Relation between high levels of myeloperoxidase in the culprit artery and microvascular obstruction, infarct size and reverse remodeling in ST-elevation myocardial infarction

To better understand the role of myeloperoxidases (MPO) in microvascular obstruction (MO) phenomenon and infarct size (IS) using cardiac magnetic resonance (CMR) data in patients with acute myocardial infarction (AMI). 40 consecutive patients classified according to the median level of MPO in the cu...

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Vydáno v:PLOS ONE Ročník 12; číslo 7; s. e0179929
Hlavní autoři: Stamboul, Karim, Zeller, Marianne, Rochette, Luc, Cottin, Yves, Cochet, Alexandre, Leclercq, Thibault, Porot, Guillaume, Guenancia, Charles, Fichot, Marie, Maillot, Nicolas, Vergely, Catherine, Lorgis, Luc, Bugiardini, Raffaele
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States Public Library of Science (PLoS) 13.07.2017
Public Library of Science
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ISSN:1932-6203, 1932-6203
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Abstract To better understand the role of myeloperoxidases (MPO) in microvascular obstruction (MO) phenomenon and infarct size (IS) using cardiac magnetic resonance (CMR) data in patients with acute myocardial infarction (AMI). 40 consecutive patients classified according to the median level of MPO in the culprit artery. A CMR study was performed during the week following AMI and at 6 months, with late gadolinium enhancement sequences. Persistent MO was observed in the same proportion (50 vs. 65%, p = 0.728) between the low vs. high MPO group levels. However, the extent of the microvascular obstruction was significantly greater in the high-MPO group (6 (0-9) vs.16.5 (0-31), p = 0.027), together with a greater infarct size, and a trend towards a lower left ventricular ejection fraction (LVEF) (p = 0.054) at one week. CMR data at 6 months showed that reverse systolic remodeling was two fold more present in the low-MPO group (p = 0.058). Interestingly, the extent of MO (8.5 (6.5-31) vs. 4.1 (3-11.55), p = 0.042) and IS remained significantly greater (24.5 (9.75-35) vs. 7.5 (2.5-18.75), p = 0.022) in the high-MPO group. Moreover, MPO in the culprit artery appeared to correlate positively with MPO in non-culprit arteries and serum, and with troponin levels and peak CK. This patient-based study revealed in patients after AMI that high MPO levels in the culprit artery were associated with more severe microvascular obstruction and greater IS. These findings may provide new insights pathophysiology explanation for the adverse prognostic impact of MO.
AbstractList To better understand the role of myeloperoxidases (MPO) in microvascular obstruction (MO) phenomenon and infarct size (IS) using cardiac magnetic resonance (CMR) data in patients with acute myocardial infarction (AMI). 40 consecutive patients classified according to the median level of MPO in the culprit artery. A CMR study was performed during the week following AMI and at 6 months, with late gadolinium enhancement sequences. Persistent MO was observed in the same proportion (50 vs. 65%, p = 0.728) between the low vs. high MPO group levels. However, the extent of the microvascular obstruction was significantly greater in the high-MPO group (6 (0-9) vs.16.5 (0-31), p = 0.027), together with a greater infarct size, and a trend towards a lower left ventricular ejection fraction (LVEF) (p = 0.054) at one week. CMR data at 6 months showed that reverse systolic remodeling was two fold more present in the low-MPO group (p = 0.058). Interestingly, the extent of MO (8.5 (6.5-31) vs. 4.1 (3-11.55), p = 0.042) and IS remained significantly greater (24.5 (9.75-35) vs. 7.5 (2.5-18.75), p = 0.022) in the high-MPO group. Moreover, MPO in the culprit artery appeared to correlate positively with MPO in non-culprit arteries and serum, and with troponin levels and peak CK. This patient-based study revealed in patients after AMI that high MPO levels in the culprit artery were associated with more severe microvascular obstruction and greater IS. These findings may provide new insights pathophysiology explanation for the adverse prognostic impact of MO.
