Outcome of clinical and subclinical myocardial injury in systemic lupus erythematosus – A prospective cohort study

  • Riette du Toit
    Division of Rheumatology, Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University and Tygerberg Academic Hospital, Cape Town, South Africa
  • Phillip G Herbst
    Division of Cardiology, Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University and Tygerberg Academic Hospital, Cape Town, South Africa
  • Christelle Ackerman
    Division of Radiodiagnosis, Department of Medical Imaging and Clinical Oncology, Faculty of Medicine and Health Sciences, Stellenbosch University and Tygerberg Academic Hospital, Cape Town, South Africa
  • Alfonso JK Pecoraro
    Division of Cardiology, Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University and Tygerberg Academic Hospital, Cape Town, South Africa
  • Dirk Claassen
    Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University and Tygerberg Academic Hospital, Cape Town, South Africa
  • Henry P Cyster
    Division of Cardiology, Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University and Tygerberg Academic Hospital, Cape Town, South Africa
  • Helmuth Reuter
    Division of Clinical Pharmacology, Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University and Tygerberg Academic Hospital, Cape Town, South Africa
  • Anton F Doubell
    Division of Cardiology, Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University and Tygerberg Academic Hospital, Cape Town, South Africa

抄録

<jats:sec><jats:title>Objectives</jats:title><jats:p> To determine the outcome of subclinical lupus myocarditis (LM) over twelve months with regards to: mortality; incidence of clinical LM and change in imaging parameters (echocardiography and cardiac magnetic resonance [CMR]). To evaluate the impact of immunosuppression on CMR evidence of myocardial tissue injury. </jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p> SLE patients with and without CMR evidence of myocardial injury (as per 2009 Lake Louise criteria [LLC]) were included. Analysis at baseline and follow-up included: clinical evaluation, laboratory and imaging analyses (echocardiography and CMR). Clinical LM was defined as clinical features of LM supported by echocardiographic and/or biochemical evidence of myocardial dysfunction. Subclinical LM was defined as CMR myocardial injury without clinical LM. </jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p> Forty-nine SLE patients were included with follow-up analyses (after 12 months) available in 36 patients. Twenty-five patients (51%) received intensified immunosuppressive therapy during follow-up for indications related to SLE. Disease activity (SLEDAI-2K) improved (p < 0.001) from 13 (median;IQR:9–20) to 7 (3–11). One patient without initial CMR evidence of myocardial injury developed clinical LM. Mortality (n = 10) and SLE clinical features were similar between patients with and without initial CMR myocardial injury. Echocardiographic left ventricular ejection fraction (LVEF) (p = 0.014), right ventricular function (p = 0.001) and wall motion abnormalities (p = 0.056) improved significantly but not strain analyses nor the left LV internal diameter index. CMR mass index (p = 0.011) and LVEF (p < 0.001) improved with follow-up but not parameters identifying myocardial tissue injury (LLC). A trend towards a reduction in the presence of CMR criteria was counterbalanced by persistence (n = 7) /development of new criteria (n = 11) in patients. Change in CMR mass index correlated with change in T2-weighted signal (myocardial oedema) (r = 386;p = 0.024). Intensified immunosuppressive therapy had no significant effect on CMR parameters. </jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p> CMR evidence of subclinical LM persisted despite improved SLEDAI-2K, serological markers, cardiac function and CMR mass index. Subclinical LM did not progress to clinical LM and had no significant prognostic implications over 12 months. Immunosuppressive therapy did not have any significant effect on the presence of CMR evidence of myocardial tissue injury. Improvement in CMR mass index correlated with reduction in myocardial oedema and may be used to monitor SLE myocardial injury. </jats:p></jats:sec>

収録刊行物

  • Lupus

    Lupus 30 (2), 256-268, 2020-12-01

    SAGE Publications

被引用文献 (1)*注記

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