Myositis-Specific Autoantibodies and QTc Changes by ECG in Idiopathic Inflammatory Myopathies

Sine Søndergaard Korsholm, Daniel C Andersson, John Bonde Knudsen, Maryam Dastmalchi, Axel C P Diederichsen, Oke Gerke, Nanna Witting, Søren Jacobsen, Redi Pecini, Tina Friis, Markus E Krogager, Ingrid E Lundberg, Louise C. Pyndt Raun Diederichsen

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Abstrakt

OBJECTIVES: The aim of this study was to investigate cardiac involvement detected by electrocardiography (ECG) in patients with idiopathic inflammatory myopathies (IIM) and to evaluate possible associations between autoantibody profile and ECG changes in these patients.

METHODS: In a Scandinavian cross-sectional study, patients were included from two Danish centres and one Swedish centre. Resting 12-lead ECG was investigated in 261 patients with IIM compared with 102 patients with systemic sclerosis (SSc) and 48 healthy controls (HCs). ECG changes were correlated to clinical manifestations and myositis-specific (MSAs) and myositis-associated (MAAs) autoantibodies.

RESULTS: Patients with IIM had longer mean QTc duration and more frequently presented with prolonged QTc (≥ 450 ms; p= 0.038) compared with HCs. Longer QTc duration was recorded in SSc compared with IIM (433 ± 23 ms vs 426 ± 24 ms, p= 0.011), yet, no significant difference in the fraction with prolonged QTc (SSc: 22%, IIM: 16%; p= 0.19). In multivariable regression analyses, anti-Mi2 (p= 0.01, p= 0.035) and anti-Pl-7 (p= 0.045, p= 0.014) were associated with QTc duration and prolonged QTc in IIM. Elevated CRP was associated with prolonged QTc (p= 0.041).

CONCLUSION: Presence of QTc abnormalities was as common in patients with IIM as in patients with SSc, including prolonged QTc seen in almost one fifth of the patients. Anti-Mi2, anti-Pl-7, and elevated CRP may serve as biomarkers for cardiac disease in IIM, but needs to be confirmed in a larger prospective study.

OriginalsprogEngelsk
TidsskriftRheumatology (Oxford, England)
ISSN1462-0324
DOI
StatusE-pub ahead of print - 20. jan. 2022

Bibliografisk note

© The Author(s) 2022. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For permissions, please email: journals.permissions@oup.com.

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