Photo Credit: Rasi Bhadramani

The following is a summary of “Assessment of Biomechanical Properties in Pulmonary Arterial Hypertension: A Computational Fluid Dynamics Study of the Extensive Pulmonary Arterial Tree,” published in the April 2025 issue of the BMC Pulmonary Medicine by Shi et al.

Pulmonary arterial hypertension (PAH) is a progressive and life-threatening disorder marked by elevated pulmonary vascular resistance and subsequent right heart failure. Emerging evidence has highlighted the critical role of biomechanical forces in the disease’s pathogenesis. However, the intricate branching and three-dimensional complexity of the pulmonary arterial system have historically hindered comprehensive hemodynamic investigations, particularly in capturing the full scope of vascular alterations in PAH. 

To address this gap, the present study applies computational fluid dynamics (CFD) to assess biomechanical parameters throughout an extensively segmented pulmonary arterial tree, encompassing up to sixth-generation branches, in patients with PAH.

A detailed CFD-based analysis was conducted to quantify key hemodynamic variables, including velocity, wall shear stress (WSS), time-averaged wall shear stress (TAWSS), oscillatory shear index (OSI), and relative residence time (RRT). These metrics were chosen for their relevance in characterizing vascular remodeling and flow abnormalities associated with PAH. The study revealed a statistically significant reduction in the cross-sectional area at distal outlets of the pulmonary arterial tree (p < 0.0001), indicative of narrowed peripheral vessels. Concomitantly, a significant elevation in velocity was observed at the arterial outlets when compared to both the proximal inlet (p < 0.05) and the main pulmonary artery trunk (p < 0.001), suggesting a compensatory increase in flow velocity due to downstream resistance.

Notably, WSS values were consistently lower in the proximal pulmonary arteries than in their distal counterparts across all analyzed subjects. This was accompanied by a marked reduction in TAWSS in proximal regions, reinforcing the presence of disturbed flow in these areas. Hemodynamic assessments also revealed prominent helical flow structures within the proximal arteries, a characteristic flow pattern often associated with vascular dysfunction in PAH. Furthermore, regions of high OSI and prolonged RRT were predominantly localized to the proximal segments, suggesting increased temporal variability in shear forces and prolonged particle residence times—factors that may contribute to endothelial dysfunction and pathological vascular remodeling.

The integrative approach employed in this study offers a high-resolution, system-wide perspective on the pulmonary arterial flow environment in PAH, advancing the understanding of the disease’s biomechanical underpinnings. Importantly, the findings underscore the diagnostic and mechanistic value of velocity, WSS, OSI, and RRT as critical indicators of vascular pathology in PAH. By mapping these parameters across a fully segmented pulmonary artery tree, this research provides a foundational framework for future investigations into targeted therapies that address hemodynamic dysfunction in patients with PAH.

Source: bmcpulmmed.biomedcentral.com/articles/10.1186/s12890-025-03647-4