Main objective To better understand the role of myeloperoxidases (MPO) in microvascular obstruction (MO) phenomenon and infarct size (IS) using cardiac magnetic resonance (CMR) data in patients with acute myocardial infarction (AMI). Method 40 consecutive patients classified according to the median level of MPO in the culprit artery. A CMR study was performed during the week following AMI and at 6 months, with late gadolinium enhancement sequences. Results Persistent MO was observed in the same proportion (50 vs. 65%, p = 0.728) between the low vs. high MPO group levels. However, the extent of the microvascular obstruction was significantly greater in the high-MPO group (6 (0–9) vs.16.5 (0–31), p = 0.027), together with a greater infarct size, and a trend towards a lower left ventricular ejection fraction (LVEF) (p = 0.054) at one week. CMR data at 6 months showed that reverse systolic remodeling was two fold more present in the low-MPO group (p = 0.058). Interestingly, the extent of MO (8.5 (6.5–31) vs. 4.1 (3–11.55), p = 0.042) and IS remained significantly greater (24.5 (9.75–35) vs. 7.5 (2.5–18.75), p = 0.022) in the high-MPO group. Moreover, MPO in the culprit artery appeared to correlate positively with MPO in non-culprit arteries and serum, and with troponin levels and peak CK. Conclusion This patient-based study revealed in patients after AMI that high MPO levels in the culprit artery were associated with more severe microvascular obstruction and greater IS. These findings may provide new insights pathophysiology explanation for the adverse prognostic impact of MO.
To better understand the role of myeloperoxidases (MPO) in microvascular obstruction (MO) phenomenon and infarct size (IS) using cardiac magnetic resonance (CMR) data in patients with acute myocardial infarction (AMI).40 consecutive patients classified according to the median level of MPO in the culprit artery. A CMR study was performed during the week following AMI and at 6 months, with late gadolinium enhancement sequences.Persistent MO was observed in the same proportion (50 vs. 65%, p = 0.728) between the low vs. high MPO group levels. However, the extent of the microvascular obstruction was significantly greater in the high-MPO group (6 (0-9) vs.16.5 (0-31), p = 0.027), together with a greater infarct size, and a trend towards a lower left ventricular ejection fraction (LVEF) (p = 0.054) at one week. CMR data at 6 months showed that reverse systolic remodeling was two fold more present in the low-MPO group (p = 0.058). Interestingly, the extent of MO (8.5 (6.5-31) vs. 4.1 (3-11.55), p = 0.042) and IS remained significantly greater (24.5 (9.75-35) vs. 7.5 (2.5-18.75), p = 0.022) in the high-MPO group. Moreover, MPO in the culprit artery appeared to correlate positively with MPO in non-culprit arteries and serum, and with troponin levels and peak CK.This patient-based study revealed in patients after AMI that high MPO levels in the culprit artery were associated with more severe microvascular obstruction and greater IS. These findings may provide new insights pathophysiology explanation for the adverse prognostic impact of MO.
Main objective To better understand the role of myeloperoxidases (MPO) in microvascular obstruction (MO) phenomenon and infarct size (IS) using cardiac magnetic resonance (CMR) data in patients with acute myocardial infarction (AMI). Method 40 consecutive patients classified according to the median level of MPO in the culprit artery. A CMR study was performed during the week following AMI and at 6 months, with late gadolinium enhancement sequences. Results Persistent MO was observed in the same proportion (50 vs. 65%, p = 0.728) between the low vs. high MPO group levels. However, the extent of the microvascular obstruction was significantly greater in the high-MPO group (6 (0-9) vs.16.5 (0-31), p = 0.027), together with a greater infarct size, and a trend towards a lower left ventricular ejection fraction (LVEF) (p = 0.054) at one week. CMR data at 6 months showed that reverse systolic remodeling was two fold more present in the low-MPO group (p = 0.058). Interestingly, the extent of MO (8.5 (6.5-31) vs. 4.1 (3-11.55), p = 0.042) and IS remained significantly greater (24.5 (9.75-35) vs. 7.5 (2.5-18.75), p = 0.022) in the high-MPO group. Moreover, MPO in the culprit artery appeared to correlate positively with MPO in non-culprit arteries and serum, and with troponin levels and peak CK. Conclusion This patient-based study revealed in patients after AMI that high MPO levels in the culprit artery were associated with more severe microvascular obstruction and greater IS. These findings may provide new insights pathophysiology explanation for the adverse prognostic impact of MO.
