Myocardial infarction induces atrial inflammation that can be prevented by C1-esterase inhibitor

Mark P. V. Begieneman, Reindert W. Emmens, Liza Rijvers, Linde Woudstra, Walter J. Paulus, Bela Kubat, Alexander B. A. Vonk, Albert C. van Rossum, Diana Wouters, Sacha Zeerleder, Marieke van Ham, Casper G. Schalkwijk, Hans W. M. Niessen, Paul A. J. Krijnen

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

AIMS: Inflammation plays an important role in the pathogenesis of myocardial infarction (MI). Whether MI induces atrial inflammation is unknown however. Here, we analysed atrial inflammation in patients with MI and in rats with experimentally induced MI. The effect of the anti-inflammatory agent C1-esterase inhibitor (C1inh) on atrial inflammation in rats was also analysed.

METHODS: In the hearts of patients who died at different time points after MI (total n=24, mean age=60), neutrophils (myeloperoxidase-positive cells), lymphocytes (CD45-positive cells) and macrophages (CD68-positive cells) were quantified in the myocardium of the left and right atria and the infarcted left and non-infarcted right ventricles and compared with control patients (n=5, mean age=59). For the left and right atria, inflammatory cells were also quantified in the atrial adipose tissue. MI was induced in 17 rats, of which 10 were subsequently treated with C1inh for 6 days. Forty-two days post-MI, lymphocytes, macrophages and the endothelial inflammation marker Nε-(carboxymethyl)lysine (CML) were analysed in the myocardium of both the atria and ventricles.

RESULTS: In all investigated areas of the human hearts increased lymphocytes and macrophages were observed to a varying extent, especially between 6 h and 5 days following MI. Similarly, in rats MI resulted in an increase of inflammatory cells and CML in the atria. C1inh treatment decreased atrial inflammation.

CONCLUSIONS: MI induces atrial inflammation in patients and in rats. C1inh treatment could counteract this MI-induced atrial inflammation in rats.

Original languageEnglish
Pages (from-to)1093-1099
Number of pages7
JournalJournal of Clinical Pathology
Volume69
Issue number12
DOIs
Publication statusPublished - Dec 2016

Cite this

Begieneman, Mark P. V. ; Emmens, Reindert W. ; Rijvers, Liza ; Woudstra, Linde ; Paulus, Walter J. ; Kubat, Bela ; Vonk, Alexander B. A. ; van Rossum, Albert C. ; Wouters, Diana ; Zeerleder, Sacha ; van Ham, Marieke ; Schalkwijk, Casper G. ; Niessen, Hans W. M. ; Krijnen, Paul A. J. / Myocardial infarction induces atrial inflammation that can be prevented by C1-esterase inhibitor. In: Journal of Clinical Pathology. 2016 ; Vol. 69, No. 12. pp. 1093-1099.
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title = "Myocardial infarction induces atrial inflammation that can be prevented by C1-esterase inhibitor",
abstract = "AIMS: Inflammation plays an important role in the pathogenesis of myocardial infarction (MI). Whether MI induces atrial inflammation is unknown however. Here, we analysed atrial inflammation in patients with MI and in rats with experimentally induced MI. The effect of the anti-inflammatory agent C1-esterase inhibitor (C1inh) on atrial inflammation in rats was also analysed.METHODS: In the hearts of patients who died at different time points after MI (total n=24, mean age=60), neutrophils (myeloperoxidase-positive cells), lymphocytes (CD45-positive cells) and macrophages (CD68-positive cells) were quantified in the myocardium of the left and right atria and the infarcted left and non-infarcted right ventricles and compared with control patients (n=5, mean age=59). For the left and right atria, inflammatory cells were also quantified in the atrial adipose tissue. MI was induced in 17 rats, of which 10 were subsequently treated with C1inh for 6 days. Forty-two days post-MI, lymphocytes, macrophages and the endothelial inflammation marker Nε-(carboxymethyl)lysine (CML) were analysed in the myocardium of both the atria and ventricles.RESULTS: In all investigated areas of the human hearts increased lymphocytes and macrophages were observed to a varying extent, especially between 6 h and 5 days following MI. Similarly, in rats MI resulted in an increase of inflammatory cells and CML in the atria. C1inh treatment decreased atrial inflammation.CONCLUSIONS: MI induces atrial inflammation in patients and in rats. C1inh treatment could counteract this MI-induced atrial inflammation in rats.",
keywords = "Animals, Anti-Inflammatory Agents, Complement C1 Inhibitor Protein, Coronary Vessels, Disease Models, Animal, Heart Atria, Heart Ventricles, Humans, Inflammation, Lymphocytes, Macrophages, Male, Middle Aged, Myocardial Infarction, Myocardium, Neutrophils, Rats, Rats, Wistar, Journal Article",
author = "Begieneman, {Mark P. V.} and Emmens, {Reindert W.} and Liza Rijvers and Linde Woudstra and Paulus, {Walter J.} and Bela Kubat and Vonk, {Alexander B. A.} and {van Rossum}, {Albert C.} and Diana Wouters and Sacha Zeerleder and {van Ham}, Marieke and Schalkwijk, {Casper G.} and Niessen, {Hans W. M.} and Krijnen, {Paul A. J.}",
note = "Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.",
year = "2016",
month = "12",
doi = "10.1136/jclinpath-2016-203639",
language = "English",
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Begieneman, MPV, Emmens, RW, Rijvers, L, Woudstra, L, Paulus, WJ, Kubat, B, Vonk, ABA, van Rossum, AC, Wouters, D, Zeerleder, S, van Ham, M, Schalkwijk, CG, Niessen, HWM & Krijnen, PAJ 2016, 'Myocardial infarction induces atrial inflammation that can be prevented by C1-esterase inhibitor' Journal of Clinical Pathology, vol. 69, no. 12, pp. 1093-1099. https://doi.org/10.1136/jclinpath-2016-203639

