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      Elevated uric acid/albumin ratio as a predictor of poor coronary collateral circulation development in patients with non‐ST segment elevation myocardial infarction

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          Abstract

          Background

          Uric acid/albumin ratio (UAR) is a novel composite biomarker with superior predictive value for cardiovascular disease.

          Objective

          To investigate the relationship between UAR and coronary collateral circulation (CCC) in patients with non‐ST segment elevation myocardial infarction (NSTEMI).

          Methods

          A total of 205 NSTEMI patients who underwent coronary arteriography with at least one major coronary stenosis, 95% were included. Patients were divided into two groups according to CCC development: poorly‐developed CCC group (Rentrop 0–1) and well‐developed CCC (Rentrop 2–3). Univariate analysis and logistic regression analysis were utilized to investigate the factors influencing adverse CCC formation in NSTEMI patients. The receiver operating characteristic (ROC) curve was plotted to evaluate the predictive value of UAR, C‐reactive protein (CRP), uric acid, and albumin for patients with poorly developed CCC, and the area under the curve (AUC) was compared.

          Results

          The UAR values of NSTEMI patients were significantly higher in the poorly developed CCC group than those in the well‐developed CCC group (10.19 [8.80–11.74] vs. 7.79 [6.28–9.55], p < .001). In the multiple logistic regression tests, UAR (odds ratio [OR]: 1.365, 95% confidence interval [CI]: 1.195–1.560, p < .001), CRP (OR: 1.149, 95% CI: 1.072–1.231, p < .001), and diabetes (OR: 2.924, 95% CI: 1.444–5.920, p = .003) were independent predictors of poorly developed CCC. The ROC curve analysis showed that the optimal cut‐off value of UAR was 8.78 in predicting poorly developed CCC with a sensitivity of 76.8% and specificity of 62.4%, with the AUC of 0.737 (95% Cl: 0.668–0.805, p < .001).

          Conclusion

          Elevated UAR may be an independent and effective biomarker for predicting poorly‐developed CCC development in NSTEMI patients.

          Abstract

          Analysis of 205 non‐ST segment elevation myocardial infarction patients reveals the uric acid/albumin ratio (UAR) as a strong predictor of poor coronary collateral circulation development, outperforming UAR, C‐reactive protein, uric acid, and albumin levels in predictive value, as evidenced by receiver operating characteristic curves.

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          Most cited references41

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          2016 European Guidelines on cardiovascular disease prevention in clinical practice: The Sixth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of 10 societies and by invited experts)Developed with the special contribution of the European Association for Cardiovascular Prevention & Rehabilitation (EACPR).

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            Fourth Universal Definition of Myocardial Infarction (2018).

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              A role for uric acid in the progression of renal disease.

              Hyperuricemia is associated with renal disease, but it is usually considered a marker of renal dysfunction rather than a risk factor for progression. Recent studies have reported that mild hyperuricemia in normal rats induced by the uricase inhibitor, oxonic acid (OA), results in hypertension, intrarenal vascular disease, and renal injury. This led to the hypothesis that uric acid may contribute to progressive renal disease. To examine the effect of hyperuricemia on renal disease progression, rats were fed 2% OA for 6 wk after 5/6 remnant kidney (RK) surgery with or without the xanthine oxidase inhibitor, allopurinol, or the uricosuric agent, benziodarone. Renal function and histologic studies were performed at 6 wk. Given observations that uric acid induces vascular disease, the effect of uric acid on vascular smooth muscle cells in culture was also examined. RK rats developed transient hyperuricemia (2.7 mg/dl at week 2), but then levels returned to baseline by week 6 (1.4 mg/dl). In contrast, RK+OA rats developed higher and more persistent hyperuricemia (6 wk, 3.2 mg/dl). Hyperuricemic rats demonstrated higher BP, greater proteinuria, and higher serum creatinine than RK rats. Hyperuricemic RK rats had more renal hypertrophy and greater glomerulosclerosis (24.2 +/- 2.5 versus 17.5 +/- 3.4%; P < 0.05) and interstitial fibrosis (1.89 +/- 0.45 versus 1.52 +/- 0.47; P < 0.05). Hyperuricemic rats developed vascular disease consisting of thickening of the preglomerular arteries with smooth muscle cell proliferation; these changes were significantly more severe than a historical RK group with similar BP. Allopurinol significantly reduced uric acid levels and blocked the renal functional and histologic changes. Benziodarone reduced uric acid levels less effectively and only partially improved BP and renal function, with minimal effect on the vascular changes. To better understand the mechanism for the vascular disease, the expression of COX-2 and renin were examined. Hyperuricemic rats showed increased renal renin and COX-2 expression, the latter especially in preglomerular arterial vessels. In in vitro studies, cultured vascular smooth muscle cells incubated with uric acid also generated COX-2 with time-dependent proliferation, which was prevented by either a COX-2 or TXA-2 receptor inhibitor. Hyperuricemia accelerates renal progression in the RK model via a mechanism linked to high systemic BP and COX-2-mediated, thromboxane-induced vascular disease. These studies provide direct evidence that uric acid may be a true mediator of renal disease and progression.
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                Author and article information

                Contributors
                chenweixiang@suda.edu.cn
                jtbsdfyy@163.com
                Journal
                Clin Cardiol
                Clin Cardiol
                10.1002/(ISSN)1932-8737
                CLC
                Clinical Cardiology
                John Wiley and Sons Inc. (Hoboken )
                0160-9289
                1932-8737
                16 January 2024
                January 2024
                : 47
                : 1 ( doiID: 10.1002/clc.v47.1 )
                : e24215
                Affiliations
                [ 1 ] Department of Cardiology The First Affiliated Hospital of Soochow University Suzhou China
                [ 2 ] Department of Cardiology Suzhou Ninth Hospital Affiliate to Soochow University Suzhou China
                Author notes
                [*] [* ] Correspondence Weixiang Chen and Tingbo Jiang, Department of Cardiology, The First Affiliated Hospital of Soochow University, Suzhou, China.

                Email: chenweixiang@ 123456suda.edu.cn and jtbsdfyy@ 123456163.com

                Author information
                http://orcid.org/0000-0001-8879-9862
                Article
                CLC24215
                10.1002/clc.24215
                10790324
                65171acb-4090-4b8d-b756-162b50dd96c4
                © 2024 The Authors. Clinical Cardiology published by Wiley Periodicals, LLC.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 16 December 2023
                : 22 September 2023
                : 28 December 2023
                Page count
                Figures: 2, Tables: 4, Pages: 8, Words: 5183
                Funding
                Funded by: Suzhou Special Project Fund for Key Clinical Disease Diagnosis and Treatment Technology
                Award ID: LCZX202232
                Categories
                Clinical Article
                Clinical Articles
                Custom metadata
                2.0
                January 2024
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.3.6 mode:remove_FC converted:16.01.2024

                Cardiovascular Medicine
                coronary collateral circulation,non‐st segment elevation myocardial infarction,rentrop grade,uric acid to albumin ratio

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