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Myocardial infarction induces atrial inflammation that can be prevented by C1-esterase inhibitor
  1. Mark PV Begieneman1,2,3,
  2. Reindert W Emmens1,2,4,
  3. Liza Rijvers1,
  4. Linde Woudstra1,2,
  5. Walter J Paulus2,5,
  6. Bela Kubat3,
  7. Alexander BA Vonk2,6,
  8. Albert C van Rossum2,7,
  9. Diana Wouters4,
  10. Sacha Zeerleder4,8,
  11. Marieke van Ham4,
  12. Casper G Schalkwijk9,
  13. Hans WM Niessen1,2,6,
  14. Paul AJ Krijnen1,2
  1. 1Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands
  2. 2ICaR-VU, Amsterdam, The Netherlands
  3. 3Netherlands Forensic Institute (NFI), The Hague, The Netherlands
  4. 4Department of Immunopathology, Sanquin Research, Amsterdam, The Netherlands
  5. 5Department of Physiology, VU University Medical Center, Amsterdam, The Netherlands
  6. 6Department of Cardiac Surgery, VU University Medical Center, Amsterdam, The Netherlands
  7. 7Department of Cardiology, VU University Medical Center, Amsterdam, The Netherlands
  8. 8Department of Hematology, Academic Medical Center, Amsterdam, The Netherlands
  9. 9Department of Internal Medicine, Maastricht University Medical Center, Maastricht, The Netherlands
  1. Correspondence to Reindert W Emmens, Department of Pathology, VU University Medical Center, Room 0E46, De Boelelaan 1117, Amsterdam 1081 HV, The Netherlands; r.emmens{at}


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.


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  • Handling editor Cheok Soon Lee

  • Contributors All authors have made significant contributions to this study, have critically reviewed the manuscript for intellectual content and approve of the submission.

  • Funding This study was funded by the Netherlands Forensic Institute (grant no 34) and an unrestricted grant from Shire—ViroPharma.

  • Competing interests None declared.

  • Ethics approval Medical Ethics Committee of the VU University Medical Center, Amsterdam, Netherlands.

  • Provenance and peer review Not commissioned; externally peer reviewed.