Correlation between aortic valve protein levels and vector flow mapping of wall shear stress and oscillatory shear index in patients supported with continuous-flow left ventricular assist devices.


Journal

The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation
ISSN: 1557-3117
Titre abrégé: J Heart Lung Transplant
Pays: United States
ID NLM: 9102703

Informations de publication

Date de publication:
01 2023
Historique:
received: 09 01 2022
revised: 16 09 2022
accepted: 23 09 2022
pubmed: 19 11 2022
medline: 24 12 2022
entrez: 18 11 2022
Statut: ppublish

Résumé

Continuous-flow left ventricular assist devices commonly lead to aortic regurgitation, which results in decreased pump efficiency and worsening heart failure. We hypothesized that non-physiological wall shear stress and oscillatory shear index alter the abundance of structural proteins in aortic valves of left ventricular assist device (LVAD) patients. Doppler images of aortic valves of patients undergoing heart transplants were obtained. Eight patients had been supported with LVADs, whereas 10 were not. Aortic valve tissue was collected and protein levels were analyzed using mass spectrometry. Echocardiographic images were analyzed and wall shear stress and oscillatory shear index were calculated. The relationship between normalized levels of individual proteins and in vivo echocardiographic measurements was evaluated. Of the 57 proteins of interest, there was a strong negative correlation between levels of 15 proteins and the wall shear stress (R < -0.500, p ≤ 0.05), and a moderate negative correlation between 16 proteins and wall shear stress (R -0.500 to -0.300, p ≤ 0.05). Gene ontology analysis demonstrated clusters of proteins involved in cellular structure. Proteins negatively correlated with WSS included those with cytoskeletal, actin/myosin, cell-cell junction and extracellular functions. C: In aortic valve tissue, 31 proteins were identified involved in cellular structure and extracellular junctions with a negative correlation between their levels and wall shear stress. These findings suggest an association between the forces acting on the aortic valve (AV) and leaflet protein abundance, and may form a mechanical basis for the increased risk of aortic leaflet degeneration in LVAD patients.

Sections du résumé

BACKGROUND
Continuous-flow left ventricular assist devices commonly lead to aortic regurgitation, which results in decreased pump efficiency and worsening heart failure. We hypothesized that non-physiological wall shear stress and oscillatory shear index alter the abundance of structural proteins in aortic valves of left ventricular assist device (LVAD) patients.
METHODS
Doppler images of aortic valves of patients undergoing heart transplants were obtained. Eight patients had been supported with LVADs, whereas 10 were not. Aortic valve tissue was collected and protein levels were analyzed using mass spectrometry. Echocardiographic images were analyzed and wall shear stress and oscillatory shear index were calculated. The relationship between normalized levels of individual proteins and in vivo echocardiographic measurements was evaluated.
RESULTS
Of the 57 proteins of interest, there was a strong negative correlation between levels of 15 proteins and the wall shear stress (R < -0.500, p ≤ 0.05), and a moderate negative correlation between 16 proteins and wall shear stress (R -0.500 to -0.300, p ≤ 0.05). Gene ontology analysis demonstrated clusters of proteins involved in cellular structure. Proteins negatively correlated with WSS included those with cytoskeletal, actin/myosin, cell-cell junction and extracellular functions. C: In aortic valve tissue, 31 proteins were identified involved in cellular structure and extracellular junctions with a negative correlation between their levels and wall shear stress. These findings suggest an association between the forces acting on the aortic valve (AV) and leaflet protein abundance, and may form a mechanical basis for the increased risk of aortic leaflet degeneration in LVAD patients.

Identifiants

pubmed: 36400676
pii: S1053-2498(22)02162-3
doi: 10.1016/j.healun.2022.09.017
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

64-75

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL122805
Pays : United States

Informations de copyright

Copyright © 2022 International Society for Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.

Auteurs

Serge Kobsa (S)

Division of Cardiac, Thoracic, and Vascular Surgery, Department of Surgery, Columbia University Medical Center, New York, New York.

Koichi Akiyama (K)

Department of Anesthesiology, Yodogawa Christian Hospital, Osaka, Japan.

Samantha K Nemeth (SK)

Division of Cardiac, Thoracic, and Vascular Surgery, Department of Surgery, Columbia University Medical Center, New York, New York.

Paul A Kurlansky (PA)

Division of Cardiac, Thoracic, and Vascular Surgery, Department of Surgery, Columbia University Medical Center, New York, New York.

Yoshifumi Naka (Y)

Department of Cardiothoracic Surgery, Weill Cornell Medical Center, New York, New York.

Koji Takeda (K)

Division of Cardiac, Thoracic, and Vascular Surgery, Department of Surgery, Columbia University Medical Center, New York, New York.

Keiichi Itatani (K)

Department of Cardiovascular Surgery, Osaka City University, Osaka, Japan.

Emily G Werth (EG)

Quantitative Proteomics and Metabolomics Center, Department of Biological Sciences, Columbia University, New York, New York.

Lewis M Brown (LM)

Quantitative Proteomics and Metabolomics Center, Department of Biological Sciences, Columbia University, New York, New York.

Giovanni Ferrari (G)

Division of Cardiac, Thoracic, and Vascular Surgery, Department of Surgery, Columbia University Medical Center, New York, New York.

Hiroo Takayama (H)

Division of Cardiac, Thoracic, and Vascular Surgery, Department of Surgery, Columbia University Medical Center, New York, New York. Electronic address: ht2225@cumc.columbia.edu.

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