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The Influence of Cardiovascular Medications on Iron Metabolism in Patients with Heart Failure
Oana Sirbu1, Victorita Sorodoc2, Irina M Jaba3
1Department of Internal Medicine, Gr. T. Popa University of Medicine and Pharmacy, 700115 Iasi, Romania.
Insights
Heart failure medications like beta blockers, ACE inhibitors, and calcium-channel blockers may affect iron metabolism. Close monitoring of iron deficiency is recommended for patients with heart failure on these drugs.
Area of Science:
- Cardiology
- Pharmacology
- Hematology
Background:
- Anemia in heart failure (HF) has complex causes, potentially involving drug therapies.
- Understanding drug effects on iron metabolism in HF is crucial.
Purpose of the Study:
- To assess the impact of beta blockers, ACE inhibitors, and calcium-channel blockers on iron metabolism in HF patients.
- To investigate drug-induced iron deficiency in heart failure.
Main Methods:
- Prospective observational study.
- Included HF patients with iron deficiency (ferritin <100 μg/L or 100-300 μg/L with TSAT <20%).
- Excluded anemia from other known causes.
Main Results:
- Beta-blocker use correlated significantly with ferritin levels (p=0.02).
- Calcium-channel blocker users had lower iron, hemoglobin, and hematocrit.
- ACE inhibitor use showed an indirect correlation with hematocrit (p=0.04).
Conclusions:
- This study adds evidence for drug-induced iron deficiency in heart failure.
- Clinicians should monitor iron deficiency parameters in HF patients due to potential drug impacts.
Abstract:
Background and objectives: The etiology of anemia associated with heart failure is not fully understood, but there are data suggesting the involvement of multiple mechanisms, including various drug therapies used in patients with heart failure. Our primary objective was to evaluate the impact of beta blockers, angiotensin-converting enzyme inhibitors, and calcium-channel blockers on iron metabolism in patients with heart failure. Materials and Methods: This was a prospective observational study that included patients diagnosed with heart failure and iron deficiency (defined by ferritin <100 μg/L, or 100-300 μg/L with transferrin saturation <20%). Patients with anemia secondary to a known cause were excluded. Results: We found a statistically significant correlation between beta-blocker treatment and ferritin values (p = 0.02). Iron, hemoglobin, and hematocrit levels were significantly lower in the patients using calcium-channel blockers than those who were not. We also found a statistically significant indirect correlation (p = 0.04) between the use of angiotensin-converting enzyme inhibitors and hematocrit levels. Conclusion: The contribution of our study arises from the additional data regarding the drug-induced etiology of iron deficiency. Practitioners should be aware of the potential impact of therapeutic recommendations and this should imply a close monitoring of the biochemical parameters of iron deficiency in this category of patients.
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