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.