To better understand the role of myeloperoxidases (MPO) in microvascular obstruction (MO) phenomenon and infarct size (IS) using cardiac magnetic resonance (CMR) data in patients with acute myocardial infarction (AMI).MAIN OBJECTIVETo better understand the role of myeloperoxidases (MPO) in microvascular obstruction (MO) phenomenon and infarct size (IS) using cardiac magnetic resonance (CMR) data in patients with acute myocardial infarction (AMI).40 consecutive patients classified according to the median level of MPO in the culprit artery. A CMR study was performed during the week following AMI and at 6 months, with late gadolinium enhancement sequences.METHOD40 consecutive patients classified according to the median level of MPO in the culprit artery. A CMR study was performed during the week following AMI and at 6 months, with late gadolinium enhancement sequences.Persistent MO was observed in the same proportion (50 vs. 65%, p = 0.728) between the low vs. high MPO group levels. However, the extent of the microvascular obstruction was significantly greater in the high-MPO group (6 (0-9) vs.16.5 (0-31), p = 0.027), together with a greater infarct size, and a trend towards a lower left ventricular ejection fraction (LVEF) (p = 0.054) at one week. CMR data at 6 months showed that reverse systolic remodeling was two fold more present in the low-MPO group (p = 0.058). Interestingly, the extent of MO (8.5 (6.5-31) vs. 4.1 (3-11.55), p = 0.042) and IS remained significantly greater (24.5 (9.75-35) vs. 7.5 (2.5-18.75), p = 0.022) in the high-MPO group. Moreover, MPO in the culprit artery appeared to correlate positively with MPO in non-culprit arteries and serum, and with troponin levels and peak CK.RESULTSPersistent MO was observed in the same proportion (50 vs. 65%, p = 0.728) between the low vs. high MPO group levels. However, the extent of the microvascular obstruction was significantly greater in the high-MPO group (6 (0-9) vs.16.5 (0-31), p = 0.027), together with a greater infarct size, and a trend towards a lower left ventricular ejection fraction (LVEF) (p = 0.054) at one week. CMR data at 6 months showed that reverse systolic remodeling was two fold more present in the low-MPO group (p = 0.058). Interestingly, the extent of MO (8.5 (6.5-31) vs. 4.1 (3-11.55), p = 0.042) and IS remained significantly greater (24.5 (9.75-35) vs. 7.5 (2.5-18.75), p = 0.022) in the high-MPO group. Moreover, MPO in the culprit artery appeared to correlate positively with MPO in non-culprit arteries and serum, and with troponin levels and peak CK.This patient-based study revealed in patients after AMI that high MPO levels in the culprit artery were associated with more severe microvascular obstruction and greater IS. These findings may provide new insights pathophysiology explanation for the adverse prognostic impact of MO.CONCLUSIONThis patient-based study revealed in patients after AMI that high MPO levels in the culprit artery were associated with more severe microvascular obstruction and greater IS. These findings may provide new insights pathophysiology explanation for the adverse prognostic impact of MO.
Main objective 40 consecutive patients classified according to the median level of MPO in the culprit artery. A CMR study was performed during the week following AMI and at 6 months, with late gadolinium enhancement sequences. Persistent MO was observed in the same proportion (50 vs. 65%, p = 0.728) between the low vs. high MPO group levels. However, the extent of the microvascular obstruction was significantly greater in the high-MPO group (6 (0-9) vs.16.5 (0-31), p = 0.027), together with a greater infarct size, and a trend towards a lower left ventricular ejection fraction (LVEF) (p = 0.054) at one week. CMR data at 6 months showed that reverse systolic remodeling was two fold more present in the low-MPO group (p = 0.058). Interestingly, the extent of MO (8.5 (6.5-31) vs. 4.1 (3-11.55), p = 0.042) and IS remained significantly greater (24.5 (9.75-35) vs. 7.5 (2.5-18.75), p = 0.022) in the high-MPO group. Moreover, MPO in the culprit artery appeared to correlate positively with MPO in non-culprit arteries and serum, and with troponin levels and peak CK. This patient-based study revealed in patients after AMI that high MPO levels in the culprit artery were associated with more severe microvascular obstruction and greater IS. These findings may provide new insights pathophysiology explanation for the adverse prognostic impact of MO.
