{
  "abstract": "Introduction Systemic sclerosis (SSc) is associated with up to a four-fold higher risk of cardiovascular involvement, and cardiac disease accounts for around one-quarter of SSc-related deaths. Cardiovascular magnetic resonance (CMR) enables detection of subclinical myocardial abnormalities. Type I interferon (IFN) plays a role in vascular and fibrotic pathways, and elevated levels correlate with disease activity, but its relationship with cardiac involvement is unclear. We aimed to evaluate whether IFN activity and its chemokine correlates associate with myocardial involvement in SSc.Material and Methods SSc patients without known SSc/non-SSc heart disease, diabetes, or more than 1 traditional cardiovascular risk factor underwent CMR on a 3 Tesla Philips Achieva MR system. Myocardial perfusion reserve (MPR) was recorded, and abnormal myocardial tissue (MT) was defined by 1 or more of: non-ischaemic late gadolinium enhancement (LGE), native T1 more than 1050 ms (diffuse interstitial changes), or extracellular volume (ECV) >30% (fibrosis). Serum IFN score was calculated from CCL2, CCL8, CCL19, CXCL9, CXCL10, and CXCL11 concentrations; ‘high IFN’ was defined as 2 SD or more above healthy control mean. χ 2 /Fisher’s exact test, correlation analyses, and logistic regression were used (p<0.05 nominally significant).Results 36 SSc patients were included in this study, 13 had normal MT and 23 had abnormal MT. Baseline characteristics are summarized in table 1 and were comparable between normal and abnormal MT groups except for high hs-TnI (more than 37 ng/L), which was significantly more frequent in the abnormal MT group (43.5% vs 15.4%, p = 0.02) and median NT-proBNP and hs-TnI numerically higher in this group. Mean Luminex IFN scores were comparable between the two MT groups (table 1), however, a high IFN signature was more frequent in the abnormal MT group (52.1% vs 23.1%, p = 0.03). IFN activity was not associated with individual quantitative CMR parameters. Among the individual chemokines, CCL19 levels were higher with abnormal MT (192.2 ± 133.1 vs 169.0 ± 122.3 pg/mL, p = 0.03). IFN signature demonstrated a moderate positive correlation with myocardial perfusion reserve (MPR) (r = 0.36, p = 0.17;), not reaching statistical significance.Conclusions Myocardial tissue changes and injury are associated with a high IFN signature, specifically, increased CCL19 levels, suggesting a link between immune dysregulation and myocardial involvement. These exploratory findings warrant validation in larger cohorts to establish IFN as a biomarker of SSc-myocardial involvement and investigation to determine whether a therapeutic target in SSc-related cardiac disease.Abstract OC.04 Table 1Abstract OC.04 Figure 1a) Violin plots showing (left) Luminex IFN levels in patients with CMR abnormal vs normal, and (right) native T1 values in patients stratitied by IFN-low vs IFN-high status. White dots represent the median, thick bars the interquartile range, and thin lines the rest of the distributionAbstract OC.04 Figure 2Scatter plots showing associations between IFN activity (Luminex) and quantitative CMR parameters: {a) native T1 (ms) and (b) ECV (%). Each dot represents an individual patient, with the red line indicating linear regression fit",
  "authors": [
    {
      "affiliations": [
        "Centre for Musculoskeletal Research, Division of Musculoskeletal & Dermatological Sciences, Manchester, UK"
      ],
      "name": "Cristiana Sieiro Santos"
    },
    {
      "affiliations": [
        "Department of Rheumatology, University Hospital Coventry & Warwickshire NHS Trust, Warwickshire, UK"
      ],
      "name": "Raluca Bianca Dimitru"
    },
    {
      "affiliations": [
        "Department of Rheumatology, Leeds Teaching Hospitals NHS Trust, Leeds, UK",
        "Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, LS2 9JT, United Kingdom, Leeds, UK"
      ],
      "name": "Lesley-Anne Bissell"
    },
    {
      "affiliations": [
        "Nottingham University Hospitals NHS Trust, Nottingham, UK"
      ],
      "name": "Bara Erhayiem"
    },
    {
      "affiliations": [
        "Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK"
      ],
      "name": "Graham Fent"
    },
    {
      "affiliations": [
        "Rheumatology Institute of Lucania (IReL) and Rheumatology Department of Lucania, San Carlo Regional Hospital, Potenza, Potenza, Italy"
      ],
      "name": "Giuseppina Abignano"
    },
    {
      "affiliations": [
        "Department of Rheumatology, Leeds Teaching Hospitals NHS Trust, Leeds, UK"
      ],
      "name": "Marco Minerba"
    },
    {
      "affiliations": [
        "Department of Rheumatology, Leeds Teaching Hospitals NHS Trust, Leeds, UK"
      ],
      "name": "Rebecca Ross"
    },
    {
      "affiliations": [
        "Department of Medical Physics and Engineering, Leeds Teaching Hospitals NHS Trust, Leed, UK"
      ],
      "name": "John Greenwood"
    },
    {
      "affiliations": [
        "Baker Heart and Diabetes Institute, Melbourne, Australia, Melbourne, Australia"
      ],
      "name": "John Biglands"
    },
    {
      "affiliations": [
        "Department of Biomedical Imaging Science, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Le, Leeds, UK"
      ],
      "name": "Sven Plein"
    },
    {
      "affiliations": [
        "Department of Rheumatology, Leeds Teaching Hospitals NHS Trust, Leeds, UK"
      ],
      "name": "Francesco Del Galdo"
    },
    {
      "affiliations": [
        "Centre for Musculoskeletal Research, Division of Musculoskeletal & Dermatological Sciences, Manchester, UK",
        "Department of Rheumatology, Leeds Teaching Hospitals NHS Trust, Leeds, UK"
      ],
      "name": "Maya Buch"
    }
  ],
  "title": "OC.04 High type 1 interferon associates with subclinical myocardial involvement in systemic sclerosis",
  "uid": "d98734a4-6c06-5d9f-aad4-226d39f33700"
}
