Abstract
The use of circulating biomarkers for heart failure (HF) is engrained in contemporary cardiovascular practice and provides objective information about various pathophysiological pathways associated with HF syndrome. However, biomarker profiles differ considerably among women and men. For instance, in the general population, markers of cardiac stretch (natriuretic peptides) and fibrosis (galectin-3) are higher in women, whereas markers of cardiac injury (cardiac troponins) and inflammation (sST2) are higher in men. Such differences may reflect sex-specific pathogenic processes associated with HF risk, but may also arise as a result of differences in sex hormone profiles and fat distribution. From a clinical perspective, sex-related differences in biomarker levels may affect the objectivity of biomarkers in HF management because what is considered to be ‘normal’ in one sex may not be so in the other. The objectives of this review are, therefore: (i) to examine the sex-specific dynamics of clinically relevant HF biomarkers in the general population, as well as in HF patients; (ii) to discuss the overlap between sex-related and obesity-related effects, and (iii) to identify knowledge gaps to stimulate research on sex-related differences in HF.
| Original language | English |
|---|---|
| Pages (from-to) | 775-788 |
| Number of pages | 14 |
| Journal | European Journal of Heart Failure |
| Volume | 22 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - 1 May 2020 |
| Externally published | Yes |
Bibliographical note
Funding Information:This work was supported by the Netherlands Heart Foundation (CVON SHE-PREDICTS-HF, grant no. 2017–21). The authors acknowledge further support from the Netherlands Heart Foundation (CVON DOSIS, grant no. 2014–40, and CVON RED-CVD, grant no. 2017–11), the Innovational Research Incentives Scheme of the Netherlands Organization for Scientific Research (NWO VIDI, grant no. 917.13.350) and the European Research Council (ERC CoG 818715, SECRETE-HF). Conflict of interest: the University Medical Centre Groningen, which employs N.S., L.M.G.M. and R.A.dB., has received research grants and/or fees from AstraZeneca, Abbott, Bristol-Myers Squibb, Novartis, Novo Nordisk and Roche. R.A.dB. has received personal fees from Abbott, AstraZeneca, Novartis and Roche. J.E.H. has received research supplies from EcoNugenics. The other authors have nothing to disclose.
Funding Information:
This work was supported by the Netherlands Heart Foundation (CVON SHE‐PREDICTS‐HF, grant no. 2017–21). The authors acknowledge further support from the Netherlands Heart Foundation (CVON DOSIS, grant no. 2014–40, and CVON RED‐CVD, grant no. 2017–11), the Innovational Research Incentives Scheme of the Netherlands Organization for Scientific Research (NWO VIDI, grant no. 917.13.350) and the European Research Council (ERC CoG 818715, SECRETE‐HF).
Publisher Copyright:
© 2020 The Authors. European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.
