The role of endothelial shear stress, shear stress gradient, and plaque topography in plaque erosion.


Journal

Atherosclerosis
ISSN: 1879-1484
Titre abrégé: Atherosclerosis
Pays: Ireland
ID NLM: 0242543

Informations de publication

Date de publication:
07 2023
Historique:
received: 23 10 2022
revised: 12 05 2023
accepted: 16 05 2023
medline: 3 7 2023
pubmed: 1 6 2023
entrez: 31 5 2023
Statut: ppublish

Résumé

Plaque erosion is a common underlying cause of acute coronary syndromes. The role of endothelial shear stress (ESS) and endothelial shear stress gradient (ESSG) in plaque erosion remains unknown. We aimed to determine the role of ESS metrics and maximum plaque slope steepness in plaques with erosion versus stable plaques. This analysis included 46 patients/plaques from TOTAL and COMPLETE trials and Brigham and Women's Hospital's database who underwent angiography and OCT. Plaques were divided into those with erosion (n = 24) and matched stable coronary plaques (n = 22). Angiographic views were used to generate a 3-D arterial reconstruction, with centerlines merged from angiography and OCT pullback. Local ESS metrics were assessed by computational fluid dynamics. Among plaque erosions, the up- and down-slope (Δ lumen area/frame) was calculated for each culprit plaque. Compared with stable plaque controls, plaques with an erosion were associated with higher max ESS (8.3 ± 4.8 vs. 5.0 ± 1.9 Pa, p = 0.02) and max ESSG any direction (9.2 ± 7.5 vs. 4.3 ± 3.11 Pa/mm, p = 0.005). Proximal erosion was associated with a steeper plaque upslope while distal erosion with a steeper plaque downslope. Max ESS and Max ESSG any direction were independent factors in the development of plaque erosion (OR 1.32, 95%CI 1.06-1.65, p = 0.014; OR 1.22, 95% CI 1.03-1.45, p = 0.009, respectively). In plaques with similar luminal stenosis, plaque erosion was strongly associated with higher ESS, ESS gradients, and plaque slope as compared with stable plaques. These data support that ESS and slope metrics play a key role in the development of plaque erosion and may help prognosticate individual plaques at risk for future erosion.

Sections du résumé

BACKGROUND AND AIMS
Plaque erosion is a common underlying cause of acute coronary syndromes. The role of endothelial shear stress (ESS) and endothelial shear stress gradient (ESSG) in plaque erosion remains unknown. We aimed to determine the role of ESS metrics and maximum plaque slope steepness in plaques with erosion versus stable plaques.
METHODS
This analysis included 46 patients/plaques from TOTAL and COMPLETE trials and Brigham and Women's Hospital's database who underwent angiography and OCT. Plaques were divided into those with erosion (n = 24) and matched stable coronary plaques (n = 22). Angiographic views were used to generate a 3-D arterial reconstruction, with centerlines merged from angiography and OCT pullback. Local ESS metrics were assessed by computational fluid dynamics. Among plaque erosions, the up- and down-slope (Δ lumen area/frame) was calculated for each culprit plaque.
RESULTS
Compared with stable plaque controls, plaques with an erosion were associated with higher max ESS (8.3 ± 4.8 vs. 5.0 ± 1.9 Pa, p = 0.02) and max ESSG any direction (9.2 ± 7.5 vs. 4.3 ± 3.11 Pa/mm, p = 0.005). Proximal erosion was associated with a steeper plaque upslope while distal erosion with a steeper plaque downslope. Max ESS and Max ESSG any direction were independent factors in the development of plaque erosion (OR 1.32, 95%CI 1.06-1.65, p = 0.014; OR 1.22, 95% CI 1.03-1.45, p = 0.009, respectively).
CONCLUSIONS
In plaques with similar luminal stenosis, plaque erosion was strongly associated with higher ESS, ESS gradients, and plaque slope as compared with stable plaques. These data support that ESS and slope metrics play a key role in the development of plaque erosion and may help prognosticate individual plaques at risk for future erosion.

Identifiants

pubmed: 37257352
pii: S0021-9150(23)00208-3
doi: 10.1016/j.atherosclerosis.2023.05.013
pii:
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

11-18

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL146144
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL140498
Pays : United States

Informations de copyright

Copyright © 2023. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Diaa Hakim (D)

Cardiovascular Division, Brigham & Women's Hospital/Harvard Medical School, Boston, MA, USA.

Natalia Pinilla-Echeverri (N)

McMaster University and Population Health Research Institute, Hamilton Health Sciences, Hamilton, Canada.

Ahmet U Coskun (AU)

Department of Mechanical and Industrial Engineering, Northeastern University, Boston, MA, USA.

Zhongyue Pu (Z)

Department of Medical Science, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Olli A Kajander (OA)

Heart Hospital, Tampere University Hospital and School of Medicine, University of Tampere, Tampere, Finland.

Deborah Rupert (D)

Medical Scientist Training Program, Stonybrook University, New York, NY, USA.

Charles Maynard (C)

Department of Health Systems and Population Health, University of Washington, Seattle, WA, USA.

Nicholas Cefalo (N)

Cardiovascular Division, Brigham & Women's Hospital/Harvard Medical School, Boston, MA, USA.

Gerasimos Siasos (G)

National and Kapodistrian University of Athens, Medical School, Athens, Greece.

Michail I Papafaklis (MI)

Cardiology Department, University of Ioannina, Ioannina, Greece.

Stefanu Kostas (S)

Cardiology Department, University of Ioannina, Ioannina, Greece.

Lampros K Michalis (LK)

Cardiology Department, University of Ioannina, Ioannina, Greece.

Sanjit Jolly (S)

McMaster University and Population Health Research Institute, Hamilton Health Sciences, Hamilton, Canada.

Shamir R Mehta (SR)

McMaster University and Population Health Research Institute, Hamilton Health Sciences, Hamilton, Canada.

Tej Sheth (T)

McMaster University and Population Health Research Institute, Hamilton Health Sciences, Hamilton, Canada.

Kevin Croce (K)

Cardiovascular Division, Brigham & Women's Hospital/Harvard Medical School, Boston, MA, USA.

Peter H Stone (PH)

Cardiovascular Division, Brigham & Women's Hospital/Harvard Medical School, Boston, MA, USA. Electronic address: pstone@bwh.harvard.edu.

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