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Baseline State for Pulmonary Vasculature with Pulmonary Arterial Hypertension: Effect of Geometric Remodeling and Metabolic Shift

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Abstract Pulmonary arterial hypertension (PAH) is a complex disease characterized by chronically elevated pulmonary arterial pressure, with early onset and progression linked to structural, metabolic and morphological changes in the pulmonary vasculature. Understanding the interplay between hemodynamics and arterial wall mechanics is essential to capture the pathology of the distal vasculature in PAH. This study aims to develop a data-driven framework that establishes a baseline state of PAH vasculature, incorporating key features of arterial wall constituents, geometry, and their interaction with PAH-specific hemodynamics. The model also explores changes in the metabolic energy costs of the arterial vasculature and hypothesize the most plausible metabolic costs based on PAH arterial wall energy consumption. Illustrative examples of symmetrically bifurcating arterial trees are used to establish baseline characteristics of PAH-affected pulmonary arteries. We establish the baseline state for PAH vasculature and compared it with healthy homeostatic vasculature in terms of arterial mechanics, morphometry, and pulsatile hemodynamics. This framework provides a representative computational model for advanced studies on PAH treatments and lays the groundwork for future pathophysiological modeling of the disease.
Title: Baseline State for Pulmonary Vasculature with Pulmonary Arterial Hypertension: Effect of Geometric Remodeling and Metabolic Shift
Description:
Abstract Pulmonary arterial hypertension (PAH) is a complex disease characterized by chronically elevated pulmonary arterial pressure, with early onset and progression linked to structural, metabolic and morphological changes in the pulmonary vasculature.
Understanding the interplay between hemodynamics and arterial wall mechanics is essential to capture the pathology of the distal vasculature in PAH.
This study aims to develop a data-driven framework that establishes a baseline state of PAH vasculature, incorporating key features of arterial wall constituents, geometry, and their interaction with PAH-specific hemodynamics.
The model also explores changes in the metabolic energy costs of the arterial vasculature and hypothesize the most plausible metabolic costs based on PAH arterial wall energy consumption.
Illustrative examples of symmetrically bifurcating arterial trees are used to establish baseline characteristics of PAH-affected pulmonary arteries.
We establish the baseline state for PAH vasculature and compared it with healthy homeostatic vasculature in terms of arterial mechanics, morphometry, and pulsatile hemodynamics.
This framework provides a representative computational model for advanced studies on PAH treatments and lays the groundwork for future pathophysiological modeling of the disease.

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