Diagnostic value of novel biomarkers for heart failure

Huang, Zenan; Zhong, Jianhui; Ling, Yesheng; Zhang, Y; Wu, Lin; Tang, Lei-lei; Liu, J; Li, S

doi:10.1007/s00059-018-4702-6

Cited by 20 publications

(17 citation statements)

References 64 publications

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“…Although the usefulness of Gal‐3 as a biomarker of heart disease has gained support from the findings of many clinical studies, more recent studies have revealed inconsistency, questioning the usefulness of Gal‐3 in predicting MACE, even though higher blood levels of Gal‐3 are consistent findings in almost all reports (Abou Ezzeddine et al, ; Arangalage et al, ; Begg et al, ; Besler et al, ; de Boer et al, ; Huang et al, ; Jansen et al, ; Lopez et al, ; Stoltze Gaborit et al, ). For instance, in studies on community cohorts or HF patients, multiple biomarkers were employed and compared for individual prognostic power and Gal‐3 was found to have insignificant clinical value (Bayes‐Genis et al, ; de Boer et al, ).…”

Section: Gal‐3 As a Biomarker Of Heart Disease: Influence Of β‐Adrenomentioning

confidence: 99%

β‐Adrenoceptor activation affects galectin‐3 as a biomarker and therapeutic target in heart disease

Zhao

Nguyen

et al. 2019

British J Pharmacology

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Myocardial fibrosis is a key histopathological component that drives the progression of heart disease leading to heart failure and constitutes a therapeutic target. Recent preclinical and clinical studies have implicated galectin‐3 (Gal‐3) as a pro‐fibrotic molecule and a biomarker of heart disease and fibrosis. However, our knowledge is poor on the mechanism(s) that determine the blood level or regulate cardiac expression of Gal‐3. Recent studies have demonstrated that enhanced β‐adrenoceptor activity is a determinant of both circulating concentration and cardiac expression of Gal‐3. Pharmacological or transgenic activation of β‐adrenoceptors leads to increased blood levels of Gal‐3 and up‐regulated cardiac Gal‐3 expression, effect that can be reversed with the use of β‐adrenoceptor antagonists. Conversely, Gal‐3 gene deletion confers protection against isoprenaline‐induced cardiotoxicity and fibrogenesis. At the transcription level, β‐adrenoceptor stimulation activates cardiac mammalian sterile‐20‐like kinase 1, a pivotal kinase of the Hippo signalling pathway, which is associated with Gal‐3 up‐regulation. Recent studies have suggested a role for the β‐adrenoceptor‐Hippo signalling pathway in the regulation of cardiac Gal‐3 expression thereby contributing to the onset and progression of heart disease. This implies a therapeutic potential of the suppression of Gal‐3 expression. In this review, we discuss the effects of β‐adrenoceptor activity on Gal‐3 as a biomarker and causative mediator in the setting of heart disease and point out pivotal knowledge gaps. Linked Articles This article is part of a themed section on Adrenoceptors—New Roles for Old Players. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.14/issuetoc

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Section: Gal‐3 As a Biomarker Of Heart Disease: Influence Of β‐Adrenomentioning

confidence: 99%

β‐Adrenoceptor activation affects galectin‐3 as a biomarker and therapeutic target in heart disease

Zhao

Nguyen

et al. 2019

British J Pharmacology

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“…Newer biomarkers, such as mid regional pro-adrenomedullin (MR-proADM) and sST2 hold significant potential for prediction and diagnosis of HF, and may augment the use of NP measurement [ 7 , 18 , 53 , 54 ]. MR-proADM and sST2 production are influenced, in part, by the hemodynamics of a fluid-overloaded state in HF, including endothelial shear stress [ 55 ], myocyte strain [ 56 , 57 ] and alveolar strain in pulmonary edema [ 58 ].…”

Section: Discussionmentioning

confidence: 99%

Inflammatory Markers and Incident Heart Failure in Older Men: the Role of Nt-Probnp

et al. 2021

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Aim: To determine the relationship between baseline inflammation (CRP and IL-6) with natriuretic peptide (NP) activity (measured by NT-proBNP) and incident heart failure (HF) in older men. Methods & results: In the British Regional Heart Study, 3569 men without prevalent myocardial infarction or HF were followed for mean 16.3 years; 327 developed HF. Baseline CRP and IL-6 were significantly and positively associated with NT-proBNP. Those in the highest CRP & IL-6 quartiles had elevated risk of HF after age and BMI adjustment (HR = 1.42 [1.01,1.98] and 1.71 [1.24,2.37] respectively), which markedly attenuated after NT-proBNP adjustment (HR = 1.15 [0.81,1.63] and 1.25 [0.89,1.75] respectively). Conclusion: NP activity is associated with pro-inflammatory biomarkers and may explain the link between inflammation and incident HF.

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“…However, Vazquez-Montes MDLA et al (2020) [85] reported that MR-proADM was not superior to NT-proBNP in the prediction of chronic HF. In a recently published meta-analysis comparing the diagnostic value of novel biomarkers for HF, Huang Z. et al (2020) [86] revealed that MR-proADM had a poor discriminative value to confirm or exclude HF. Whether a serial measurement of MR-proADM is able to reclassify a risk of death due to HF individually depending on the presence of other CV risk factors including T2DM is not yet fully understood, because no correlation between T2DM and levels of MR-proADM has been found for mortality or HF hospitalization [87].…”

Section: Adrenomedullinmentioning

confidence: 99%

Heart Failure and Diabetes Mellitus: Biomarkers in Risk Stratification and Prognostication

et al. 2021

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Heart failure (HF) and type 2 diabetes mellitus (T2DM) have a synergistic effect on cardiovascular (CV) morbidity and mortality in patients with established CV disease (CVD). The aim of this review is to summarize the knowledge regarding the discriminative abilities of conventional and novel biomarkers in T2DM patients with established HF or at higher risk of developing HF. While conventional biomarkers, such as natriuretic peptides and high-sensitivity troponins demonstrate high predictive ability in HF with reduced ejection fraction (HFrEF), this is not the case for HF with preserved ejection fraction (HFpEF). HFpEF is a heterogeneous disease with a high variability of CVD and conventional risk factors including T2DM, hypertension, renal disease, older age, and female sex; therefore, the extrapolation of predictive abilities of traditional biomarkers on this population is constrained. New biomarker-based approaches are disputed to be sufficient for improving risk stratification and the prediction of poor clinical outcomes in patients with HFpEF. Novel biomarkers of biomechanical stress, fibrosis, inflammation, oxidative stress, and collagen turn-over have shown potential benefits in determining prognosis in T2DM patients with HF regardless of natriuretic peptides, but their role in point-to-care and in routine practice requires elucidation in large clinical trials.

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Diagnostic value of novel biomarkers for heart failure

Abstract: The overall diagnostic accuracy of copeptin, galectin-3, hs-cTnT, MR-proANP, and ST2 was relatively good. MR-proADM had a poor capacity to confirm or exclude HF. Improving the diagnostic accuracy of HF by a combination of biomarkers could be considered in the future.

Cited by 20 publications

References 64 publications

β‐Adrenoceptor activation affects galectin‐3 as a biomarker and therapeutic target in heart disease

β‐Adrenoceptor activation affects galectin‐3 as a biomarker and therapeutic target in heart disease

Inflammatory Markers and Incident Heart Failure in Older Men: the Role of Nt-Probnp

Heart Failure and Diabetes Mellitus: Biomarkers in Risk Stratification and Prognostication

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