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

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