Abstract
Background Antimalarial (AM)-induced cardiomyopathy (AMIC) has been rarely reported in systemic lupus erythematosus (SLE). However, given the large number of patients treated, it seems possible that AMIC is under-recognized and may run undiagnosed as an ill-defined heart failure syndrome. Specific cardiac biomarkers may identify patients at risk. We sought to investigate the prevalence and associated factors for such biomarkers in SLE.
Methods One hundred sixty-eight consecutive patients (153 females) attending the a large lupus clinic, without past history of cardiac disease (heart failure, coronary artery disease, valvulopathy etc.) and/or pulmonary hypertension, were enrolled. None had chest pain or electrocardiographic (ECG) abnormalities suggestive of acute coronary syndrome. High-sensitivity cardiac troponin I (cTnI) and B-natriuretic peptide (BNP) were measured simultaneously in serum and plasma samples, respectively. Patients were categorized according to normal or abnormal BNP and/or cTnI. For the assessment of the impact of AM duration on abnormal cardiac biomarkers, patients were divided in two groups according to the median duration of use, which was calculated at 5.6 years in the current cohort. Statistical analysis was performed with SAS 9.0 software; p<0.05 was considered significant.
Results Sixteen patients (9.5%) had elevated BNP and/or cTnI. Compared to subjects with normal biomarkers, they were older, had longer disease and AM use duration and more frequently persistent creatine phosphokinase (CPK) elevation (table 1). Multivariable regression analysis showed prolonged AM treatment (>5.6 years) and persistent CPK elevation to be important predictors for elevated cardiac biomarkers [HR=5.43, 95% CI=1.14 to 25.9, p=0.034 and HR=4.62, 95% CI=1.22 to 17.51, p=0.024, respectively]. Two patients were diagnosed with AMIC on endomyocardial biopsy; both had CPK and BNP/cTnI elevation.
Conclusions Approximately 9% of SLE patients had elevated myocardial biomarkers, in the absence of prior cardiac disease or pulmonary arterial hypertension. Prolonged AM therapy and persistent CPK elevation conferred an increased risk for abnormal BNP and cTnI, which might predict AMIC.