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可溶性ST2用于预测伴或不伴肾功能不全的冠心病患者发生心力衰竭、心房颤动及死亡的情况。

Soluble ST2 for predicting heart failure, atrial fibrillation and death in patients with coronary heart disease with or without renal insufficiency.

作者信息

Li Huiying, Zhu Qiwei, Bai Jing, Chen Jianqiao, Zhu Zifan, Hao Benchuan, Wang Wei, Bai Yongyi, Liu Hongbin

机构信息

Department of Cardiology, The Second Medical Center & National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, 100853, Beijing, China.

Medical School of Chinese PLA, 100853, Beijing, China.

出版信息

Heliyon. 2024 Apr 20;10(9):e29804. doi: 10.1016/j.heliyon.2024.e29804. eCollection 2024 May 15.

DOI:10.1016/j.heliyon.2024.e29804
PMID:38698979
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11064070/
Abstract

BACKGROUND

This study aimed to investigate the relationship between baseline soluble suppression of tumorigenesis-2 (sST2) concentration and the outcomes of heart failure (HF), atrial fibrillation (AF) or death in patients with coronary heart disease (CHD) with or without renal insufficiency (RI).

METHODS

Between March 2011 and December 2015, 3454 patients with CHD from the Chinese PLA General Hospital were enrolled in this cohort study. The patients were followed up until October 2021. AF, HF, and death events were recorded. Associations between baseline sST2 concentrations and clinical outcomes were assessed using Kaplan-Meier (K-M) curves, and Cox regression and generalised additive models. Subgroup analysis were carried out between RI and non-RI groups.

RESULTS

Among the patients with CHD (61.5 ± 11.8 years; 78.6 % men), 415 (12.02 %) had RI. During a median follow-up of 8.37 years, HF and AF were reported in 216 (6.25 %) and 174 (5.04 %) patients, respectively, and 297 (8.60 %) died. The K-M curves indicated that patients in the higher quartiles of sST2 concentrations were correlated with a poor survival rate of HF, AF, or death (all  < 0.001). Generalised additive model (GAM) demonstrated a nonlinear positive association between sST2 concentration and the risk of HF, AF, and death in CHD patients. The cut-off value of sST2 for predicting HF, AF and death were 32.1, 25.4 and 28.6 ng/mL, respectively. CHD patients with sST2 higher than the cut-off value had higher risks of HF (HR: 3.02, 95%CI: 2.24-4.05), AF (HR: 2.86; 95%CI: 2.10-3.90), and death (HR:2.11, 95%CI: 1.67-2.67). Furthermore, in patients with RI (12.02 %, n = 415), the prognostic value of sST2 over the cut-off value for HF and death remained unchanged (HR: 3.21 and 2.35;  < 0.05). In patients with CHD with or without RI, sST2 improved the area under the curve (AUC) of traditional risk models for predicting clinical endpoint events.

CONCLUSIONS

The biomarker sST2 may be useful for predicting HF, AF, and death in patients with CHD. The predicted value was not affected by renal function.

摘要

背景

本研究旨在探讨基线可溶性肿瘤发生抑制因子2(sST2)浓度与合并或不合并肾功能不全(RI)的冠心病(CHD)患者发生心力衰竭(HF)、心房颤动(AF)或死亡结局之间的关系。

方法

2011年3月至2015年12月,来自中国人民解放军总医院的3454例冠心病患者纳入了本队列研究。对患者进行随访至2021年10月。记录AF、HF和死亡事件。使用Kaplan-Meier(K-M)曲线、Cox回归和广义相加模型评估基线sST2浓度与临床结局之间的关联。在RI组和非RI组之间进行亚组分析。

结果

在冠心病患者(61.5±11.8岁;78.6%为男性)中,415例(12.02%)有RI。在中位随访8.37年期间,分别有216例(6.25%)和174例(5.04%)患者报告发生HF和AF,297例(8.60%)死亡。K-M曲线表明,sST2浓度处于较高四分位数的患者与HF、AF或死亡的较差生存率相关(均P<0.001)。广义相加模型(GAM)显示sST2浓度与冠心病患者发生HF、AF和死亡的风险之间呈非线性正相关。预测HF、AF和死亡的sST2临界值分别为32.1、25.4和28.6 ng/mL。sST2高于临界值的冠心病患者发生HF(HR:3.02,95%CI:2.24-4.05)、AF(HR:2.86;95%CI:2.10-3.90)和死亡(HR:2.11,95%CI:1.67-2.67)的风险更高。此外,在有RI的患者(12.02%,n = 415)中,sST2高于临界值对HF和死亡的预后价值保持不变(HR:3.21和2.35;P<0.05)。在合并或不合并RI的冠心病患者中,sST2改善了预测临床终点事件的传统风险模型的曲线下面积(AUC)。

结论

生物标志物sST2可能有助于预测冠心病患者发生HF、AF和死亡。预测价值不受肾功能影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7144/11064070/4b8b7367ab50/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7144/11064070/840c76cdd55f/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7144/11064070/6dead8f50d8b/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7144/11064070/1a209f0bbab2/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7144/11064070/946a17839347/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7144/11064070/4b8b7367ab50/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7144/11064070/840c76cdd55f/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7144/11064070/6dead8f50d8b/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7144/11064070/1a209f0bbab2/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7144/11064070/946a17839347/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7144/11064070/4b8b7367ab50/gr5.jpg

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