Myocardial infarction induces atrial inflammation that can be prevented by C1-esterase inhibitor. Issue 12 (6th May 2016)

• Record Type: Journal Article
• Authors: Begieneman, Mark PV; Emmens, Reindert W; Rijvers, Liza; Woudstra, Linde; Paulus, Walter J; Kubat, Bela; Vonk, Alexander BA; van Rossum, Albert C; Wouters, Diana; Zeerleder, Sacha; van Ham, Marieke; Schalkwijk, Casper G; Niessen, Hans WM; Krijnen, Paul AJ
• Is Part Of: Journal of clinical pathology. Volume 69:Issue 12(2016)
• Page Start: 1093
• Page End: 1099
• Publication Date: 2016-05-06
• Subjects: INFLAMMATION -- LEUCOCYTES -- HEART; Pathology -- Periodicals; Pathology, Molecular -- Periodicals; 616.0705
• DOI: 10.1136/jclinpath-2016-203639
• Languages: English
• ISSNs: 0021-9746

Abstract

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 N ε -(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.