Blood Monocyte Phenotype Fingerprint of Stable Coronary Artery Disease: A Cross-Sectional Substudy of SMARTool Clinical Trial.


Journal

BioMed research international
ISSN: 2314-6141
Titre abrégé: Biomed Res Int
Pays: United States
ID NLM: 101600173

Informations de publication

Date de publication:
2020
Historique:
received: 23 04 2020
accepted: 20 05 2020
entrez: 18 8 2020
pubmed: 18 8 2020
medline: 23 4 2021
Statut: epublish

Résumé

Atherosclerosis is an inflammatory disease with long-lasting activation of innate immunity and monocytes are the main blood cellular effectors. We aimed to investigate monocyte phenotype (subset fraction and marker expression) at different stages of coronary atherosclerosis in stable coronary artery disease (CAD) patients. 73 patients with chronic coronary syndrome were evaluated by CT coronary angiography (CTCA) and classified by maximal diameter stenosis of major vessels into three groups of CAD severity: CAD1 (no CAD/minimal CAD, Total cell count and fraction of Mon2 were higher in CAD2 and CAD3 compared to CAD1. By multivariate regression analysis, Mon2 cell fraction and Mon2 expression of CX3CR1, CD18, and CD16 showed a statistically significant and independent increase, parallel to stenosis severity, from CAD1 to CAD2 and CAD3 groups. A similar trend was also present for CX3CR1 and HLA-DR expressions on total monocyte population. A less calcified plaque composition was associated to a higher Mon2 expression of CD16 and higher TNF- The results of this study suggest that a specific pattern of inflammation-correlated monocyte marker expression is associated to higher stenosis severity and less calcified lesions in stable CAD. The clinical trial Identifier is NCT04448691.

Sections du résumé

BACKGROUND AND AIMS OBJECTIVE
Atherosclerosis is an inflammatory disease with long-lasting activation of innate immunity and monocytes are the main blood cellular effectors. We aimed to investigate monocyte phenotype (subset fraction and marker expression) at different stages of coronary atherosclerosis in stable coronary artery disease (CAD) patients.
METHODS METHODS
73 patients with chronic coronary syndrome were evaluated by CT coronary angiography (CTCA) and classified by maximal diameter stenosis of major vessels into three groups of CAD severity: CAD1 (no CAD/minimal CAD,
RESULTS RESULTS
Total cell count and fraction of Mon2 were higher in CAD2 and CAD3 compared to CAD1. By multivariate regression analysis, Mon2 cell fraction and Mon2 expression of CX3CR1, CD18, and CD16 showed a statistically significant and independent increase, parallel to stenosis severity, from CAD1 to CAD2 and CAD3 groups. A similar trend was also present for CX3CR1 and HLA-DR expressions on total monocyte population. A less calcified plaque composition was associated to a higher Mon2 expression of CD16 and higher TNF-
CONCLUSIONS CONCLUSIONS
The results of this study suggest that a specific pattern of inflammation-correlated monocyte marker expression is associated to higher stenosis severity and less calcified lesions in stable CAD. The clinical trial Identifier is NCT04448691.

Identifiants

pubmed: 32802883
doi: 10.1155/2020/8748934
pmc: PMC7403909
doi:

Substances chimiques

Antigens, CD 0
Cytokines 0
HLA-DR Antigens 0
Receptors, Chemokine 0

Banques de données

ClinicalTrials.gov
['NCT04448691']

Types de publication

Clinical Trial Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

8748934

Informations de copyright

Copyright © 2020 Silverio Sbrana et al.

Déclaration de conflit d'intérêts

The authors declare that there is no conflict of interest regarding the publication of this paper.

