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Tissue factor is unregulated in microvascular endothelial cells of patients with heart failure
  1. Edyta Reichman-Warmusz1,
  2. Dorota Domal-Kwiatkowska2,
  3. Natalia Matysiak1,
  4. Józef Kurek3,
  5. Dominik Spinczyk4,
  6. Damian Dudek1,
  7. Krzysztof Helewski1,
  8. Romuald Wojnicz1,5
  1. 1Department of Histology, School of Medicine with the Division of Dentistry, Medical University of Silesia in Katowice, Zabrze, Poland
  2. 2Department of Biochemistry, School of Pharmacy, Medical University of Silesia in Katowice, Sosnowiec, Poland
  3. 3Department of Surgery, Municipal Hospital, Jaworzno, Poland
  4. 4Faculty of Biomedical Engineering, Silesian University of Technology in Gliwice, Zabrze, Poland
  5. 5Silesian Centre for Heart Disease, Zabrze, Poland
  1. Correspondence to Professor Romuald Wojnicz, Department of Histology with Cell Pathology Laboratory, Jordana 19, Zabrze 41-808, Poland; wojnicz{at}dom.zabrze.pl/rwojnicz{at}sum.edu.pl

Abstract

Aims Several lines of evidence point to hypercoagulability as an important factor for heart failure (HF) pathogenesis.

Methods We hypothesised that endothelial tissue factor (TF) expression reflects altered tissue haemostasis which is related to the severity of HF. Accordingly, we investigated TF expression in the biopsies of 60 patients with HF and 22 without HF. In addition, we assessed the relationship between endothelial TF expression and clinical markers of HF severity.

Results The control subjects without HF presented absent or weak TF expression in few microvessels, while the endomyocardial biopsies of patients with HF, capillary vessels presented both weak and severe staining patterns by immunohistochemistry usually with regional distribution. This was collaborated by the immune electron microscopic study. The severe microvessel TF antigen expression was found in 11 (18.3%) patients with HF. The endothelial TF expression was inversely associated with left ventricular ejection fraction (r=−0.42, p=0.001) and positively with N-terminal brain natriuretic peptide (r=0.36, p<0.023), markers of HF severity.

Conclusions Regional upregulation of the TF in the capillary endothelial cells suggests local myocardial thrombogenicity. Furthermore, the relationship between endothelial TF and HF severity would be keeping in line with the hypothesis that an altered tissue haemostasis is most profoundly expressed in patients with severe HF. Weak TF expression found in several microvessels of the biopsy specimens patients without HF pathology might be potentially related to a low basal level of activation of the clotting system in normal individuals.

  • BLOOD VESSELS
  • IMMUNOHISTOCHEMISTRY
  • CLOTTING
  • ELECTRON MICROSCOPY
  • HEART

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