Role of Non-Transferrin-Bound Iron in the pathogenesis of cardiotoxicity in patients with ST-elevation myocardial infarction assessed by Cardiac Magnetic Resonance Imaging

Alberto Roghi, Erika Poggiali, Lorena Duca, Antonio Mafrici, Patrizia Pedrotti, Stefania Paccagnini, Sergio Brenna, Alessio Galli, Dario Consonni, Maria Domenica Cappellini

Research output: Contribution to journalArticle

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.

Original languageEnglish
Pages (from-to)326-332
Number of pages7
JournalInternational Journal of Cardiology
Volume199
DOIs
Publication statusPublished - Sep 15 2015

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Iron
Magnetic Resonance Imaging
Hemorrhage
Percutaneous Coronary Intervention
ST Elevation Myocardial Infarction
Cardiotoxicity
Troponin T
Thalassemia
Hemochromatosis
Myelodysplastic Syndromes
Gadolinium
Malondialdehyde
Lipid Peroxidation
Interleukin-6
Reactive Oxygen Species
Edema
Magnetic Resonance Spectroscopy
Heart Failure

Keywords

  • Iron
  • Myocardial infarction
  • Non-Transferrin Bound Iron
  • Reperfusion injury

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Role of Non-Transferrin-Bound Iron in the pathogenesis of cardiotoxicity in patients with ST-elevation myocardial infarction assessed by Cardiac Magnetic Resonance Imaging. / Roghi, Alberto; Poggiali, Erika; Duca, Lorena; Mafrici, Antonio; Pedrotti, Patrizia; Paccagnini, Stefania; Brenna, Sergio; Galli, Alessio; Consonni, Dario; Cappellini, Maria Domenica.

In: International Journal of Cardiology, Vol. 199, 15.09.2015, p. 326-332.

Research output: Contribution to journalArticle

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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.",
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T1 - Role of Non-Transferrin-Bound Iron in the pathogenesis of cardiotoxicity in patients with ST-elevation myocardial infarction assessed by Cardiac Magnetic Resonance Imaging

AU - Roghi, Alberto

AU - Poggiali, Erika

AU - Duca, Lorena

AU - Mafrici, Antonio

AU - Pedrotti, Patrizia

AU - Paccagnini, Stefania

AU - Brenna, Sergio

AU - Galli, Alessio

AU - Consonni, Dario

AU - Cappellini, Maria Domenica

PY - 2015/9/15

Y1 - 2015/9/15

N2 - 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.

AB - 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.

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KW - Myocardial infarction

KW - Non-Transferrin Bound Iron

KW - Reperfusion injury

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