Autoimmune diseases in patients undergoing percutaneous coronary intervention: A risk factor for in-stent restenosis?


Journal

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

Informations de publication

Date de publication:
09 2021
Historique:
received: 27 01 2021
revised: 25 06 2021
accepted: 04 08 2021
pubmed: 22 8 2021
medline: 27 10 2021
entrez: 21 8 2021
Statut: ppublish

Résumé

Despite the relation between autoimmune diseases and increased atherosclerotic risk is established, the influence of autoimmune disorders on in-stent restenosis (ISR) after percutaneous coronary intervention (PCI) is only partly known. ISR is an aberrant reparative process mainly characterized by an increased number of vascular smooth muscle cells and excessive deposition of extracellular proteoglycans and type III collagen. Chronic inflammation, always present in autoimmune diseases, modulates the endothelial response to PCI. Aim of this review is to resume the current evidence on the association between ISR and autoimmune diseases, focusing on pathogenic mechanisms and therapeutic targets. We conducted a comprehensive review of the literature on the relationship between ISR and insulin-dependent diabetes mellitus (IDDM), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), antiphospholipid-antibodies syndrome (APS), inflammatory bowel diseases (IBD), and Hashimoto's thyroiditis (HT). Patients affected with IDDM, RA, SLE, APS, IBD and HT proved to face higher rates of ISR compared to the general population. The endothelial dysfunction seems the principal common pathogenic pathway for ISR and is attributed to both the immune system disorder and the systemic inflammation. Some evidence suggested that methotrexate and anti-tumor necrosis factor treatments can be effective in reducing ISR, while antibodies against vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 showed to reduce neointimal hyperplasia in animal models. Autoimmune diseases are a risk factor for ISR. The study of the potential cardiovascular benefits of the current therapies, mainly anti-inflammatory drugs, and the pursuit of innovative treatments appear of paramount interest.

Sections du résumé

BACKGROUND AND AIMS
Despite the relation between autoimmune diseases and increased atherosclerotic risk is established, the influence of autoimmune disorders on in-stent restenosis (ISR) after percutaneous coronary intervention (PCI) is only partly known. ISR is an aberrant reparative process mainly characterized by an increased number of vascular smooth muscle cells and excessive deposition of extracellular proteoglycans and type III collagen. Chronic inflammation, always present in autoimmune diseases, modulates the endothelial response to PCI. Aim of this review is to resume the current evidence on the association between ISR and autoimmune diseases, focusing on pathogenic mechanisms and therapeutic targets.
METHODS
We conducted a comprehensive review of the literature on the relationship between ISR and insulin-dependent diabetes mellitus (IDDM), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), antiphospholipid-antibodies syndrome (APS), inflammatory bowel diseases (IBD), and Hashimoto's thyroiditis (HT).
RESULTS
Patients affected with IDDM, RA, SLE, APS, IBD and HT proved to face higher rates of ISR compared to the general population. The endothelial dysfunction seems the principal common pathogenic pathway for ISR and is attributed to both the immune system disorder and the systemic inflammation. Some evidence suggested that methotrexate and anti-tumor necrosis factor treatments can be effective in reducing ISR, while antibodies against vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 showed to reduce neointimal hyperplasia in animal models.
CONCLUSIONS
Autoimmune diseases are a risk factor for ISR. The study of the potential cardiovascular benefits of the current therapies, mainly anti-inflammatory drugs, and the pursuit of innovative treatments appear of paramount interest.

Identifiants

pubmed: 34418682
pii: S0021-9150(21)01268-5
doi: 10.1016/j.atherosclerosis.2021.08.007
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

24-31

Informations de copyright

Copyright © 2021 Elsevier B.V. All rights reserved.

Auteurs

Martino Pepe (M)

Cardiovascular Diseases Section, Department of Emergency and Organ Transplantation (DETO), University of Bari, Piazza G. Cesare 11, Bari (BA), 70120, Italy. Electronic address: drmartinopepe@gmail.com.

Gianluigi Napoli (G)

Cardiovascular Diseases Section, Department of Emergency and Organ Transplantation (DETO), University of Bari, Piazza G. Cesare 11, Bari (BA), 70120, Italy.

Eugenio Carulli (E)

Cardiovascular Diseases Section, Department of Emergency and Organ Transplantation (DETO), University of Bari, Piazza G. Cesare 11, Bari (BA), 70120, Italy.

Marco Moscarelli (M)

Cardiothoracic and Vascular Department, Maria Cecilia Hospital GVM Care & Research, Via Via Corriera 1,Cotignola, 48033, Ravenna, Italy.

Cinzia Forleo (C)

Cardiovascular Diseases Section, Department of Emergency and Organ Transplantation (DETO), University of Bari, Piazza G. Cesare 11, Bari (BA), 70120, Italy.

Palma Luisa Nestola (PL)

Cardiovascular Diseases Section, Department of Emergency and Organ Transplantation (DETO), University of Bari, Piazza G. Cesare 11, Bari (BA), 70120, Italy.

Giuseppe Biondi-Zoccai (G)

Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Corso della Republica 79, Latina, 04100,Latina, Italy; Mediterranea Cardiocentro, Via Orazio 2, Napoli, 80122, Napoli, Italy.

Arturo Giordano (A)

Invasive Cardiology Unit, "Pineta Grande" Hospital, Via Domitiana km 30, Castel Volturno, 81030, Caserta, Italy.

Stefano Favale (S)

Cardiovascular Diseases Section, Department of Emergency and Organ Transplantation (DETO), University of Bari, Piazza G. Cesare 11, Bari (BA), 70120, Italy.

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