Heart failure & cardiomyopathies
Inflammatory and catabolic activity mediate the association of plasma β-hydroxybutyrate and mortality in heart failure
Authors' conclusion
Elevated β-hydroxybutyrate levels predict mortality in chronic HF, independent of established risk factors. Proteomic analysis links elevated β-hydroxybutyrate to heightened inflammation and catabolism, and these pathways largely mediated the association between β-hydroxybutyrate and mortality. These findings suggest that elevated ketone bodies may reflect underlying metabolic stress in patients at risk of adverse outcome.
Study context
- Population
- Patients with heart failure (HF) from the BIOSTAT-CHF cohortpatients with HF with plasma β-hydroxybutyrate measured
- Participants
- 478 patients
- Exposure
- Association of plasma β-hydroxybutyrate with mortality and HF hospitalization
- Outcome
- Cohort characteristics
Main finding
As reported in the abstract
Male patients
64.2%
Observational data: associations, not effects.
Further findings
| Outcome | Estimate | |
|---|---|---|
| Mortality per doubling of β-hydroxybutyrateEvery doubling of β-hydroxybutyrate · 36.4% increase in mortality | unadjusted hazard ratio 1.364 (95% CI 1.089–1.707) | |
| Mortality per doubling of β-hydroxybutyrateEvery doubling of β-hydroxybutyrate · after accounting for known risk factors | adjusted hazard ratio 1.389 (95% CI 1.150–1.677) | |
| 0.512Ratio (log scale) |
Correlates of elevated β-hydroxybutyrate
- Independently associated with higher heart rate, lower iron levels, and lower body mass index
Differential expression and ingenuity pathway analyses
- Higher β-hydroxybutyrate associated with upregulation of pathways associated with acute inflammation and cachexia; lipogenic and anabolic pathways down-regulated
Multiple mediation analysis
- Share of association between β-hydroxybutyrate and mortality explained by these pathways
- 76%
Original publication
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