Background: Rheumatoid arthritis (RA) was historically associated with an increased incidence of major adverse cardiovascular events (MACE). Recent literature has shown a reduction in this incidence in patients diagnosed after the year 2000 (“modern RA”), with the MACE incidence gap between RA and the general population closing. In contrast to this, osteoarthritis (OA) has now been linked to higher MACE incidence than population controls. OA is another common condition referred to and seen in rheumatology and has conventionally been regarded as a degenerative disease caused by “mechanical wear and tear”. However, it has increasingly been recognised as having an inflammatory basis, with some potential overlap with the signalling pathways seen in RA. Conventional MACE risk factors, including age, smoking and deprivation index are important contributors in both RA and OA populations, though other disease specific factors are likely to be implicated given the inflammatory nature, such as circulating inflammatory cytokines (more so in RA). Treatment for OA still follows a symptomatic management pathway; however, adoption of a “treat-to-target” management approach with disease modifying therapies for RA in recent decades has led to more rapid and sustained control of this disease.

Objectives: Firstly, to compare MACE incidence in a “real world” single centre population of modern RA and OA patients. Secondly, to determine if good clinical response to initial disease modifying treatments within the first 6 months of diagnosis in the early RA cohort influences longer-term MACE incidence.

Methods: We performed a single-centre retrospective review of individuals attending the North-East Arthritis Clinic (NEAC) receiving a new diagnosis of RA or OA between December 2011 to November 2021. All patients were followed up until 30 ^th April 2024 and MACE events recorded. MACE included stroke, transient ischaemic attack (TIA), myocardial infarction (MI) and new diagnosis of ischaemic heart disease (IHD). Clinical co-morbidities and characteristics were recorded along with symptom duration prior to diagnosis and socioeconomic factors, including smoking status and the level of deprivation, determined by an index score generated as per the “English indices of deprivation 2019” calculator. The Charlson Co-morbidity Index (CCI) was used and included measurement of conventional MACE risk factors. For the RA cohort, additional data collected included serostatus (seropositive defined as rheumatoid factor (RF) and/or anti-citrullinated protein antibody (ACPA) positive, seronegative defined as both RF and ACPA negative), baseline RA disease activity (DAS-28) and measures of early RA disease control (6-month EULAR response). Analysis included censoring to account for variable follow-up time. Survival and cox proportional hazards modelling were applied with co-variates included, such as age sex, baseline BMI, CCI, hypertension, deprivation index, smoking status, and symptom duration prior to diagnosis. R studio and JMP statistical software was used with significance taken at p<0.05.

Results: Cohorts included 278 early RA patients and 397 OA patients. RA patients were significantly older (mean age 67.3 years [range 25-95]) than OA patients (mean age 64.3 years [range 27-97]), (p=2.926e-05). Sex ratio (F:M) was ~2:1 for RA and ~4:1 for OA, (p=3.846e-06). There was a slight increase in smoking status in RA with 41.4% being current or previous smokers compared to 32.7% in the OA group (p=0.0284) and a higher co-morbidity burden was seen in OA than RA (CCI, p=0.0001). Mean BMI was significantly higher (p=0.0188) in the OA group at 29.14 kg/m ² [range 15.52-59.66] compared with RA (27.82 kg/m ² [range 16.54-47.67]). Deprivation index was comparable between cohorts (p=0.1448). Mean symptom duration prior to diagnosis was 21.84 weeks for RA and 43.92 weeks for OA. Study follow up-time were similar in both groups, with a median time of 8 years in OA versus 7 years in RA [range 2 to 12 for both]. Cox regression analyses identified increased incidence of MACE in both cohorts relating to traditional risk factors, such as smoking status (CI 1.1423-2.734), deprivation index (1.0101-1.243) and CCI (CI = 1.1817-1.460). However, when accounting for population characteristics, including MACE risk factors, there was no significant difference in MACE incidence between the RA and OA cohorts (Kaplan Meier, p value = 0.60). Furthermore, there were equivocal subcategory breakdowns of MACE events across the two groups (stroke 16 OA vs 16 RA, MI 16 OA vs 19 RA and IHD 18 OA vs 17 RA). Subgroup analyses within the RA cohort found no significant difference in MACE risk, when split into 1) seropositive versus seronegative (p=0.08), 2) EULAR response at 6 months (p=0.66), 3) baseline disease activity at diagnosis (DAS28-CRP p=0.72, DAS28-ESR p=0.92), and 4) symptom duration prior to diagnosis (p=0.16).

Conclusion: In this large retrospective cohort study, MACE incidence was similar in our OA and RA groups and in RA was independent of early clinical response to DMARDs. This could be secondary to a shift towards a more modern RA cohort. This is globally characterised by earlier review in early arthritis clinics, tighter disease control as well as the introduction and use of newer drugs including biologics, thus negating any effects of sustained high inflammatory responses that would have been historically observed in RA. Alternatively, this could be explained by recent understanding of an inflammatory component in OA as a potential risk factor for MACE. Therefore to better improve patient morbidity, modern OA patients, as well as modern RA patients, may benefit from early cardiovascular review and timely input to reduce longer-term cardiovascular risk.

REFERENCES: NIL.

Acknowledgements: The views expressed are those of the author(s) and not necessarily those of the NIHR or the Department of Health and Social Care.

Disclosure of Interests: None declared.

© The Authors 2025. This abstract is an open access article published in Annals of Rheumatic Diseases under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ). Neither EULAR nor the publisher make any representation as to the accuracy of the content. The authors are solely responsible for the content in their abstract including accuracy of the facts, statements, results, conclusion, citing resources etc.