Team: Michelle Bartolo, Megan Chambers, Amanda Colunga, & Mette Olufsen
Collaborators: Naomi Chesler, Rachel Clipp, Mansoor Haider, Nicholas Hill, M. Umar Qureshi
- Numerical predictions of shear stress and cyclic stretch in the healthy pulmonary vasculature
- A multiscale model of vascular function in chronic thromboembolic pulmonary hypertension
- Structural and hemodynamic properties in murine pulmonary arterial networks under hypoxia-induced pulmonary hypertension
Pulmonary hypertension (PH) is defined by an elevated blood pressure in the pulmonary arteries, leading to right ventricular dysfunction and alterations in typical oxygen exchange in the lungs. There are five main etiologies of PH, including PH due to left heart impairment (group II), PH due to lung disease, such as COPD and hypoxia (group III), and chronic thromboembolic PH (group IV). PH leads to remodeling in large and small arteries as well as arterioles, which changes both the structure and function of the pulmonary vasculature. Using mathematical modeling, our group investigates how both local and systems-level changes in hemodynamic parameters impact pressure, cardiac output, and heart function in patients with PH. Our long-term goal is to use mathematical modeling to monitor disease progression in PH patients in a non-invasive manner and further understand the underlying disease mechanism.
- Remodeling of pulmonary cardiovascular networks in the presence of hypertension
- Uncertainty propagation
- Extraction, visualization, analysis and modeling of large tree networks
- Predicting mechanical stress in pulmonary capillaries using a sheet model
Click here to return to our general research page!