Chronic thromboembolic pulmonary hypertension (CTEPH) results from
single or recurrent pulmonary thromboemboli arising from sites of
venous thrombosis. In patients with CTEPH thro+mboemboli do not
resolve, but rather they form endothelialized, fibrotic
obstructions of the pulmonary vascular bed. Mechanisms underlying
thrombus organisation are poorly understood. Because of the
observation that infected intravenous leads enhance the likelihood
of CTEPH, the hypothesis that bacterial infection causes a failure
of thrombus resolution, has been tested. A mouse model of venous
thrombus formation was employed to investigate thrombus resolution
in the absence and in presence of low doses staphylococcus aureus.
On days 3, 7, 14 and 28 after thrombus induction, animals were
sacrificed, thrombi were harvested, fixed and embedded in paraffin.
Thrombi of infected mice were larger than controls. Furthermore,
fibrosis markers showed a different expression pattern.
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