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AB0202 Cardiac Troponin T and Anti-Cardiac Troponin I Antibodies in Patients with Systemic Sclerosis: A Monocentric, Retrospective Pilot Study
  1. M. Vasile1,
  2. Z. Kaya2,
  3. M. Frerix3,
  4. U. Mueller-Ladner4,
  5. A. Rolf5,
  6. F. Meier6
  1. 1Department of Rheumatology, Kerckhoff Clinic, University of Giessen, Bad-Nauheim
  2. 2Department of Cardiology, University of Heidelberg, Heidelberg
  3. 3Department of Rheumatology, Kerkhoff Clinic, University of Giessen
  4. 4Department of Rheumatology, Kerckhoff-Clinic, University of Giessen
  5. 5Department of Cardiology, Kerckhoff Clinic, University of Giessen, Bad-Nauheim, Germany
  6. 6Institue of Infection, Immunity and Inflammation, Coll of Medical, Veterinary amnd Life Sciences, Glasgow, United Kingdom


Background Cardiac troponins (cTn) are widely used as biomarkers for the diagnosis and quantitation of cardiac injury (1). Autoantibodies against cTn, especially against cTnI (anti-cTnI), have been recently described in association with cardiac dysfunction (2). However, their clinical significance is still unclear. Systemic sclerosis (SSc) is a chronic autoimmune connective tissue disease that is associated with heart involvement, although often clinically occult (3,4).

Objectives Hence, the value of elevated cTn levels and a possible autoimmune response against cTnI as biomarkers in patients with SSc were the aims of this study.

Methods Out of our monocentric SSc cohort we retrospectively identified 113 of 190 patients in whom routine laboratory assessment including high-sensitive cTnT was performed. Stored biosamples, available for 60/113 patients (53.1%), were used to assess auto-cTnI titres as previously described (5). A 2x2 table, using chi-square test, compared the results of cTnT and anti-cTnI. If available, cardiac magnetic-resonance-imaging (cMRI) data were retrospectively evaluated to assess early myocardial gadolinium enhancement (T1 ratio, as a marker for hyperemia and capillary leakage) as well as edema (T2 ratio).

Results Out of 113 patients with available results for cTNT, 41 patients (36.3%) had a positive and 72 (63.7%) a negative result. Biosamples were available for 21 cTNT positive and 39 cTNT negative patients. Anti-cTnI were detected in 17 samples (28.3%): in 8 (38.1%) cTNT positive compared to 9 (23.1%) cTNT negative patients (p=0.218). Anti-cTnI-titres were 1:40 in 7, 1:80 in 6 and 1:160 in 4 samples. cMRI data were available for three anti-cTnI positive patients (all diffuse cutaneous subtype). All of them had a distinct change in the T1 ratio (6.4-8.9), not in the T2 ratio. Late enhancement (gold standard for the detection of myocarditis) was present in one patient (6).

Conclusions The preliminary results of this pilot study suggest that cTnT levels are elevated in about one third of SSc patients, and anti-cTnI are present in about a third of cTNT positive patients. Additionally, anti-cTnI can be detected in about a quarter of cTNT negative patients. Whether cTNT and/or anti-cTnI autoantibodies might serve as new biomarkers in SSc heart disease need to be evaluated in further prospective trials.


  1. Kaya Z Clin. Immunol. 134,80–88(2010).

  2. Kaya Z Circulation Research 110,145–158(2012).

  3. Allanore Y Curr Opin Rheumatol 20,697–702(2008).

  4. Meune C Arch Cardiovasc Dis 103,46–52(2010).

  5. Leuschner F Eur. Heart J. 29, 1949–1955(2008).

  6. Desai CS Curr Opin Rheumatol 23,545–554(2011).

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.3595

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