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Objectives: The objectives are to assess smoking abstinence and its effects on vascular risk and to report tobacco-cessation counselling and pharmacotherapy use in patients who had a recent minor stroke or transient ischaemic attack (TIA)., Design and Setting: The TIA registry.org project is a prospective, observational registry of patients with TIA and minor stroke that occurred in the previous 7 days with a 5-year follow-up, involving 61 sites with stroke specialists in 21 countries (Europe, Asia, Latin America and Middle East). Of those, 42 sites had 5-year follow-up data on more than 50% of their patients and were included in the present study., Participants: From June 2009 through December 2011, 3847 patients were eligible for the study (80% of the initial cohort)., Outcomes: Tobacco counselling and smoking-cessation pharmacotherapy use in smoking patients were reported at discharge. Association between 3-month smoking status and risk of a major cardiovascular event (MACE) was analysed with multivariable Cox regression model., Results: Among 3801 patients included, 835 (22%) were smokers. At discharge, only 35.2% have been advised to quit and 12.5% had smoking-cessation pharmacotherapy prescription. At 3 months, 383/835 (46.9%) baseline smokers were continuers. Living alone and alcohol abuse were associated with persistent smoking; high level of education, aphasia and dyslipidaemia with quitting. The adjusted HRs for MACE at 5 years were 1.13 (95% CI 0.90 to 1.43) in former smokers, 1.31 (95% CI 0.93 to 1.84) in quitters and 1.31 (95% CI 0.94 to 1.83) in continuers. Using time-varying analysis, current smoking at the time of MACE non-significantly increased the risk of MACE (HR 1.31 (95% CI 0.97 to 1.78); p=0.080)., Conclusion: In the TIAregistry.org, smoking-cessation intervention was used in a minority of patients. Surprisingly, in this population in which, at 5 years, other vascular risk factors were well controlled and antithrombotic treatment maintained, smoking cessation non-significantly decreased the risk of MACE., Competing Interests: Competing interests: PL has nothing to disclose. PA reports receipt of research grant support from Pfizer, Sanofi, Bristol-Myers-Squibb, AstraZeneca, Boston Scientific, AltheraPharmaceutical, and from the French government, and consulting fees from Pfizer, BMS, AstraZeneca, Johnson and Johnson, Kowa, Amgen, and lecture fees from Amgen, Pfizer, Sanofi. P-JT reports royalties from IP in IMT Company and is a stockholder in IMT. GWA reports equity interest: iSchemaView, and consultant fees from Medtronic, iSchemaView, Janssen, and Biogen. GAD reports unrestricted research grant from Sanofi, speaker and advisory board fees from Boehringer Ingelheim, Bristol Myer Squibb, Pfizer and Bayer companies. JMF reports having received fees as speakers bureau from Boehringer-Ingelheim, consultant fees from GSK, Ferrer and Servier. PGS discloses the following relationships: research grants: Amarin, AstraZeneca, Bayer, Sanofi, and Servier Clinical Trials (Steering committee, CEC, DSMB): Amarin, AstraZeneca, Bayer, Bristol-Myers Squibb, Idorsia, Janssen, Novartis, PhaseBio, Pfizer, Sanofi, Servier Consulting or speaking: Amarin, Amgen, BMS, Novo-Nordisk, Regeneron Senior Associate Editor at Circulation Bayer, Boehringer-Ingelheim, BristolMyersSquibb, Idorsia, Mylan, NovoNordisk, Novartis, Pfizer, Regeneron, Sanofi, Servier. HC has nothing to disclose. JL has nothing to disclose. MGH has nothing to disclose. SU reports receipt of research grants, consultancy fees, and lecture fees from Sanofi, Bayer, Otsuka, Boehringer-Ingelheim, and Daiichi-Sankyo, and research grants from the Japanese Ministry of Health, Labour, and Welfare and Japan Cardiovascular Research Foundation. EV reports Consulting/speaking honoraria from Abbott, Amgen, BMS, Fresenius, GSK, Medtronic, Pfizer, Sanofi, Stallergenes. LKSW reports honoraria as a member of a steering committee for Johnson & Johnson, Astra Zeneca and Bayer; honoraria for participation in clinical trials, contributions to advisory boards, or oral presentations from Bayer, Sanofi-Aventis, Bristol-Myers Squibb, Boehringer Ingelheim, and Pfizer. CAM serves in the Steering Committee of CLOTBUST-ER trial (Cerevast); SOCRATES (AstraZeneca), IMPACT-24b (Brainsgate), REVASCAT (Fundació Ictus