Our proposed project consists of two aims, both based on our previously established model of thrombus persistence after repetitive pulmonary embolisms resulting in elevated pulmonary pressure, pulmonary arterial endothelial dysfunction and increased ROS. Aim 1 will expand our model to enable noninvasive assessment of thrombus burden in correlation with right ventricular dysfunction. Aim 2 will take advantage of the same experimental setup and investigate the interplay of thrombus persistence, pulmonary hypertension, increased ROS and telomere homeostasis.