Literature DB >> 30261750

Neutrophil gelatinase-associated lipocalin (NGAL) and cardiovascular events in patients with stable coronary artery disease.

Zenthuja Sivalingam1, Nils Erik Magnusson2, Erik Lerkevang Grove1,3, Anne-Mette Hvas3,4, Steen Dalby Kristensen1,3, Sanne Bøjet Larsen1.   

Abstract

Inflammation is an important mediator in the pathogenesis of atherosclerosis. Neutrophil gelatinase-associated lipocalin (NGAL) is a small glycoprotein secreted by neutrophils. NGAL regulates the activity of matrix metalloproteinase-9, which plays a role in plaque instability. It has therefore been hypothesised that NGAL may modulate inflammation and promote the development and progression of atherosclerosis. Our aim was to assess the predictive value of plasma NGAL in a prospective cohort study of 876 high-risk patients with stable coronary artery disease (CAD). NGAL levels were measured using the NGAL TestTM from BioPorto Diagnostics. Clinical follow-up was performed after a median of 3.1 years. The endpoint was a combination of non-fatal acute myocardial infarction (MI), cardiovascular death (CVD), or ischaemic stroke. The NGAL concentration was (median [25;75%]: 64.3 µg/L [51.3;81.4]). The area under the receiver operating characteristic curve (AUC) was 0.56 (95% confidence interval (CI): 0.49;0.64) for the diagnosis of the composite endpoint and 0.66 (95% CI: 0.56;0.75) after adding NGAL to high-sensitive C-reactive protein (hs-CRP), leucocyte count, interleukin-6 (IL-6), calprotectin, age, sex, body mass index (BMI), diabetes mellitus, smoking and creatinine. However, the AUC for hs-CRP, leucocyte count, IL-6, calprotectin, age, sex, BMI, diabetes mellitus, smoking and creatinine without NGAL was similar at 0.66 (95% CI: 0.56;0.76). NGAL alone had no predictive value with respect to the composite endpoint of non-fatal AMI, ischaemic stroke, or CVD in stable CAD patients. NGAL did not add any predictive value to the endpoint compared with existing inflammatory biomarkers and cardiovascular risk factors.

Entities:  

Keywords:  Atherosclerosis; biomarkers; coronary artery disease; inflammation; neutrophil gelatinase-associated lipocalin

Mesh:

Substances:

Year:  2018        PMID: 30261750     DOI: 10.1080/00365513.2018.1499956

Source DB:  PubMed          Journal:  Scand J Clin Lab Invest        ISSN: 0036-5513            Impact factor:   1.713


  5 in total

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Journal:  Sci Rep       Date:  2020-04-28       Impact factor: 4.379

3.  Neutrophil Gelatinase-Associated Lipocalin 2 Accelerates Hypoxia-Induced Endothelial Cell Injury via eNOS/NRF2 Signalling.

Authors:  Yang Gu; Wei Sun; Z Huo Xu; Jing Wang; Xiao Hu; Zhou-Zhou Lu; Xi-Wen Zhang
Journal:  Cell J       Date:  2021-08-29       Impact factor: 2.479

4.  Serum Biomarkers of Cardiovascular Remodelling Reflect Extra-Valvular Cardiac Damage in Patients with Severe Aortic Stenosis.

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5.  Plasma neutrophil gelatinase-associated lipocalin levels are associated with the presence and severity of coronary heart disease.

Authors:  Chao Li; Zheng Zhang; Yu Peng; Hanxiang Gao; Yongxiang Wang; Jing Zhao; Chenliang Pan
Journal:  PLoS One       Date:  2019-08-06       Impact factor: 3.240

  5 in total

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