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177 Association between chronic antimalarial therapy and elevated myocardial biomarkers in patients with systemic lupus erythematosus and no prior heart disease: a preliminary report
  1. K Tselios1,
  2. D Gladman1,
  3. P Harvey2,
  4. J Su1 and
  5. M Urowitz1
  1. 1University of Toronto and Toronto Western Hospital, Rheumatology, Toronto, Canada
  2. 2University of Toronto and Women’s College Hospital, Medicine, Toronto, Canada


Background and aims Antimalarial (AM)-induced cardiomyopathy is an extremely rare complication of AM treatment in systemic lupus erythematosus (SLE). The use of specific cardiac biomarkers may identify patients at risk. We sought to investigate the prevalence and associated factors for abnormal myocardial biomarkers in lupus patients.

Methods Consecutive patients (n=179) attending the Toronto Lupus Clinic were enrolled. BNP (brain natriuretic peptide, assessing pressure and/or volume overload) and cTnI (cardiac troponin I, assessing myocardial necrosis) were measured simultaneously. None had ECG abnormalities suggestive of acute coronary syndrome. Analysis was performed with SAS 9.3; p<0.05 was considered significant.

Results Twenty-seven patients (15.1%) had elevated BNP and/or cTnI; 11 with prior history of heart failure, coronary artery disease, pulmonary hypertension and/or exertional dyspnea were excluded. Compared to subjects with normal biomarkers, the remaining patients (n=16) were older [54.7±15.1 vs. 47.8±12.2 years, p=0.037], had longer disease duration [22.6±10.4 vs. 15.5±10.1 years, p<0.001], longer AM use [12.5±9.6 vs. 7.9±8 years, p=0.034] and more frequently persistent CPK elevation [44.4 vs. 16.4%, p<0.001]. Multi-variable regression analysis showed chronic AM treatment combined with CPK elevation to be an important predictor for elevated myocardial biomarkers [HR=1.41, 95%CI=1.06–1.89, p=0.02]. Two patients were diagnosed with AM-induced cardiomyopathy on endomyocardial biopsy; both had CPK and BNP/cTnI elevation.

Conclusions Approximately 9% of unselected SLE patients had elevated myocardial biomarkers, in the absence of prior cardiac disease. Chronic AM therapy accompanied by persistent CPK elevation conferred an increased risk for abnormal BNP and cTnI, which might predict cardiomyopathy in such patients.

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