Malaltia Vascular). He has received honoraria for participation in clinical trials, contribution to advisory boards or oral presentations from: Astra Zeneca: Boeringher Ingelheim, Daichii Sankyo, BMS, Covidien, Cerevast, Brainsgate. CAM has no ownership interest and does not own stocks of any pharmaceutical or medical device company. PR has received Advisory Board fees from Pfizer, Sanofi, Bristol-Myers-Squibb, AstraZeneca, Boehringer-Ingelheim, Bayer and Daiichi-Sankyo., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Purpose of Review: This review summarizes the recent evidence available regarding the epidemiology of cardiovascular disease in spondyloarthritis (SpA), including the effect of disease modifying drugs on cardiovascular risk., Recent Findings: People with SpA suffer from an increased risk of cardiovascular disease compared to the general population. This elevated risk is explained by the high prevalence of traditional cardiovascular risk factors and inflammation from disease activity leading to endothelial dysfunction and accelerated atherosclerosis. Consequently, the American College of Cardiology/American Heart Association and the European League Against Rheumatism recommend enhanced cardiovascular risk screening in SpA patients. There is evidence from observational studies that methotrexate and tumor necrosis factor inhibitors reduce the risk of cardiovascular events in SpA. Unlike what is observed in the general population, the use of nonsteroidal anti-inflammatory drugs does not appear to increase cardiovascular disease risk in SpA., Summary: Cardiovascular diseases are increasingly recognized in patients suffering from SpA, especially axial SpA and psoriatic arthritis. Cardiovascular diseases can cause significant morbidity, mortality, and add to the overall disease burden. Disease modifying drugs may mitigate some of the cardiovascular risk; however, a multidisciplinary team is needed to monitor patients and improve cardiovascular health status., (Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)

Objective: Polymorphisms in the antifungal signalling molecule CARD9 are associated with ankylosing spondylitis (AS). Here, we investigated the cellular mechanism by which CARD9 controls pathogenic Th17 responses and the onset of disease in both experimental murine AS and patients., Methods: Experiments in SKG, Card9 -/- SKG, neutrophil-deplete SKG mice along with in vitro murine, neutrophil and CD4 + T cell cocultures examined Card9 function in neutrophil activation, Th17 induction and arthritis in experimental AS. In AS patients the neutrophil: Bath Ankylosing Spondylitis Functional Index relationship was analysed. In vitro studies with autologous neutrophil: T cell cocultures examined endogenous CARD9 versus the AS-associated variant (rs4075515) of CARD9 in T cellular production of IL-17A., Results: Card9 functioned downstream of Dectin-1 and was essential for induction of Th17 cells, arthritis and spondylitis in SKG mice. Card9 expression within T cells was dispensable for arthritis onset in SKG mice. Rather, Card9 expression controlled neutrophil function; and neutrophils in turn, were responsible for triggering Th17 expansion and disease in SKG mice. Mechanistically, cocultures of zymosan prestimulated neutrophils and SKG T cells revealed a direct cellular function for Card9 within neutrophils in the potentiation of IL-17 production by CD4 + T cells on TCR-ligation. The clinical relevance of the neutrophil-Card9-coupled mechanism in Th17-mediated disease is supported by a similar observation in AS patients. Neutrophils from HLA-B27 + AS patients expanded autologous Th17 cells in vitro , and the AS-associated CARD9 S12N variant increased IL-17A., Conclusions: These data reveal a novel neutrophil-intrinsic role for Card9 in arthritogenic Th17 responses and AS pathogenesis. These data provide valuable utility in our future understanding of CARD9-specific mechanisms in spondyloarthritis ., Competing Interests: Competing interests: AAD consults for the pharmaceuticals (AbbVie, Amgen, Aurinia, Bristol Myers Squibb, Celgene, Eli Lilly, Glaxo Smith & Kline, Janssen, Moonlake, Novartis, Pfizer, UCB) and has received funding support from AbbVie, Bristol Myers Squibb, Eli Lilly, Glaxo Smith & Kline, Janssen, Novartis, Pfizer, UCB., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)