Références

Clin Imaging. 2019 Sep - Oct;57:7-14
pubmed: 31078917
Cytometry B Clin Cytom. 2005 May;65(1):14-21
pubmed: 15786508
Arterioscler Thromb Vasc Biol. 2015 Feb;35(2):272-9
pubmed: 25538208
Eur Heart J. 2018 Oct 7;39(38):3521-3527
pubmed: 29069365
Int J Cardiovasc Imaging. 2013 Jun;29(5):1177-90
pubmed: 23417447
Eur Radiol. 2018 Apr;28(4):1365-1372
pubmed: 29116390
Circulation. 1975 Apr;51(4 Suppl):5-40
pubmed: 1116248
Blood. 1989 Nov 15;74(7):2527-34
pubmed: 2478233
Thromb Haemost. 2016 Sep 27;116(4):626-37
pubmed: 27412877
Nat Rev Cardiol. 2010 Feb;7(2):77-86
pubmed: 20065951
J Thromb Haemost. 2011 May;9(5):1056-66
pubmed: 21342432
Eur Heart J. 2020 Jan 14;41(3):407-477
pubmed: 31504439
JACC Cardiovasc Imaging. 2019 Oct;12(10):1987-1997
pubmed: 30660516
Eur Heart J. 2011 Jan;32(1):84-92
pubmed: 20943670
Perfusion. 2020 Jan;35(1):48-56
pubmed: 31151363
Cardiovasc Diabetol. 2017 Aug 8;16(1):96
pubmed: 28789689
Cytometry. 1988 Nov;9(6):619-26
pubmed: 3061754
Atherosclerosis. 2016 Oct;253:128-134
pubmed: 27615596
Annu Rev Immunol. 2009;27:165-97
pubmed: 19302038
JAMA Cardiol. 2018 Feb 1;3(2):144-152
pubmed: 29322167
Cytometry B Clin Cytom. 2004 Mar;58(1):17-24
pubmed: 14994371
Semin Immunol. 2016 Aug;28(4):384-93
pubmed: 27113267
Int J Cardiovasc Imaging. 2017 Aug;33(8):1223-1236
pubmed: 28239800
Curr Opin Lipidol. 2019 Oct;30(5):395-400
pubmed: 31335332
Blood. 2010 Oct 21;116(16):e74-80
pubmed: 20628149
Atherosclerosis. 2017 Nov;266:95-102
pubmed: 29017104
Atherosclerosis. 2018 Feb;269:245-251
pubmed: 29407600
Atherosclerosis. 2016 Nov;254:228-236
pubmed: 27764724
J Cardiovasc Comput Tomogr. 2016 Jul-Aug;10(4):269-81
pubmed: 27318587
Trends Immunol. 2018 Jun;39(6):438-445
pubmed: 29716792
Circulation. 2004 Oct 26;110(17):2638-43
pubmed: 15492297
Arterioscler Thromb Vasc Biol. 2009 Oct;29(10):1412-8
pubmed: 19759373
Thromb Res. 2007;121(3):387-95
pubmed: 17521710

Auteurs

Silverio Sbrana (S)

CNR Institute of Clinical Physiology, 54100 Massa, Italy.

Jonica Campolo (J)

CNR Institute of Clinical Physiology, 20162 Milan, Italy.

Alberto Clemente (A)

Fondazione Toscana Gabriele Monasterio, 56124 Pisa, Italy.

Luca Bastiani (L)

CNR Institute of Clinical Physiology, 54100 Massa, Italy.

Antonella Cecchettini (A)

Department of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy.
CNR Institute of Clinical Physiology, 56124 Pisa, Italy.

Elisa Ceccherini (E)

CNR Institute of Clinical Physiology, 56124 Pisa, Italy.

Chiara Caselli (C)

CNR Institute of Clinical Physiology, 56124 Pisa, Italy.

Danilo Neglia (D)

Fondazione Toscana Gabriele Monasterio, 56124 Pisa, Italy.

Oberdan Parodi (O)

CNR Institute of Clinical Physiology, 56124 Pisa, Italy.

Dante Chiappino (D)

Fondazione Toscana Gabriele Monasterio, 56124 Pisa, Italy.

Jeff M Smit (JM)

Department of Cardiology, Leiden University Medical Center, 2333 ZA, Leiden, Netherlands.

Arthur J Scholte (AJ)

Department of Cardiology, Leiden University Medical Center, 2333 ZA, Leiden, Netherlands.

Gualtiero Pelosi (G)

CNR Institute of Clinical Physiology, 56124 Pisa, Italy.

Silvia Rocchiccioli (S)

CNR Institute of Clinical Physiology, 56124 Pisa, Italy.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH