RT Journal Article
SR Electronic
T1 Myocardial infarction induces atrial inflammation that can be prevented by C1-esterase inhibitor
JF Journal of Clinical Pathology
JO J Clin Pathol
FD BMJ Publishing Group Ltd and Association of Clinical Pathologists
SP 1093
OP 1099
DO 10.1136/jclinpath-2016-203639
VO 69
IS 12
A1 Begieneman, Mark PV
A1 Emmens, Reindert W
A1 Rijvers, Liza
A1 Woudstra, Linde
A1 Paulus, Walter J
A1 Kubat, Bela
A1 Vonk, Alexander BA
A1 van Rossum, Albert C
A1 Wouters, Diana
A1 Zeerleder, Sacha
A1 van Ham, Marieke
A1 Schalkwijk, Casper G
A1 Niessen, Hans WM
A1 Krijnen, Paul AJ
YR 2016
UL http://jcp.bmj.com/content/69/12/1093.abstract
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.