Iron Deficiency and Bone Metabolism in Heart Failure
Ryosuke Sato1,2, Tania Garfias-Veitl1,2, Angelika Hafke3
1Department of Cardiology and Pneumology, University Medical Center Göttingen, Göttingen, Germany.
Insights
Iron deficiency in heart failure patients is linked to higher bone mineral density, potentially due to altered FGF-23 and vitamin D levels. Further research into bone microstructure is recommended.
Area of Science:
- Cardiology
- Endocrinology
- Bone Metabolism
Background:
- Iron deficiency (ID) is prevalent in chronic heart failure (HF).
- ID may negatively impact bone metabolism in HF patients.
- The interplay between ID, bone mineral density (BMD), and specific biomarkers is not fully understood.
Purpose of the Study:
- To investigate the association between ID and BMD in chronic HF patients.
- To explore the potential mediating roles of fibroblast growth factor 23 (FGF-23) and 1,25-dihydroxy vitamin D (1,25(OH)2 vitamin D) in this relationship.
- To analyze data from the Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF) cohort.
Main Methods:
- Defined ID as transferrin saturation (TSAT) <20%.
- Analyzed BMD, serum FGF-23, and plasma 1,25(OH)2 vitamin D levels in 198 chronic HF patients.
- Utilized multivariable analyses to assess associations and potential mediation.
Main Results:
- A significant proportion of patients (29.8%) had ID (TSAT <20%).
- ID was associated with higher BMD (p=0.009) and a dose-response relationship was observed across TSAT quartiles (p for trend=0.0009).
- ID correlated with elevated FGF-23 and reduced 1,25(OH)2 vitamin D. Lower 1,25(OH)2 vitamin D was independently associated with higher BMD (aOR 0.54, p=0.002).
Conclusions:
- In chronic HF, ID (TSAT <20%) is linked to disturbed bone metabolism.
- Increased FGF-23 and decreased 1,25(OH)2 vitamin D may mediate this association.
- Further investigation into bone microstructure in HF patients with ID is warranted.
Aims:
Iron deficiency (ID) is common in chronic heart failure (HF) and may disturb bone metabolism.We investigated the association of ID with bone mineral density (BMD), and the potential mediating roles of fibroblast growth factor 23 (FGF-23) and 1,25-dihydroxy vitamin D (1,25(OH)2 vitamin D) in patients with chronic HF from the Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF).
Methods And Results:
ID was defined as a transferrin saturation (TSAT) <20%. Among 198 patients (69 [61-76] years, 80% men), TSAT was <20% in 29.8% and associated with higher BMD (1.25 vs. 1.20 g/cm2, p=0.009), with a graded dose-response across TSAT quartiles (p for trend=0.0009). ID was also associated with higher serum FGF-23 (pg/mL; adjusted β=0.20, p=0.0009) and lower plasma 1,25(OH)2 vitamin D (30 vs. 35 pg/mL, p=0.03). In multivariable analyses, both TSAT <20% (adjusted odds ratio (aOR) 3.45, p=0.01) and lower plasma 1,25(OH)2 vitamin D (aOR 0.54, p=0.002) were associated with BMD above sex-specific medians.
Conclusions:
In HF, a TSAT <20% is associated with disturbed bone metabolism, possibly mediated by increases in serum FGF-23 and reductions in 1,25(OH)2 vitamin D concentrations. Detailed analyses of bone microstructure in HF are warranted.
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