Audience Academic
Author Cochet, Alexandre
Stamboul, Karim
Cottin, Yves
Maillot, Nicolas
Bugiardini, Raffaele
Rochette, Luc
Lorgis, Luc
Vergely, Catherine
Zeller, Marianne
Guenancia, Charles
Fichot, Marie
Leclercq, Thibault
Porot, Guillaume
AuthorAffiliation 3 Laboratory of Cerebro-Vascular Pathophysiology and epidemiology (PEC2), University of Burgundy, Dijon, France.University of Burgundy, Dijon, France
2 MRI Unit and LE2I UMR CNRS 6306, University Hospital, Dijon, France
1 Department of Cardiology, University Hospital, Bd de Lattre de Tassigny, Dijon Cedex, France
University of Bologna, ITALY
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Conseil Régional de Bourgogne
Service de radiologie et d'Imagerie médicale diagnostique et thérapeutique (CHU de Dijon) ; Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon)
Laboratoire Electronique, Informatique et Image [UMR6306] (Le2i) ; Université de Bourgogne (UB)-École Nationale Supérieure d'Arts et Métiers (ENSAM) ; Arts et Métiers Sciences et Technologies ; HESAM Université (HESAM)-HESAM Université (HESAM)-Arts et Métiers Sciences et Technologies ; HESAM Université (HESAM)-HESAM Université (HESAM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Centre National de la Recherche Scientifique (CNRS)
Fédération Francaise de Cardiologie (FFC)
Union Régionale des Caisses d'Assurance Maladie de Bourgogne (URCAM)
Université de Bourgogne (UB)
Association de Cardiologie de Bourgog
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Copyright COPYRIGHT 2017 Public Library of Science
2017 Stamboul et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Distributed under a Creative Commons Attribution 4.0 International License
2017 Stamboul et al 2017 Stamboul et al
Copyright_xml – notice: COPYRIGHT 2017 Public Library of Science
– notice: 2017 Stamboul et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
– notice: Distributed under a Creative Commons Attribution 4.0 International License
– notice: 2017 Stamboul et al 2017 Stamboul et al
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Issue 7
Keywords Acute Coronary Syndromes
Disease
Leukocyte
Mortality
Definition
Long-Term
Dimethylarginine
No-Reflow
Language English
License Distributed under a Creative Commons Attribution 4.0 International License: http://creativecommons.org/licenses/by/4.0
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Snippet To better understand the role of myeloperoxidases (MPO) in microvascular obstruction (MO) phenomenon and infarct size (IS) using cardiac magnetic resonance...
Main objective To better understand the role of myeloperoxidases (MPO) in microvascular obstruction (MO) phenomenon and infarct size (IS) using cardiac...
Main objective 40 consecutive patients classified according to the median level of MPO in the culprit artery. A CMR study was performed during the week...
Main objective To better understand the role of myeloperoxidases (MPO) in microvascular obstruction (MO) phenomenon and infarct size (IS) using cardiac...
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SubjectTerms [SDV.IB]Life Sciences [q-bio]/Bioengineering
[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system
Acute Coronary Syndromes
Acute Coronary Syndromes, No-Reflow, Long-Term, Leukocyte, Dimethylarginine, Definition, Mortality, Disease
Aged
Arteries
Arteries - enzymology
Arteries - pathology
Biology and Life Sciences
Calcium-binding protein
Cardiac patients
Cardiology
Cardiology and cardiovascular system
Cardiovascular disease
Definition
Dimethylarginine
Disease
Epidemiology
Female
Gadolinium
Health aspects
Heart
Heart attack
Heart attacks
Heart diseases
Human health and pathology
Humans
Hypertension
Infarction
Ischemia
Laboratories
Leukocyte
Life Sciences
Long-Term
Magnetic resonance
Magnetic resonance imaging
Magnetic Resonance Imaging, Cine
Magnetic Resonance Imaging, Cine - methods
Male
Medicine
Medicine and Health Sciences
Microcirculation
Microvasculature
Middle Aged
Mortality
Myocardial infarction
Neutrophils
Nitric oxide
NMR
No-Reflow
Nuclear magnetic resonance
Patients
Peroxidase
Peroxidase - metabolism
Plasma
Prognosis
Q
R
Remodeling
Research Article
Resonance
Science
ST Elevation Myocardial Infarction
ST Elevation Myocardial Infarction - blood
ST Elevation Myocardial Infarction - enzymology
ST Elevation Myocardial Infarction - pathology
Stroke Volume
Troponin
Ventricle
Ventricular Function, Left
Ventricular Remodeling
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Title Relation between high levels of myeloperoxidase in the culprit artery and microvascular obstruction, infarct size and reverse remodeling in ST-elevation myocardial infarction
URI https://cir.nii.ac.jp/crid/1871428068002141824
https://www.ncbi.nlm.nih.gov/pubmed/28704420
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http://dx.doi.org/10.1371/journal.pone.0179929
Volume 12
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