TY - JOUR
T1 - Uric Acid, Heart Failure Survival, and the Impact of Xanthine Oxidase Inhibition
AU - Harzand, Arash
AU - Tamariz, Leonardo
AU - Hare, Joshua M.
PY - 2012/5
Y1 - 2012/5
N2 - Increasing evidence suggests that serum uric acid (UA), a product of xanthine oxidase (XO), may be a useful marker for metabolic, hemodynamic, and functional staging in heart failure (HF) and a valid predictor of survival in HF patients. Recent data support an expanded role for UA and the XO pathway in the pathogenesis of HF, as studies have shown that an elevation in the enzymatic activity of XO can lead to increases in oxidative stress, endothelial dysfunction, and reduced myocardial function. Numerous population studies have previously reported that elevated UA levels are an independent predictor of cardiovascular mortality, and recent evidence suggests that lowering serum levels of UA may lead to improved outcomes in HF patients. The question of whether UA is only a marker rather than a causal factor in the pathogenesis of HF remains. Regardless of whether UA levels are ready for routine clinical use, either as a prognostic factor or novel therapeutic target, further prospective studies are necessary to demonstrate that routine measurement or reduction of UA levels improves outcomes in HF patients.
AB - Increasing evidence suggests that serum uric acid (UA), a product of xanthine oxidase (XO), may be a useful marker for metabolic, hemodynamic, and functional staging in heart failure (HF) and a valid predictor of survival in HF patients. Recent data support an expanded role for UA and the XO pathway in the pathogenesis of HF, as studies have shown that an elevation in the enzymatic activity of XO can lead to increases in oxidative stress, endothelial dysfunction, and reduced myocardial function. Numerous population studies have previously reported that elevated UA levels are an independent predictor of cardiovascular mortality, and recent evidence suggests that lowering serum levels of UA may lead to improved outcomes in HF patients. The question of whether UA is only a marker rather than a causal factor in the pathogenesis of HF remains. Regardless of whether UA levels are ready for routine clinical use, either as a prognostic factor or novel therapeutic target, further prospective studies are necessary to demonstrate that routine measurement or reduction of UA levels improves outcomes in HF patients.
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U2 - 10.1111/j.1751-7133.2011.00262.x
DO - 10.1111/j.1751-7133.2011.00262.x
M3 - Article
C2 - 22587748
AN - SCOPUS:84861189813
VL - 18
SP - 179
EP - 182
JO - Prevention and Management of Congestive Heart Failure
JF - Prevention and Management of Congestive Heart Failure
SN - 1527-5299
IS - 3
ER -