Circulating heart failure biomarkers beyond natriuretic peptides: review from the Biomarker Study Group of the Heart Failure Association (<scp>HFA</scp>), European Society of Cardiology (<scp>ESC</scp>)

Meijers, Wouter C.; Bayés‐Genís, Antoni; Mebazaa, Alexandre; Bauersachs, Johann; Cleland, John G.F.; Coats, Andrew J.S.; Januzzi, James L.; Maisel, Alan S.; McDonald, Kenneth; Mueller, Thomas; Richards, A. Mark; Seferović, Petar; Mueller, Christian; Boer, Rudolf A. de

doi:10.1002/ejhf.2346

Cited by 85 publications

(99 citation statements)

References 222 publications

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“…IL-33 was thought to exert beneficial actions via ST2L that are related to cardiac repair or attenuation of adverse cardiac remodeling ( 15 ). Acting as a soluble truncated form of ST2L, sST2 functions as a decoy receptor for IL-33 and thereby attenuates beneficial effects of IL-33/ST2L signaling in the context of the heart ( 18 ). Previous clinical and experimental studies showed a strong correlation between ST2 and HF ( 19 ).…”

Section: Discussionmentioning

confidence: 99%

Exploring the Causal Effects of Circulating ST2 and Galectin-3 on Heart Failure Risk: A Mendelian Randomization Study

Wang

Zhu

et al. 2022

Front. Cardiovasc. Med.

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BackgroundHeart failure (HF), primarily caused by conditions such as coronary heart disease or cardiomyopathy, is a global health problem with poor prognosis and heavy burden on healthcare systems. As biomarkers of myocardial injury and fibrosis, suppression of tumorigenicity 2 (ST2) and galectin-3 were recommended for prognosis stratification in HF guidelines. However, the causality between these two mediators and HF remains obscure. This study aimed to explore the causal relationship of genetically determined ST2 and galectin-3 with the risk of HF.MethodsWe used the two-sample Mendelian randomization (MR) method, incorporating available genome-wide association summary statistics, to investigate the causal association of ST2 and galectin-3 with HF risk. We applied inverse-variance weighted analysis as the main method of analysis.ResultsIn our final MR analysis, 4 single-nucleotide polymorphisms (SNPs) of ST2 and galectin-3, respectively, were identified as valid instrumental variables. Fixed-effect inverse variance weighted (IVW) analysis indicated that genetically predicted ST2 and galectin-3 were not causally associated with HF risk 3. [odds ratio (OR) = 0.9999, 95% confidence interval [CI] = 0.9994–1.0004, p = 0.73; OR = 1.0002, 95% CI = 0.9994–1.0010, p = 0.60, respectively]. These findings were robust in sensitivity analyses, including MR-Egger regression and leave-one-out analysis.ConclusionThis MR study provided no evidence for the causal effects of ST2 and galectin-3 on HF risk.

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Section: Discussionmentioning

confidence: 99%

Exploring the Causal Effects of Circulating ST2 and Galectin-3 on Heart Failure Risk: A Mendelian Randomization Study

Wang

Zhu

et al. 2022

Front. Cardiovasc. Med.

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“…Moreover, natriuretic peptides are elevated also in other conditions, such as ischaemic heart disease and pulmonary embolism, not being a specific HF biomarker [71,72]. Baseline high sensitivity cardiac troponin T and its increase are associated with mortality, disease worsening and acute decompensation, in HF patients [72][73][74][75][76][77][78][79]. Sensitive contemporary cardiac troponin I is also a predictive biomarker of all-cause and cardiovascular mortality, in HF outpatients [73].…”

Section: Heart Failure Pathophysiology Paradigm: What Is Beyond Left ...mentioning

confidence: 99%

Do the Current Guidelines for Heart Failure Diagnosis and Treatment Fit with Clinical Complexity?

Severino

D’Amato

Prosperi

et al. 2022

JCM

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Heart failure (HF) is a clinical syndrome defined by specific symptoms and signs due to structural and/or functional heart abnormalities, which lead to inadequate cardiac output and/or increased intraventricular filling pressure. Importantly, HF becomes progressively a multisystemic disease. However, in August 2021, the European Society of Cardiology published the new Guidelines for the diagnosis and treatment of acute and chronic HF, according to which the left ventricular ejection fraction (LVEF) continues to represent the pivotal parameter for HF patients’ evaluation, risk stratification and therapeutic management despite its limitations are well known. Indeed, HF has a complex pathophysiology because it first involves the heart, progressively becoming a multisystemic disease, leading to multiorgan failure and death. In these terms, HF is comparable to cancer. As for cancer, surviving, morbidity and hospitalisation are related not only to the primary neoplastic mass but mainly to the metastatic involvement. In HF, multiorgan involvement has a great impact on prognosis, and multiorgan protective therapies are equally important as conventional cardioprotective therapies. In the light of these considerations, a revision of the HF concept is needed, starting from its definition up to its therapy, to overcome the old and simplistic HF perspective.

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“…Interestingly, GDF15 levels have been reported to be elevated in patients with HF and negatively associated with clinical outcome and mortality [ 24 , 25 , 26 , 27 ]. Higher levels of GDF15 were found in patients with HF who were older and with higher New York Heart Association functional class and had lower body mass index and exercise capacity [ 27 ].…”

Section: Introductionmentioning

confidence: 99%

Neutralization of GDF15 Prevents Anorexia and Weight Loss in the Monocrotaline-Induced Cardiac Cachexia Rat Model

Albuquerque

Chen

Hirenallur-Shanthappa

et al. 2022

Cells

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Growth and differentiation factor 15 (GDF15) is a cytokine reported to cause anorexia and weight loss in animal models. Neutralization of GDF15 was efficacious in mitigating cachexia and improving survival in cachectic tumor models. Interestingly, elevated circulating GDF15 was reported in patients with pulmonary arterial hypertension and heart failure, but it is unclear whether GDF15 contributes to cachexia in these disease conditions. In this study, rats treated with monocrotaline (MCT) manifested a progressive decrease in body weight, food intake, and lean and fat mass concomitant with elevated circulating GDF15, as well as development of right-ventricular dysfunction. Cotreatment of GDF15 antibody mAb2 with MCT prevented MCT-induced anorexia and weight loss, as well as preserved lean and fat mass. These results indicate that elevated GDF15 by MCT is causal to anorexia and weight loss. GDF15 mAb2 is efficacious in mitigating MCT-induced cachexia in vivo. Furthermore, the results suggest GDF15 inhibition is a potential therapeutic approach to alleviate cardiac cachexia in patients.

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Circulating heart failure biomarkers beyond natriuretic peptides: review from the Biomarker Study Group of the Heart Failure Association (HFA), European Society of Cardiology (ESC)

Cited by 85 publications

References 222 publications

Exploring the Causal Effects of Circulating ST2 and Galectin-3 on Heart Failure Risk: A Mendelian Randomization Study

Exploring the Causal Effects of Circulating ST2 and Galectin-3 on Heart Failure Risk: A Mendelian Randomization Study

Do the Current Guidelines for Heart Failure Diagnosis and Treatment Fit with Clinical Complexity?

Neutralization of GDF15 Prevents Anorexia and Weight Loss in the Monocrotaline-Induced Cardiac Cachexia Rat Model

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