Hyperuricemia and the Risk of Heart Failure: Pathophysiology and Therapeutic Implications

The association between hyperuricemia and cardiovascular disease (CVD) has been reported and studied in the past two decades. Xanthine oxidase (XO) induced uric acid (UA) serves as a risk factor and has the independent prognostic and functional impact of heart failure (HF), but whether it plays a po...

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Autores principales: Ke Si, Chijing Wei, Lili Xu, Yue Zhou, Wenshan Lv, Bingzi Dong, Zhongchao Wang, Yajing Huang, Yangang Wang, Ying Chen
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Publicado: Frontiers Media S.A. 2021
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Acceso en línea:https://doaj.org/article/57aeda73599d4342b95ff0dce856d7c3
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spelling oai:doaj.org-article:57aeda73599d4342b95ff0dce856d7c32021-11-12T13:12:46ZHyperuricemia and the Risk of Heart Failure: Pathophysiology and Therapeutic Implications1664-239210.3389/fendo.2021.770815https://doaj.org/article/57aeda73599d4342b95ff0dce856d7c32021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fendo.2021.770815/fullhttps://doaj.org/toc/1664-2392The association between hyperuricemia and cardiovascular disease (CVD) has been reported and studied in the past two decades. Xanthine oxidase (XO) induced uric acid (UA) serves as a risk factor and has the independent prognostic and functional impact of heart failure (HF), but whether it plays a positive role in the pathogenesis of HF has remained unclear. Growing evidence suggest the up-regulated XO avtivity and increased production of free oxygen radical (ROS) correspondingly are the core pathogenesis of HF with hyperuricemia, which results in a whole cluster of pathophysiologic cardiovascular effects such as oxidative stress, endothelial dysfunction, vascular inflammation, left ventricular (LV) dysfunction as well as insulin resistance (IR). The use of XO inhibition represents a promising therapeutic choice in patients with HF due to its dual effect of lowering serum UA levels as well as reducing ROS production. This review will discuss the pathophysiologic mechanisms of hyperuricemia with HF, the targeted therapeutic interventions of UA lowering therapies (ULT) with XO inhibition and mechanism underlying beneficial effects of ULT. In addition, the review also summarizes current evidence on the role of ULT in HF and compares CV risk between allopurinol and febuxostat for practical and clinical purposes. Guidelines and implementation of CV risk management in daily practice will be discussed as well.Ke SiChijing WeiLili XuYue ZhouWenshan LvBingzi DongZhongchao WangYajing HuangYangang WangYing ChenFrontiers Media S.A.articlehyperuricemiaheart failurecardiovascular diseasepathophysiologytreatmentDiseases of the endocrine glands. Clinical endocrinologyRC648-665ENFrontiers in Endocrinology, Vol 12 (2021)
institution DOAJ
collection DOAJ
language EN
topic hyperuricemia
heart failure
cardiovascular disease
pathophysiology
treatment
Diseases of the endocrine glands. Clinical endocrinology
RC648-665
spellingShingle hyperuricemia
heart failure
cardiovascular disease
pathophysiology
treatment
Diseases of the endocrine glands. Clinical endocrinology
RC648-665
Ke Si
Chijing Wei
Lili Xu
Yue Zhou
Wenshan Lv
Bingzi Dong
Zhongchao Wang
Yajing Huang
Yangang Wang
Ying Chen
Hyperuricemia and the Risk of Heart Failure: Pathophysiology and Therapeutic Implications
description The association between hyperuricemia and cardiovascular disease (CVD) has been reported and studied in the past two decades. Xanthine oxidase (XO) induced uric acid (UA) serves as a risk factor and has the independent prognostic and functional impact of heart failure (HF), but whether it plays a positive role in the pathogenesis of HF has remained unclear. Growing evidence suggest the up-regulated XO avtivity and increased production of free oxygen radical (ROS) correspondingly are the core pathogenesis of HF with hyperuricemia, which results in a whole cluster of pathophysiologic cardiovascular effects such as oxidative stress, endothelial dysfunction, vascular inflammation, left ventricular (LV) dysfunction as well as insulin resistance (IR). The use of XO inhibition represents a promising therapeutic choice in patients with HF due to its dual effect of lowering serum UA levels as well as reducing ROS production. This review will discuss the pathophysiologic mechanisms of hyperuricemia with HF, the targeted therapeutic interventions of UA lowering therapies (ULT) with XO inhibition and mechanism underlying beneficial effects of ULT. In addition, the review also summarizes current evidence on the role of ULT in HF and compares CV risk between allopurinol and febuxostat for practical and clinical purposes. Guidelines and implementation of CV risk management in daily practice will be discussed as well.
format article
author Ke Si
Chijing Wei
Lili Xu
Yue Zhou
Wenshan Lv
Bingzi Dong
Zhongchao Wang
Yajing Huang
Yangang Wang
Ying Chen
author_facet Ke Si
Chijing Wei
Lili Xu
Yue Zhou
Wenshan Lv
Bingzi Dong
Zhongchao Wang
Yajing Huang
Yangang Wang
Ying Chen
author_sort Ke Si
title Hyperuricemia and the Risk of Heart Failure: Pathophysiology and Therapeutic Implications
title_short Hyperuricemia and the Risk of Heart Failure: Pathophysiology and Therapeutic Implications
title_full Hyperuricemia and the Risk of Heart Failure: Pathophysiology and Therapeutic Implications
title_fullStr Hyperuricemia and the Risk of Heart Failure: Pathophysiology and Therapeutic Implications
title_full_unstemmed Hyperuricemia and the Risk of Heart Failure: Pathophysiology and Therapeutic Implications
title_sort hyperuricemia and the risk of heart failure: pathophysiology and therapeutic implications
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/57aeda73599d4342b95ff0dce856d7c3
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