Autoimmune Diseases and Cardiovascular System: Physiopathology, Epidemiology, Clinical Characteristics and Therapeutic Strategies

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Immunology".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 1302

Special Issue Editor


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Guest Editor
Dipartimento di Medicina, Chirurgia e Farmacia, University of Sassari, 07100 Sassari, Italy
Interests: autoimmune disorders; rheumatic diseases; clinical rheumatology; rheumatoid arthritis; autoimmunity; atherosclerosis; endothelial dysfunction; cardiovascular disease; arterial stiffness; atrial myopathy

Special Issue Information

Dear Colleagues,

The impact of chronic autoimmune conditions on the development of cardiovascular disease is due to a broad range of conditions, including a chronic inflammatory burden, oxidative stress, the loss of tolerance, and the adverse effects of immunosuppressive and anti-inflammatory drugs. Patients with autoimmune diseases, including rheumatoid arthritis, lupus, psoriasis, multiple sclerosis, and type 1 diabetes, are exposed to the dangerous effects of inflammation, which leads to endothelial dysfunction, early atherosclerosis, and arterial stiffening, causing irreversible damage to blood vessels, heart muscle, and other components of the cardiovascular system. This can result in a higher risk of premature cardiovascular events, such as heart attacks and strokes, in individuals with autoimmune diseases, compared with the general population.

This Special Issue aims to provide a platform for scholars to share their valuable insights on topics such as the prevalence of cardiovascular events and the performance of commonly used cardiovascular risk scores in assessing the risk of future events in patients affected by autoimmune conditions. Further potential topics of interest of this Special Issue include, but are not limited to, the following: the role of inflammation in the development of atherosclerosis; oxidative stress and autoimmunity in atherosclerosis; novel biomarkers of subclinical cardiovascular disease under autoimmune conditions; microbiomes and atherosclerosis in autoimmune diseases; the effects of drugs on cardiovascular disease under autoimmune conditions; and clonal hematopoiesis and cardiovascular disease in autoimmune diseases.

Understanding the mechanisms and risk factors for cardiovascular involvement in autoimmune diseases is crucial for developing effective prevention and treatment strategies to minimize the cardiovascular risk and to protect patients from excessive cardiovascular morbidity and mortality.

We encourage submissions of both original research articles and reviews.

Prof. Dr. Gian Luca Erre
Guest Editor

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Keywords

  • cardiovascular events
  • cardiovascular risk
  • atherosclerosis
  • autoimmune diseases
  • treatment

Published Papers (1 paper)

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Research

13 pages, 261 KiB  
Article
Real-Life Comparison of Four JAK Inhibitors in Rheumatoid Arthritis (ELECTRA-i Study)
by Maurizio Benucci, Francesca Li Gobbi, Arianna Damiani, Edda Russo, Serena Guiducci, Mariangela Manfredi, Barbara Lari, Valentina Grossi and Maria Infantino
J. Clin. Med. 2024, 13(6), 1821; https://doi.org/10.3390/jcm13061821 - 21 Mar 2024
Viewed by 1134
Abstract
Background: Real-world evidence of the efficacy and adverse events of JAK inhibitor treatment (Tofacitinib, Baricitinib, Upadacitinib, and Filgotinib) in rheumatoid arthritis is still limited. Methods: We studied 115 patients from the Rheumatology Unit of S. Giovanni di Dio Hospital affected by D2T-RA, according [...] Read more.
Background: Real-world evidence of the efficacy and adverse events of JAK inhibitor treatment (Tofacitinib, Baricitinib, Upadacitinib, and Filgotinib) in rheumatoid arthritis is still limited. Methods: We studied 115 patients from the Rheumatology Unit of S. Giovanni di Dio Hospital affected by D2T-RA, according to the 2010 EULAR criteria. Out of the 115 patients, 17 had been treated with Baricitinib 8 mg/daily, 32 with Filgotinib 200 mg/daily, 21 with Tofacitinib 10 mg/daily, and 45 with Upadacitinib 15 mg/daily. We evaluated the clinical response after 3, 6, and 12 months of treatment and the follow-up from September 2022 to September 2023. All patients were evaluated according to the number of tender joints (NTJs), number of swollen joints (NSJs), visual analog scale (VAS), global assessment (GA), health assessment questionnaire (HAQ), Disease Activity Score (DAS28), and CDAI. Furthermore, laboratory parameters of efficacy and tolerability were evaluated. Results: All treatments demonstrated a statistically significant decrease in the DAS28 and CDAI scores, tender and swollen joint counts, VAS, HAQ, and patient global assessment (PGA) after 3, 6, and 12 months of treatment. All treatments showed similar behavior, and statistically significant decreases in circulating calprotectin, TNFα, and IL-6 were observed for all drugs after 12 months of treatment. In addition, soluble urokinase plasminogen activator receptor (suPAR) values showed significant differences at baseline and after 12 months of treatment for Filgotinib: 4.87 ± 4.53 vs. 3.61 ± 0.9 (0.009) and Upadacitinib: 6.64 ± 7.12 vs. 4.06 ± 3.61 (0.0003), while no statistically significant differences were found for Baricitinib: 3.4 ± 0.1 vs. 3.78 ± 0.1 and Tofacitinib: 3.95 ± 1.77 vs. 2.58 ± 0.1. The TC/HDL-C ratio (atherogenic index) showed significant differences when comparing Baricitinib vs. Filgotinib (0.0012), Filgotinib vs. Tofacitinib (0.0095), and Filgotinib vs. Upadacitinib (0.0001); furthermore, the LDL-C/HDL-C ratio in the Filgotinib group did not change (2.37 ± 0.45 vs. 2.35 ± 2.13 (NS)) after 12 months of treatment. Venous Thrombotic Events (VTEs) and major adverse cardiovascular events (MACEs) accounted for 1% of adverse events after treatment with Baricitinib. Herpes zoster reactivation accounted for 1% of adverse events after treatment with Filgotinib and Tofacitinib, while non-melanoma skin cancer (NMSC) accounted for 1% of adverse events after Upadacitinib treatment. Conclusions: Our real-world data from patients with RA show differences in some laboratory parameters and in the impact of lipid metabolism in JAK inhibitor treatment. Full article
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