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不同糖代谢状态冠心病患者的纤维蛋白原与白蛋白比值及长期死亡率

Fibrinogen-to-Albumin Ratio and Long-Term Mortality in Coronary Artery Disease Patients with Different Glucose Metabolism Status.

作者信息

Xie Yun, Xu Xiayan, Wang Dongmei, Zhou Yang, Kang Yu, Lai Wenguang, Lu Hongyu, Liu Jin, Chen Shiqun, Xu Junyan, Yan Xiaoming, Huang Xiaoyu, Liu Yong

机构信息

School of Biology and Biological Engineering, South China University of Technology, 510006 Guangzhou, Guangdong, China.

Department of Cardiology, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, 510080 Guangzhou, Guangdong, China.

出版信息

Rev Cardiovasc Med. 2023 Nov 16;24(11):317. doi: 10.31083/j.rcm2411317. eCollection 2023 Nov.

DOI:10.31083/j.rcm2411317
PMID:39076427
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11272855/
Abstract

BACKGROUND

Abnormal glucose metabolism is present in most patients with coronary artery disease (CAD). Inflammation is considered to be a common risk factor for CAD and diabetes. Fibrinogen-to-albumin ratio (FAR), a novel inflammation biomarker, has been proposed as a predictor for cardiovascular disease. However, the relationship between the level of FAR and long-term mortality including all-cause, cardiovascular and cancer mortality, remains unknown in CAD patients, especially those with prediabetes.

METHODS

We enrolled 66,761 CAD patients from 2007 to 2020 from a multi-center registry cohort study. The primary outcomes were the all-cause, cardiovascular and cancer mortality. FAR was calculated using the following formula: Fibrinogen (g/L)/Albumin (g/L). Patients were divided into three groups by FAR tertile (low FAR (FAR-L), median FAR (FAR-M), high FAR (FAR-H)), and further categorized into 9 groups according to FAR and glucose metabolism status (normal glucose regulation (NGR), prediabetes mellitus (PreDM), diabetes mellitus (DM)). Cox regression models and competing risk models were used to examine the relationships between FAR and clinical outcomes.

RESULTS

66,761 patients (63.1 11.0 years, 75.3% male) were enrolled. During the follow-up, 10,534 patients died, including 4991 cardiovascular deaths and 1092 cancer deaths. After adjusting for confounders, higher FAR was associated with increased risk of all-cause and cause-specific mortality in CAD patients with NGR, PreDM and DM. The risk of all-cause and cardiovascular mortality was highest in FAR-H with DM (HR (95% CI) = 1.71 (1.58-1.86), 2.11 (1.86-2.38), respectively; 0.001). FAR-H with PreDM was significantly associated with the highest risk of cancer mortality (HR (95% CI) = 2.27 (1.70-3.02), 0.001). Adding FAR to the original model significantly improved the prediction of long-term mortality.

CONCLUSIONS

Increased FAR was significantly associated with higher risk of all-cause and cause-specific mortality in CAD patients with NGR, PreDM and DM. Abnormal glucose metabolism augments the relationship between FAR and mortality.

CLINICAL TRIAL REGISTRATION

ClinicalTrials.gov NCT05050877.

摘要

背景

大多数冠状动脉疾病(CAD)患者存在糖代谢异常。炎症被认为是CAD和糖尿病的常见危险因素。纤维蛋白原与白蛋白比值(FAR)作为一种新的炎症生物标志物,已被提出作为心血管疾病的预测指标。然而,在CAD患者,尤其是糖尿病前期患者中,FAR水平与包括全因、心血管和癌症死亡率在内的长期死亡率之间的关系尚不清楚。

方法

我们从一项多中心注册队列研究中纳入了2007年至2020年的66761例CAD患者。主要结局是全因、心血管和癌症死亡率。FAR采用以下公式计算:纤维蛋白原(g/L)/白蛋白(g/L)。患者按FAR三分位数分为三组(低FAR(FAR-L)、中等FAR(FAR-M)、高FAR(FAR-H)),并根据FAR和糖代谢状态(正常血糖调节(NGR)、糖尿病前期(PreDM)、糖尿病(DM))进一步分为9组。采用Cox回归模型和竞争风险模型来研究FAR与临床结局之间的关系。

结果

共纳入66761例患者(63.1±11.0岁,75.3%为男性)。随访期间,10534例患者死亡,包括4991例心血管死亡和1092例癌症死亡。在调整混杂因素后,较高的FAR与NGR、PreDM和DM的CAD患者全因和特定病因死亡率增加相关。在患有DM的FAR-H组中,全因和心血管死亡率风险最高(HR(95%CI)分别为1.71(1.58 - 1.86)、2.11(1.86 - 2.38);P<0.001)。患有PreDM的FAR-H组与最高的癌症死亡率风险显著相关(HR(95%CI)=2.27(1.70 - 3.02),P<0.001)。将FAR添加到原模型中显著改善了长期死亡率的预测。

结论

在NGR、PreDM和DM的CAD患者中,FAR升高与全因和特定病因死亡率较高显著相关。糖代谢异常增强了FAR与死亡率之间的关系。

临床试验注册

ClinicalTrials.gov NCT05050877。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06e6/11272855/900d6bef9036/2153-8174-24-11-317-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06e6/11272855/cabd7404bd0b/2153-8174-24-11-317-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06e6/11272855/df9cf9b2caca/2153-8174-24-11-317-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06e6/11272855/7b36f7dbb823/2153-8174-24-11-317-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06e6/11272855/900d6bef9036/2153-8174-24-11-317-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06e6/11272855/cabd7404bd0b/2153-8174-24-11-317-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06e6/11272855/df9cf9b2caca/2153-8174-24-11-317-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06e6/11272855/7b36f7dbb823/2153-8174-24-11-317-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06e6/11272855/900d6bef9036/2153-8174-24-11-317-g4.jpg

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