Myocardial infarction induces atrial inflammation that can be prevented by C1-esterase inhibitor. / Begieneman, Mark P. V.; Emmens, Reindert W.; Rijvers, Liza; Woudstra, Linde; Paulus, Walter J.; Kubat, Bela; Vonk, Alexander B. A.; van Rossum, Albert C.; Wouters, Diana; Zeerleder, Sacha; van Ham, Marieke; Schalkwijk, Casper G.; Niessen, Hans W. M.; Krijnen, Paul A. J.

In: Journal of Clinical Pathology, Vol. 69, No. 12, 12.2016, p. 1093-1099.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - Myocardial infarction induces atrial inflammation that can be prevented by C1-esterase inhibitor

AU - Begieneman, Mark P. V.

AU - Emmens, Reindert W.

AU - Rijvers, Liza

AU - Woudstra, Linde

AU - Paulus, Walter J.

AU - Kubat, Bela

AU - Vonk, Alexander B. A.

AU - van Rossum, Albert C.

AU - Wouters, Diana

AU - Zeerleder, Sacha

AU - van Ham, Marieke

AU - Schalkwijk, Casper G.

AU - Niessen, Hans W. M.

AU - Krijnen, Paul A. J.

N1 - Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.

PY - 2016/12

Y1 - 2016/12

N2 - AIMS: Inflammation plays an important role in the pathogenesis of myocardial infarction (MI). Whether MI induces atrial inflammation is unknown however. Here, we analysed atrial inflammation in patients with MI and in rats with experimentally induced MI. The effect of the anti-inflammatory agent C1-esterase inhibitor (C1inh) on atrial inflammation in rats was also analysed.METHODS: In the hearts of patients who died at different time points after MI (total n=24, mean age=60), neutrophils (myeloperoxidase-positive cells), lymphocytes (CD45-positive cells) and macrophages (CD68-positive cells) were quantified in the myocardium of the left and right atria and the infarcted left and non-infarcted right ventricles and compared with control patients (n=5, mean age=59). For the left and right atria, inflammatory cells were also quantified in the atrial adipose tissue. MI was induced in 17 rats, of which 10 were subsequently treated with C1inh for 6 days. Forty-two days post-MI, lymphocytes, macrophages and the endothelial inflammation marker Nε-(carboxymethyl)lysine (CML) were analysed in the myocardium of both the atria and ventricles.RESULTS: In all investigated areas of the human hearts increased lymphocytes and macrophages were observed to a varying extent, especially between 6 h and 5 days following MI. Similarly, in rats MI resulted in an increase of inflammatory cells and CML in the atria. C1inh treatment decreased atrial inflammation.CONCLUSIONS: MI induces atrial inflammation in patients and in rats. C1inh treatment could counteract this MI-induced atrial inflammation in rats.

AB - AIMS: Inflammation plays an important role in the pathogenesis of myocardial infarction (MI). Whether MI induces atrial inflammation is unknown however. Here, we analysed atrial inflammation in patients with MI and in rats with experimentally induced MI. The effect of the anti-inflammatory agent C1-esterase inhibitor (C1inh) on atrial inflammation in rats was also analysed.METHODS: In the hearts of patients who died at different time points after MI (total n=24, mean age=60), neutrophils (myeloperoxidase-positive cells), lymphocytes (CD45-positive cells) and macrophages (CD68-positive cells) were quantified in the myocardium of the left and right atria and the infarcted left and non-infarcted right ventricles and compared with control patients (n=5, mean age=59). For the left and right atria, inflammatory cells were also quantified in the atrial adipose tissue. MI was induced in 17 rats, of which 10 were subsequently treated with C1inh for 6 days. Forty-two days post-MI, lymphocytes, macrophages and the endothelial inflammation marker Nε-(carboxymethyl)lysine (CML) were analysed in the myocardium of both the atria and ventricles.RESULTS: In all investigated areas of the human hearts increased lymphocytes and macrophages were observed to a varying extent, especially between 6 h and 5 days following MI. Similarly, in rats MI resulted in an increase of inflammatory cells and CML in the atria. C1inh treatment decreased atrial inflammation.CONCLUSIONS: MI induces atrial inflammation in patients and in rats. C1inh treatment could counteract this MI-induced atrial inflammation in rats.

KW - Animals

KW - Anti-Inflammatory Agents

KW - Complement C1 Inhibitor Protein

KW - Coronary Vessels

KW - Disease Models, Animal

KW - Heart Atria

KW - Heart Ventricles

KW - Humans

KW - Inflammation

KW - Lymphocytes

KW - Macrophages

KW - Male

KW - Middle Aged

KW - Myocardial Infarction

KW - Myocardium

KW - Neutrophils

KW - Rats

KW - Rats, Wistar

KW - Journal Article

U2 - 10.1136/jclinpath-2016-203639

DO - 10.1136/jclinpath-2016-203639

M3 - Article

VL - 69

SP - 1093

EP - 1099

JO - Journal of Clinical Pathology

JF - Journal of Clinical Pathology

SN - 0021-9746

IS - 12

ER -