Iron Deficiency Is Associated With Impaired Myocardial Reperfusion in ST‐Segment–Elevation Myocardial Infarction: Influence of the Definition Used

Abstract

Acute myocardial infarction; Iron deficiency; Reperfusion

Infarto agudo de miocardio; Deficiencia de hierro; Reperfusión

Infart agut de miocardi; Deficiència de ferro; Reperfusió

Background The role of iron deficiency (ID) in ST‐segment–elevation myocardial infarction (STEMI) remains unclear. This study aimed to assess whether ID is associated with impaired myocardial reperfusion in STEMI and whether this association is affected by ID definition. Methods We included 942 consecutive patients with STEMI successfully treated with primary percutaneous coronary intervention. ID was defined either as recommended by international guidelines or, alternatively, as ferritin <100 ng/mL, transferrin saturation <20%, or serum iron ≤13 μmol/L. In 595 patients, serum soluble transferrin receptor levels were measured. Impaired myocardial reperfusion was defined as lack of ST‐segment resolution ≥50% 60 to 90 minutes after percutaneous coronary intervention. Results ID prevalence varied across these definitions. Impaired reperfusion was present in 12.7% of patients without ID and 41.0% of those with ID defined by transferrin saturation <20% (P<0.001). This association was less pronounced for serum iron ≤13 μmol/L, weaker for guideline criteria, and absent for high (≥1.59 mg/L) soluble transferrin receptor levels or low ferritin. Transferrin saturation <20%, but not ferritin‐based criteria, was associated with poorer clinical course and left ventricular function and higher in‐hospital mortality and remained an independent predictor of impaired reperfusion after adjusting for baseline predictors and anemia. Conclusions ID defined by transferrin saturation <20% is strongly related to impaired ST resolution and predicts a worse in‐hospital outcome in patients with STEMI treated with primary percutaneous coronary intervention. The association of other ID criteria with myocardial reperfusion or with the clinical course is weaker or absent. The potential preventive or therapeutic strategies targeting ID in STEMI warrant further investigation.

This study was funded by Instituto de Salud Carlos III, Spain, through the projects AES PI16/00232 and AES PI23/00068 and the research network CIBERCV (CB16/11/00479), both co‐funded by European Regional Development Fund, and by the Sociedad Española de Cardiología y Fundación Española del Corazón (SEC/FEC‐INV‐BAS 23/11).