Article Text
Abstract
Background Cardiovascular (CV) involvement in patients with systemic lupus erythematosus (SLE) is presumably subclinical for the major part of its evolution. We evaluated the associations between high-sensitive troponin T (hs-TropT), a sensitive marker of myocardial injury, and CV involvement using cardiac magnetic resonance (CMR).
Methods and results This is a two-centre (London and Frankfurt) CMR imaging study at 3.0 Tesla of consecutive 92 patients with SLE free of cardiac symptoms, undergoing screening for cardiac involvement. Venous samples were drawn and analysed post-hoc for cardiac biomarkers, including hs-TropT, high-sensitive C reactive protein and N-terminal pro brain natriuretic peptide. Compared with age-matched/gender-matched non-SLE controls (n=78), patients had significantly raised cardiac biomarker levels, native T1 and T2, aortic and ventricular stiffness, and reduced global longitudinal strain (p<0.01). In SLE, hs-TropT was significantly and independently associated with native T2, followed by the models including native T1 and aortic stiffness (Χ2 0.462, p<0.01). There were no relationships between hs-TropT and age, gender, CV risk factors, duration of systemic disease, cardiac structure or function, or late gadolinium enhancement.
Conclusions Patients with SLE have a high prevalence of subclinical myocardial injury as demonstrated by raised high-sensitive troponin levels. CMR with T2 mapping reveals myocardial oedema as the strongest predictor of hs-TropT release, underscoring the inflammatory interstitial remodelling as the main mechanism of injury. Patients without active myocardial inflammation demonstrate diffuse interstitial remodelling and increased vascular stiffness. These findings substantiate the role of CMR in screening of subclinical cardiac involvement.
Trial registration numer NCT02407197; Results.
- inflammation
- systemic lupus erythematosus
- cardiovascular disease
- magnetic resonance imaging
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Footnotes
Handling editor Josef S Smolen
Contributors All authors have made relevant contributions to this manuscript as outlined by the International Committee of Medical Journal Editors. Substantial contributions to the conception or design of the work; or the acquisition, analysis or interpretation of data for the work: LW, RH, AB, UD, HB, SS, DPD’C, GC-W, MM, KS, CA, KK, TJV, AMZ, EN, VOP. Drafting the work or revising it critically for important intellectual content: LW, RH, AB, UD, HB, EN, VOP. Final approval of the version to be published: LW, RH, AB, UD, HB, SS, DPD’C, GC-W, MM, KS, CA, KK, TJV, AMZ, EN, VOP. Agreement to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved: LW, EN, VOP.
Funding Department of Health via the National Institute for Health Research (NIHR) comprehensive Biomedical Research Centre (BRC) award to Guy’s and St Thomas’ NHS Foundation Trust in partnership with King’s College London and King’s College Hospital NHS Foundation Trust. Spanish Cardiology Society Fellowship to RH. German Ministry of Education and Research via the German Centre for Cardiovascular Research (DZHK) to VOP, AMZ and EN.
Competing interests None declared.
Patient consent Obtained.
Ethics approval The study protocol was reviewed and approved by the respective local ethics committee (Guy’s and St Thomas' Ethics Committee (London site), and Ethikkommission, Goethe University Frankfurt, Germany). All procedures were carried out in accordance with the Declaration of Helsinki.
Provenance and peer review Not commissioned; externally peer reviewed.