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Pulmonary embolism causes endomyocarditis in the human heart
  1. M P V Begieneman1,2,3,
  2. F R W van de Goot1,2,3,
  3. I A C van der Bilt3,4,
  4. A Vonk Noordegraaf3,5,
  5. M D Spreeuwenberg6,
  6. W J Paulus3,7,
  7. V W M van Hinsbergh3,7,
  8. F C Visser3,4,
  9. H W M Niessen1,3,8
  1. 1
    Department of Pathology, VU University Medical Centre, Amsterdam, The Netherlands
  2. 2
    Dutch Forensic Institute, The Hague, The Netherlands
  3. 3
    ICaR-VU, Amsterdam, The Netherlands
  4. 4
    Department of Cardiology, VU University Medical Centre, Amsterdam, The Netherlands
  5. 5
    Department of Pulmonology, VU University Medical Centre, Amsterdam, The Netherlands
  6. 6
    Department of Epidemiology and Biostatistics, VU University Medical Centre, Amsterdam, The Netherlands
  7. 7
    Department of Physiology, VU University Medical Centre, Amsterdam, The Netherlands
  8. 8
    Department of Cardiac Surgery, VU University Medical Centre, Amsterdam, The Netherlands
  1. Dr M P V Begieneman, VU University Medical Centre, Department of Pathology, Room No 0E46, De Boelelaan 1117, 1007 HV Amsterdam, The Netherlands; mpv.begieneman{at}vumc.nl

Abstract

Background: Pulmonary embolism (PE) is a significant cause of morbidity and mortality. In a recent study in patients with PE, an increased level of macrophages was found in the right ventricle.

Objective: To evaluate the presence of inflammatory cells, myocytolysis and intracavitary thrombi in the left and right ventricle of patients who died because of PE as a putative new source of heart failure.

Patients and methods: 22 patients with PE were studied. For comparison, eight controls and 11 patients who died of chronic pulmonary hypertension (PHT) were used. Slides of the left and right ventricle were stained with antibodies, identifying neutrophilic granulocytes, lymphocytes and macrophages, which were subsequently quantified. Myocytolysis was visualised using complement staining. Thrombi were identified by conventional staining.

Results: Compared with controls, in patients with PE a significant increase in extravascular localisation of all three inflammatory cells was found both in the right and left ventricle, coinciding with myocytolysis, indicative for myocarditis. No increase in inflammatory cells was found in patients with PHT. Endocardial cellular infiltration was also found, partly coinciding with the presence of ventricular thrombi.

Conclusions: In patients with PE, endomyocarditis and intracavitary thrombi in the left and right ventricle were found. These abnormalities may be an additional new explanation for the observed cardiac enzyme release and functional abnormalities of the heart in these patients and may contribute to the morbidity and mortality of the disease.

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Footnotes

  • Funding: This project was financed by the Dutch Forensic Institute (Nederlands Forensisch Instituut), project No 34. The Hague, the Netherlands.

  • Competing interests: None.

  • Ethics approval: The study was approved by and performed according to the guidelines of the ethics committee of the VU University Medical Centre, Amsterdam, The Netherlands.

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