Objectives To investigate a potential shared susceptibility between rheumatoid arthritis (RA) and acute coronary syndrome (ACS) by estimation of the risk of ACS among full siblings of patients with RA.
Methods By linking nation-wide Swedish registers, we identified a cohort of patients with new-onset RA 1996–2016, age- and sex-matched (5:1) general population comparator subjects, full siblings of RA and comparator subjects, and incident ACS events through 31 December 2016. We used Cox regression to estimate the HR of ACS among patients with RA and the siblings of patients with RA versus the general population, overall and stratified by RA serostatus. We explored the impact of traditional cardiovascular (CV) risk factors on the observed associations.
Results We identified 8109 patients with incident RA, and 11 562 full siblings of these. Compared with the general population, the HR of ACS in RA was 1.46 (95% CI 1.28 to 1.67) and 1.22 (95% CI 1.09 to 1.38) among their siblings. The increased risks seemed confined to seropositive RA (patients: 1.52 [1.30 to 1.79], their siblings: 1.27 [1.10 to 1.46]); no significant risk increase was observed among siblings of patients with seronegative RA (HR 1.13 [95% CI 0.92 to 1.39]). Adjustment for 19 traditional CV risk factors did not appreciably alter these associations.
Conclusion Siblings of patients with RA are at increased risk of ACS, suggesting shared susceptibility between RA and ACS, indicating the need and potential for additional cardio-preventive measures in RA (and their siblings).
- rheumatoid arthritis
- cardiovascular risk
- familial risk
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Handling editor Josef S Smolen
Contributors HW had full access to all of the data used for the analysis in this study and takes full responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: JA, HW and TF. Acquisition of data: JA, TF and HW. Statistical analysis: HW, TF and JA. Analysis and interpretation of data: all authors. Drafting of manuscript: HW and JA. Critical revision of manuscript and final approval given: all authors. Obtained funding: JA. Study supervision: JA.
Funding This work was supported by the Swedish Research Council, the Swedish Foundation for Strategic Research, Stockholm County Council (ALF), the Heart Lung Foundation, Karolinska Institutet (Strategic Research Area Epidemiology), The Nordic Research Council (Nordforsk) and the Rheumatology Research Foundation (FOREUM). Funders had no impact on the design or interpretation of the study or its results.
Competing interests JA has or has had research agreements with Abbvie, Astra-Zeneca, BMS, Eli Lilly, MSD, Pfizer, Roche, Samsung Bioepis, and UCB, mainly in the context of safety monitoring of biologics via ARTIS/Swedish Biologics Register. Karolinska Institutet has received remuneration for JA participating in advisory boards arranged by Pfizer and Lilly.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.
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