Abstract
Uric acid (UA) is the final product of the catabolism of endogenous and exogenous purine nucleotides. While its association with articular gout and kidney disease has been known for a long time, new data have demonstrated that UA is also related to cardiovascular (CV) diseases. UA has been identified as a significant determinant of many different outcomes, such as all-cause and CV mortality, and also of CV events (mainly Acute Coronary Syndromes (ACS) and even strokes). Furthermore, UA has been related to the development of Heart Failure, and to a higher mortality in decompensated patients, as well as to the onset of atrial fibrillation. After a brief introduction on the general role of UA in CV disorders, this review will be focused on UA’s relationship with CV outcomes, as well as on the specific features of patients with ACS and Chronic Coronary Syndrome. Finally, two issues which remain open will be discussed: the first is about the identification of a CV UA cut-off value, while the second concerns the possibility that the pharmacological reduction of UA is able to lower the incidence of CV events.
Highlights
Uric Acid (UA) is the final product of the catabolism of purine nucleotides from endogenous and exogenous origins
This occurrence showed differences in terms of its statistical correlation depending on gender: while women showed a linear trend in the link between UA and all-cause mortality, a J-shaped association was found in men, in which a lower-cut off of 3.4 mg/dL was identified as a significant threshold of adverse outcomes [62]
From a pathophysiological point of view, the question of whether hyperuricemia contributes directly to the genesis of ACS and CCS, or if it is just an innocent bystander determined by an increased catabolism in ischemic myocardium is still a matter of debate
Summary
Uric Acid (UA) is the final product of the catabolism of purine nucleotides from endogenous (cellular nucleoproteins) and exogenous origins (alimentary). Conditions which may raise UA levels include the increased production which occurs with a purine-rich diet, tumor lysis syndrome or specific drugs (chemotherapy and pyrazinamide), and with a decrease in UA excretion, mainly in renal diseases. UA is correlated with the development of Heart Failure (HF) [5], and with a higher mortality in this group of patients [6], as well as with the onset of atrial fibrillation [7] All of these significant findings led the latest European Guidelines of Arterial Hypertension to introduce UA among CV risk factors that should be assessed in order to stratify a patient’s risk [8]. These two fundamental points will be discussed in this research paper
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