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Updated: Jan 27, 2026
A Method to Study the Correlation Between Local Collagen Structure and Mechanical Properties of Atherosclerotic Plaque Fibrous Tissue
Published on: November 11, 2022
Implications of the local haemodynamic forces on the phenotype of coronary plaques
Christos V Bourantas1,2,3, Thomas Zanchin1,4,5, Antonis Sakellarios6
1Department of Cardiology, Barts Heart Centre, Barts Health NHS Trust, London, UK.
Insights
Endothelial shear stress (ESS) impacts plaque progression similarly across all plaque types. Accurate assessment requires multimodality imaging, as intravascular ultrasound-virtual histology alone misclassifies plaque morphology.
Area of Science:
- Cardiovascular Medicine
- Biomedical Engineering
- Medical Imaging
Background:
- Atherosclerotic plaque progression is a dynamic process influenced by hemodynamic forces.
- Endothelial shear stress (ESS) is a critical factor modulating vascular health and disease.
- Understanding ESS's role in plaque phenotype changes is vital for managing cardiovascular disease.
Purpose of the Study:
- To investigate the impact of endothelial shear stress (ESS) on the dynamic evolution of atherosclerotic plaque phenotypes.
- To evaluate the accuracy of intravascular ultrasound-virtual histology (IVUS-VH) and optical coherence tomography (OCT) in assessing ESS-related plaque changes.
Main Methods:
- Analysis of 68 vessels from myocardial infarction patients with baseline and 13-month follow-up IVUS-VH and OCT data.
- Reconstruction of nonculprit vessels using IVUS-VH to estimate ESS in 3 mm segments.
- Assessment of plaque morphology and disease progression using combined IVUS-VH and OCT data.
Main Results:
- Low ESS was associated with plaque progression across all plaque phenotypes.
- ESS affected lumen dimensions differently across plaque types: most prominent in disease-free, less in fibrotic/calcific and lipid-rich plaques.
- Standalone IVUS-VH misclassified plaque morphology in one-third of cases, leading to inaccurate ESS effect estimations.
Conclusions:
- The effect of ESS on plaque progression is consistent across different plaque phenotypes.
- Standalone IVUS-VH is insufficient for accurately assessing ESS's impact on plaque evolution due to morphology misclassification.
- Multimodality imaging is recommended for comprehensive evaluation of ESS's role in plaque development.
Aim:
To examine the effect of endothelial shear stress (ESS) on the dynamic changes in plaque phenotype.
Methods:
Patients with myocardial infarction that had intravascular ultrasound-virtual histology (IVUS-VH) and optical coherence tomography (OCT) at baseline and 13-month follow-up were studied. The IVUS-VH data were used to reconstruct the nonculprit vessels, and in the obtained models the ESS was estimated in 3 mm segments. Plaque morphology was derived in each segment from IVUS-VH and OCT. Disease progression was defined as the presence of ≥2 out of the following criteria: reduction in lumen area, increase in plaque burden and change of plaque morphology to a more vulnerable phenotype. Linear mixed effects models were used to assess the effect of ESS in different phenotypes.
Results:
Sixty-eight vessels were included in the analysis. Low ESS was associated with plaque progression in all phenotypes. The effect of ESS on plaque burden (p for interaction=0.467) and phenotype (p for interaction=0.188) was similar in all plaque types, whereas the effect of ESS on the changes in lumen dimensions was more prominent in disease-free (β=0.70, p<0.001) than fibrotic/fibrocalcific (β=0.28, p<0.001) or lipid-rich plaques (β=0.15, p=0.015). Standalone IVUS-VH misclassified plaque morphology in one-third of the cases leading to erroneous estimations about the effect of ESS on plaque evolution in different phenotypes.
Conclusions:
The effect of ESS on plaque progression is similar in all phenotypes and cannot be accurately assessed by standalone IVUS-VH which often misclassifies plaque morphology. Therefore, multimodality imaging should be considered to examine the implications of ESS on plaque evolution.
Clinical Trial Registration:
NCT00962416; Post-results.
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