrolled hypertensive
patients when compared to normotensives and controlled hypertensive patients. Pulse
wave velocity (PWV) was significantly higher (p < 0.001) in undiagnosed and uncontrolled hypertensive patients, while controlled hypertensive
patients had PWV values comparable to normotensive controls. A similar trend has been
observed for the augmentation index (AI). A worse BP control was associated with SUA
levels (OR 1277, 95% CI 1134–1600 per mg/dL), AI (OR 1066, 95%CI 1041–1092 per unit),
and PWV (OR 1201, 95% CI 1089–1423, per m/s), but not with age, body mass index, nor
estimated glomerular filtration rate.
Conclusion
Based on our data, SUA seems to be associated with an inadequate BP control in subjects
treated with antihypertensive drugs, and subjects with both uncontrolled BP and relatively
high SUA levels have also an increased arterial stiffness that (per se) could be a
cause of worse BP control under treatment.
Keywords
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Article info
Publication history
Published online: August 03, 2016
Accepted:
July 24,
2016
Received in revised form:
July 17,
2016
Received:
January 10,
2016
Identification
Copyright
© 2016 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.
