# Hemodynamic simulation in the aortic arch under anemic, diabetic, and healthy blood flow conditions using computational fluid dynamics

**Authors:** Farzana Akter Tina, Hashnayne Ahmed, Hena Rani Biswas, Hafiz Muhammad Umer Farooqi, Hafiz Muhammad Umer Farooqi, Hafiz Muhammad Umer Farooqi, Hafiz Muhammad Umer Farooqi

PMC · DOI: 10.1371/journal.pone.0334297 · 2026-03-11

## TL;DR

This study uses computer simulations to compare blood flow in the aortic arch under anemic, diabetic, and healthy conditions, showing how blood properties affect vascular stress.

## Contribution

The study introduces a computational model to analyze hemodynamic differences caused by anemic and diabetic blood conditions in the aortic arch.

## Key findings

- Anemic blood flow showed reduced wall shear stress and low resistance, potentially impairing perfusion.
- Diabetic blood flow exhibited higher viscosity and wall shear stress, linked to vascular stiffening and remodeling risk.
- Healthy blood maintained balanced hemodynamics within normal physiological ranges.

## Abstract

This study examines the hemodynamic impact of anemic, diabetic, and healthy blood conditions in the human aortic arch using computational modeling. Blood rheology was represented by the shear-thinning Carreau–Yasuda model, and simulations were carried out in a patient-inspired aortic geometry under pulsatile flow. Velocity fields, pressure gradients, and wall shear stress (WSS) distributions were quantified to assess how altered hematocrit and viscosity affect vascular loading. Anemic blood, characterized by low viscosity, showed smooth low-resistance flow with reduced WSS, potentially limiting endothelial stimulation and impairing perfusion. Diabetic blood exhibited elevated viscosity and hematocrit, producing higher flow resistance, increased WSS, and disturbed secondary flows, consistent with vascular stiffening and remodeling risk. Healthy cases maintained balanced hemodynamics within physiological ranges. These findings highlight the mechanistic links between blood rheology and vascular stress, offering non-invasive insights for risk stratification in hematological and metabolic disorders, and supporting the integration of CFD-based analysis into clinical decision-making.

## Linked entities

- **Diseases:** anemia (MONDO:0002280), diabetes (MONDO:0005015)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Diseases:** atherogenic (MESH:D050197), hematological and metabolic disorders (MESH:D006402), hypertension (MESH:D006973), thrombosis (MESH:D013927), CFD (MESH:C563256), platelet aggregation (MESH:D001791), inflammation (MESH:D007249), orthostatic intolerance (MESH:D054971), Anemia (MESH:D000740), vascular stiffening (MESH:D057772), vascular dysfunction (MESH:D002561), endothelial dysfunction (MESH:D014652), Diabetic (MESH:D003920), cardiovascular disease (MESH:D002318), aortic dilation (MESH:D002311), aneurysm (MESH:D000783), ACADEMIC EDITOR (MESH:D007859), endothelial (MESH:D005642), perfusion (MESH:D001480), atherosclerotic plaques (MESH:D058226), stenosis (MESH:D003251)
- **Chemicals:** O2 (MESH:D010100), PONE-D-25-52209R2 (-), lipid (MESH:D008055), nitric oxide (MESH:D009569)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

50 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12978756/full.md

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Source: https://tomesphere.com/paper/PMC12978756