ArticleAnnals of biomedical engineering2021
Patient-Specific Computational Analysis of Hemodynamics in Adult Pulmonary Hypertension.
Article in Annals of biomedical engineering, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Pulmonary Vascular Signaling in Pulmonary Hypertension: Potential Role of Endothelial CaArteriosclerosis, thrombosis, and vascular biology · 2026Review
- Vascular Remodelling in COPD: An In Silico Tool to Represent Pulmonary Haemodynamics in Obstructive Lung Disease.Annals of biomedical engineering · 2026Article
- Patient-specific modelling of pulmonary arterial hypertension: wall shear stress correlates with disease severity.Frontiers in bioengineering and biotechnology · 2025Article
- Impact of Vein Wall Hyperelasticity and Blood Flow Turbulence on Hemodynamic Parameters in the Inferior Vena Cava with a Filter.Micromachines · 2024Article
- Simulating Multi-Scale Pulmonary Vascular Function by Coupling Computational Fluid Dynamics With an Anatomic Network Model.Frontiers in network physiology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Pulmonary hypertension (PH) is a progressive disease characterized by elevated pressure and vascular resistance in the pulmonary arteries. Nearly 250,000 hospitalizations occur annually in the US with PH as the primary or secondary condition. A definitive diagnosis of PH requires right heart catheterization (RHC) in addition to a chest computed tomography, a walking test, and others. While RHC is the gold standard for diagnosing PH, it is invasive and posseses inherent risks and contraindications. In this work, we characterized the patient-specific pulmonary hemodynamics in silico for diverse PH WHO groups. We grouped patients on the basis of mean pulmonary arterial pressure (mPAP) into three disease severity groups: at-risk ([Formula: see text], denoted with A), mild ([Formula: see text], denoted with M), and severe ([Formula: see text], denoted with S). The pulsatile flow hemodynamics was simulated by evaluating the three-dimensional Navier-Stokes system of equations using a flow solver developed by customizing OpenFOAM libraries (v5.0, The OpenFOAM Foundation). Quasi patient-specific boundary conditions were implemented using a Womersley inlet velocity profile and transient resistance outflow conditions. Hemodynamic indices such as spatially averaged wall shear stress ([Formula: see text]), wall shear stress gradient ([Formula: see text]), time-averaged wall shear stress ([Formula: see text]), oscillatory shear index ([Formula: see text]), and relative residence time ([Formula: see text]), were evaluated along with the clinical metrics pulmonary vascular resistance ([Formula: see text]), stroke volume ([Formula: see text]) and compliance ([Formula: see text]), to assess possible spatiotemporal correlations. We observed statistically significant decreases in [Formula: see text], [Formula: see text], and [Formula: see text], and increases in [Formula: see text] and [Formula: see text] with disease severity. [Formula: see text] was moderately correlated with [Formula: see text] and [Formula: see text] at the mid-notch stage of the cardiac cycle when these indices were computed using the global pulmonary arterial geometry. These results are promising in the context of a long-term goal of identifying computational biomarkers that can serve as surrogates for invasive diagnostic protocols of PH.
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