AI Article Synopsis
- Myo-inositol is elevated in patients with heart failure (HF), particularly in those with heart failure with preserved ejection fraction (HFpEF), and is associated with negative clinical outcomes.
- The study measured plasmatic myo-inositol levels in large cohorts from Belgium and Canada, revealing significant increases in HF patients compared to those without.
- Elevated myo-inositol levels correlate with worsening kidney function and cardiac markers, suggesting a potential role in the development and progression of HFpEF.
Article Abstract
Background: The metabolic environment plays a crucial role in the development of heart failure (HF). Our prior research demonstrated that myo-inositol, a metabolite transported by the sodium-myo-inositol co-transporter 1 (SMIT-1), can induce oxidative stress and may be detrimental to heart function. However, plasmatic myo-inositol concentration has not been comprehensively assessed in large cohorts of patients with heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF).
Methods: Plasmatic myo-inositol levels were measured using mass spectrometry and correlated with clinical characteristics in no HF subjects and patients with HFrEF and HFpEF from Belgian (male, no HF, 53%; HFrEF, 84% and HFpEF, 40%) and Canadian cohorts (male, no HF, 51%; HFrEF, 92% and HFpEF, 62%).
Findings: Myo-inositol levels were significantly elevated in patients with HF, with a more pronounced increase observed in the HFpEF population of both cohorts. After adjusting for age, sex, body mass index, hypertension, diabetes, and atrial fibrillation, we observed that both HFpEF status and impaired kidney function were associated with elevated plasma myo-inositol. Unlike HFrEF, abnormally high myo-inositol (≥69.8 μM) was linked to unfavourable clinical outcomes (hazard ratio, 1.62; 95% confidence interval, [1.05-2.5]) in patients with HFpEF. These elevated levels were correlated with NTproBNP, troponin, and cardiac fibrosis in this subset of patients.
Interpretation: Myo-inositol is a metabolite elevated in patients with HF and strongly correlated to kidney failure. In patients with HFpEF, high myo-inositol levels predict poor clinical outcomes and are linked to markers of cardiac adverse remodelling. This suggests that myo-inositol and its transporter SMIT1 may have a role in the pathophysiology of HFpEF.
Funding: BECAME-HF was supported by Collaborative Bilateral Research Program Québec - Wallonie-Brussels Federation.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11363489 | PMC |
| http://dx.doi.org/10.1016/j.ebiom.2024.105264 | DOI Listing |
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