A computational growth and remodeling framework for adaptive and maladaptive pulmonary arterial hemodynamics.

Autor: Szafron JM; Department of Pediatrics (Cardiology), Stanford University, Stanford, CA, 94305, USA.; Cardiovascular Institute, Stanford University, Palo Alto, CA, 94305, USA., Yang W; Department of Pediatrics (Cardiology), Stanford University, Stanford, CA, 94305, USA., Feinstein JA; Department of Pediatrics (Cardiology), Stanford University, Stanford, CA, 94305, USA.; Cardiovascular Institute, Stanford University, Palo Alto, CA, 94305, USA., Rabinovitch M; Department of Pediatrics (Cardiology), Stanford University, Stanford, CA, 94305, USA.; Cardiovascular Institute, Stanford University, Palo Alto, CA, 94305, USA., Marsden AL; Department of Pediatrics (Cardiology), Stanford University, Stanford, CA, 94305, USA. amarsden@stanford.edu.; Cardiovascular Institute, Stanford University, Palo Alto, CA, 94305, USA. amarsden@stanford.edu.
Jazyk: angličtina
Zdroj: Biomechanics and modeling in mechanobiology [Biomech Model Mechanobiol] 2023 Dec; Vol. 22 (6), pp. 1935-1951. Date of Electronic Publication: 2023 Sep 02.
DOI: 10.1007/s10237-023-01744-z
Abstrakt: Hemodynamic loading is known to contribute to the development and progression of pulmonary arterial hypertension (PAH). This loading drives changes in mechanobiological stimuli that affect cellular phenotypes and lead to pulmonary vascular remodeling. Computational models have been used to simulate mechanobiological metrics of interest, such as wall shear stress, at single time points for PAH patients. However, there is a need for new approaches that simulate disease evolution to allow for prediction of long-term outcomes. In this work, we develop a framework that models the pulmonary arterial tree through adaptive and maladaptive responses to mechanical and biological perturbations. We coupled a constrained mixture theory-based growth and remodeling framework for the vessel wall with a morphometric tree representation of the pulmonary arterial vasculature. We show that non-uniform mechanical behavior is important to establish the homeostatic state of the pulmonary arterial tree, and that hemodynamic feedback is essential for simulating disease time courses. We also employed a series of maladaptive constitutive models, such as smooth muscle hyperproliferation and stiffening, to identify critical contributors to development of PAH phenotypes. Together, these simulations demonstrate an important step toward predicting changes in metrics of clinical interest for PAH patients and simulating potential treatment approaches.
(© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)
Databáze: MEDLINE
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