Iron Deficiency and Bone Metabolism in Heart Failure
Ryosuke Sato, Tania Garfias-Veitl, Angelika Hafke, Andreas Fischer, Guglielmo Fibbi, Mirela Vatic, Breno Wozne, Constanze Schmidt, Jürgen Kolos, Max Diesner, Thomas Bernd Dschietzig, Goran Loncar, John G F Cleland, Stefan D Anker, Stephan von HaehlingAbstract
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.