  Microvascular disease is a contributor to persistent pulmonary hypertension
in those with chronic thromboembolic pulmonary hypertension (CTEPH). The
heterogenous nature of the micro and macrovascular defects motivates the use of
personalized computational models, which can predict flow dynamics within
multiple generations of the arterial tree and into the microvasculature. Our
study uses computational hemodynamics models and Gaussian processes for rapid,
subject-specific calibration using retrospective data from a large animal model
of CTEPH. Our subject-specific predictions shed light on microvascular
dysfunction and arterial wall shear stress changes in CTEPH.
