Implications of Iron Deficiency in STEMI Patients and in a Murine Model of Myocardial Infarction
Javier Inserte, José A. Barrabés, David Aluja, Imanol Otaegui, Jordi Bañeras, Laura Castellote, Ana Sánchez, José F. Rodríguez‐Palomares, Víctor Pineda, Elisabet Miró‐Casas, Laia Milà, Rosa-María Lidón, Antonia Sambola, Filipa Valente, Agnès Rafecas, Marisol Ruiz‐Meana, Antonio Rodríguez‐Sinovas, Begoña Benito, Irene Buera, Sara Delgado‐Tomás, David Benéitez, Ignacio Ferreira‐González
Abstract
In patients with a first anterior ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention, iron deficiency (ID) was associated with larger infarcts, more extensive microvascular obstruction, and higher frequency of adverse left ventricular remodeling as assessed by cardiac magnetic resonance imaging. In mice, an ID diet reduced the activity of the endothelial nitric oxide synthase/soluble guanylate cyclase/protein kinase G pathway in association with oxidative/nitrosative stress and increased infarct size after transient coronary occlusion. Iron supplementation or administration of an sGC activator before ischemia prevented the effects of the ID diet in mice. Not only iron excess, but also ID, may have deleterious effects in the setting of ischemia and reperfusion.