Role of Non-Transferrin-Bound Iron in the pathogenesis of cardiotoxicity in patients with ST-elevation myocardial infarction assessed by Cardiac Magnetic Resonance Imaging. (15th November 2015)

• Record Type: Journal Article
• Authors: Roghi, Alberto; Poggiali, Erika; Duca, Lorena; Mafrici, Antonio; Pedrotti, Patrizia; Paccagnini, Stefania; Brenna, Sergio; Galli, Alessio; Consonni, Dario; Cappellini, Maria Domenica
• Is Part Of: International journal of cardiology. Volume 199(2015)
• Page Start: 326
• Page End: 332
• Publication Date: 2015-11-15
• Subjects: Myocardial infarction -- Non-Transferrin Bound Iron -- Iron -- Reperfusion injury; Cardiology -- Periodicals; Electronic journals; 616.12
• DOI: 10.1016/j.ijcard.2015.07.056
• Languages: English
• ISSNs: 0167-5273

Abstract

Abstract: Background: Hereditary hemochromatosis, thalassemia and myelodysplastic syndromes represent disease models with evidence of iron-related heart failure. Non-Transferrin Bound Iron (NTBI) induces cardiac toxicity through the production of reactive oxygen species and lipid peroxidation. In ST-elevation acute myocardial infarction (STEMI) with evidence of microvascular obstruction (MVO) and hemorrhage (HEM), HEM may be a source of iron-related cardiac toxicity through NTBI and pro-inflammatory mediators. Aim of the study: The study aims to assess NTBI in patients with STEMI and its possible relationship with MVO and HEM. Methods and results: NTBI, LPO–Malondialdehyde (MDA) and interleukin-6 (IL-6) were assessed in 15 patients with STEMI immediately before primary percutaneous coronary intervention (PPCI) and at 3, 6, 9, 12, and 24 h post-PPCI. Cardiac Magnetic Resonance (CMR) was performed at 5 days and 6 months after STEMI. Myocardial edema and HEM were assessed by T2 and T2* mapping. MVO and necrotic area were assessed by early and late gadolinium enhancement (LGE). NTBI was detected in 13/15 patients with the highest values in 4 patients with evidence of MVO and HEM. NTBI levels were significantly related to CK-MB and troponin T values. NTBI kinetics appeared to be different in patients with MVO and HEM (7/15 patients), with a peak value at 6 h after PCI, in comparison with those with no evidence of MVO and HEM, in whom NTBI values were lower and remained indeterminable after the first 24 h. Conclusions: The detection of elevated NTBI values in patients with STEMI, MVO and HEM suggests a possible role of iron cardiotoxicity in myocardial damage.