As a reminder iron deficiency (ID) in HF is commonly defined as either:
- ferritin < 100 or
- ferritin < 300 and TSAT < 20%
Acute Heart Failure
The AFFIRM-AHF multicentre RCT showed that treatment with IV ferric carboxymaltose (FCM) initiated in hospital decreased 1-yr hospitalizations (by 25%) but not mortality in patients with ADHF requiring furosemide 40 mg IV or greater and LVEF < 50%.
Additional data shows that other metrics such as QOL is significantly improved with this approach between 4-24 weeks of treatment initiation as compared to placebo.
Stable Heart Failure
A 2019 Am. J. Med meta-analysis by Zhou et al. of 10 studies shows that IV iron in stable HFrEF:
- Reduced hospitalizations for worsening HF (5.3 versus 14.5 percent; odds ratio 3.9, 95% CI 0.19-0.80)
- Improved New York Heart Association (NYHA) class (weighted mean difference [WMD] -0.68, 95% CI -1.13 to -0.24)
- Improved six-minute walk test (WMD 32.7, 95% CI 4.47-60.83)
- Improved left ventricular ejection fraction (LVEF; WMD 3.81, 95% CI 1.11-6.51)
- Improved serum markers of HF and inflammation (N-terminal pro-B-type natriuretic peptide and C-reactive protein, respectively)
- These patients were generally NYHA II+ and LVEF <40-50%.
FAIR-HF (NEJM 2009) showed that IV iron therapy in patients with symptomatic HFrEF and concomitant iron deficiency (ferritin <100 ug/L or ferritin 100-299 ug/L with iron saturation < 20%) with mild or no anemia (hemoglobin 9.5-13.5 g/dL) resulted in symptomatic improvement or gains in functional status.
Takeaways
- In ADHF, you should check for ID and consider treating with IV iron to reduce symptoms and hospitalization. This does not impact mortality.
- You can consider using IV ferric gluconate over several days to accelerate this process and potentially avoid outpatient IV therapy. Source
- In stable HF(r)EF, IV iron reduces symptoms and biochemical/echocardiographic markers of HF and inflammation. PO iron does not achieve this.
- Stop iron replacement when ID is resolved as excess iron is cardiotoxic