Introduction and objectives: Iron deficiency (ID) is a well-known prognostic marker in heart failure (HF), independent of anemia. However, its impact in acute coronary syndromes (ACSs) is not well established.
Methods: This is a retrospective analysis of patients admitted with ACS from January to December 2019. The population was evaluated according to basal characteristics and divided in two groups, with or without ID, compared according to several variables, namely demographic, index hospitalization, comorbidities, analytical and echocardiographic. We determined their predictive value on the occurrence of hemorrhage or need for red blood cell transfusion, all-cause hospitalizations, and all-cause death.
Results: We included 287 patients, with median age 66 (interquartile range [IQR] 21) years and 72% male. ID was present in 48% of patients. Most presented with ST-elevation myocardial infarction (STEMI) (57%), and 13% were admitted in Killip-Kimball class III or IV. Almost 40% had a left ventricle ejection fraction < 50% on admission. Patients with non-ST-elevation myocardial infarction presented more frequently with ID, compared with patients with STEMI. Of note, 33% of patients with ID had concomitant anemia. During a median follow-up of 28 (IQR 7) months, 10% had an urgent care admission for HF, 7% were hospitalized for HF, and 18% died. There was a significantly higher rate of emergency department admissions for HF in the group with ID. Age, anemia, and NT-proBNP levels predicted the occurrence of all-cause death, with ID having no impact on none of the evaluated events.
Conclusion: ID was prevalent in patients with ACS, affecting almost half of the population. In the acute setting of an ACS, anemia seems to have a greater impact on mortality and the role of ID in promoting HF needs further investigation.
Keywords: acute coronary syndrome; heart failure; iron deficiency.
Copyright © 2025 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of PBJ-Associação Porto Biomedical/Porto Biomedical Society.