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Pulmonary embolism causes endomyocarditis in the human heart
  1. Mark PV Begieneman (mpv.begieneman{at}vumc.nl)
  1. VUMC, Netherlands
    1. Frank van de Goot
    1. VUMC, Netherlands
      1. Ivo van der Bilt
      1. VUMC, Netherlands
        1. Anton Vonk Noordegraaf
        1. VUMC, Netherlands
          1. Marieke Spreeuwenberg
          1. VUMC, Netherlands
            1. Walter Paulus
            1. VUMC, Netherlands
              1. Victor van Hinsbergh
              1. VUMC, Netherlands
                1. Frans Visser
                1. VUMC, Netherlands
                  1. Hans Niessen
                  1. VUMC, Netherlands

                    Abstract

                    Objectives Pulmonary embolism (PE) is a significant cause of morbidity and mortality. In a recent study in patients with PE, an increased amount of macrophages in the right ventricle was found. In the present study the presence of inflammatory cells, myocytolysis and intracavitary thrombi in the left and right ventricle of patients who died because of PE was evaluated as a putative new source of heart failure.

                    Design 22 PE patients were studied. For comparison, 8 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 using conventional staining.

                    Results Compared to controls, in patients with PE a significant increase in extravascular localization 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 PHT patients. Also endocardial cellular infiltration was found, partly coinciding with the presence of ventricular thrombi.

                    Conclusions In PE patients endomyocarditis and intracavitary thrombi in the left and right ventricle were found. These abnormalities could form an additional and novel 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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