Serum uric acid as a metabolic regulator of endothelial function in heart failure

Abstract

Citation: Berezin AE (2017) Serum uric acid as a metabolic regulator of endothelial function in heart failure. Arch Clin Hypertens 3(1): 027-029. DOI: http://dx.doi.org/10.17352/ach.000016 AbstractThe development of heart failure (HF) associated with elevated level of serum uric acid (SUA). Additionally, the majority of individuals with traditional cardiovascular risk factors contributing in HF risk exhibited increased levels of SUA. Although SUA lowering drugs are widely used in patients with symptomatic hyperuricemia and gout beyond their etiologies, there is no agreement of SUA below target level 6.0 mg/dL in asymptomatic individuals with kidney injury and CV disease and data of ones in heart failure (HF) are suffi ciently controversial. First SUA plays an important role in inducing oxidative stress, infl ammation, neurohumoral activation, and endothelial dysfunction. Secondary, SUA may act as antioxidant contributing in restoring of vascular function. Moreover, SUA is able to epigenetically regulate a survival of endothelial precursors, mediate their mobbing and differentiation, as well as coordinate a turn-over effect of metabolic memory phenomenon into repair capability of cell precursors. However, elevated SUA level was found a predictor of adverse clinical outcomes of HF. The short communication is depicted the importance of new clinical data to confi rm the emerging reparative ability of SUA in HF and its role as promising target for treatment in cardiac failure. Short Communication Serum uric acid as a metabolic regulator of endothelial function in heart failureAlexander E Berezin* Short CommunicationThere is a large body of evidence regarding the role of serum uric acid (SUA) in pathogenesis of cardiovascular diseases (CVD) including heart failure (HF). Although SUA levels above the current international reference limit equal 6.0 mg/dL are highly prevalent in chronic kidney disease (CKD), hyperuricemia strongly associates with in-hospital CV mortality independently from CKD etiology and renal function in individuals admitted to the hospital due to several causes, i.e. acute myocardial infarction, stroke, hypertensive emergencies, acute / chronic heart failure, arrhythmia, shock and sepsis.In contrast, hypouricemia did not associate with increased mortality rate in patient populations with established CVD [1]. In HF an elevated SUA level was found due to several mechanisms including an increased activity of xanthine oxidase (XO), which is a key enzyme in uric acid synthesis and is under control of infl ammatory cytokines / chemokines, some growth factors, and intermediates (blood glucose). Whether SUA could be an independent predictor of HF development is not fully clear. Recent clinical studies and some meta-analysis have shown that elevated SUA levels were associated with an increased risk of incident HF, observed in majority of patients with established chronic HF and relate to adverse clinical outcomes in HF [8][9][10][11]. However, the impact of uric acid on all-cause mortality and HF-related dea...