Background: Detecting impaired left ventricle (LV) or right ventricle (RV) mechanics could aid in fully understanding the process of cardiac involvement in patients with systemic lupus erythematosus (SLE). This study aimed to evaluate biventricular strain parameters derived from cardiac magnetic resonance (CMR) tissue tracking in SLE patients and their association with other clinical variables.Methods: A group of 47 SLE patients and 27 healthy controls were enrolled and underwent CMR examination, including cine and late gadolinium enhancement (LGE) imaging. Aside from RV strain parameters in the radial direction, biventricular global peak strain and peak systolic/diastolic global strain rate in radial, circumferential, and longitudinal directions were assessed for each participant. Multivariate linear regression analysis was used to analyze the factors related to the biventricular strain parameters.Receiver operating characteristic (ROC) analysis was used to identify RV dysfunction.Results: Compared with the controls, part of the biventricular strain parameters in the SLE subgroup with preserved ejection fraction (EF) were impaired, which was more significant in the SLE subgroup with reduced EF (all P<0.05). The SLE patients with RV dysfunction (15/47) included patients with LV dysfunction (8/47).The RVEF was associated with impaired LV global peak strain and peak diastolic strain rate in the SLE patients (absolute value of β=0.406-0.715, all P<0.05). The LV LGE in SLE patients (12/47) was associated with LV global longitudinal peak strain and peak diastolic global longitudinal strain rate (β=0.378 and −0.342; all P<0.05). There were independent correlations between pulmonary arterial hypertension and RV global longitudinal peak strain, anti-ribonucleoprotein (RNP) antibody and RV global circumferential peak strain, and pericardial effusion and RV peak diastolic global circumferential strain rate, respectively (β=0.319, 0.359, and −0.285, respectively; all P<0.05). The LV global longitudinal peak strain had greater diagnostic accuracy for RV dysfunction RV dysfunction [area under curve (AUC): 0.933, cut-off value: −13.38%).Conclusions: Biventricular strain parameters derived from CMR are sensitive markers of subclinical ventricular function impairment before EF reduction at an early stage of SLE. Biventricular strain analysis could be considered for inclusion in early cardiac functional assessment in SLE patients, particularly LV global longitudinal peak strain, which might assist in therapeutic decision-making and disease monitoring.

Objectives Myocardial injury (MInj) in systemic lupus erythematosus (SLE) has been observed in several studies. However, clinical predictors of MInj remain unclear. We aim to explore the effects of community-acquired pneumonia (CAP) on MInj in SLE patients according to cardiac magnetic resonance (CMR) T1 mapping. Methods SLE patients with or without CAP and healthy controls underwent CMR screening. The CMR protocol included: cines, T1- and T2 mapping, and late gadolinium enhancement (LGE). Clinical characteristics, CMR findings, and T1 mapping measuremments were compared between subgroups. Clinical assessment was performed on the subjects. Results Thirty-eight SLE patients were screened, including 18 patients with CAP (CAP group) and 20 age- and gender-matched patients without CAP (non-CAP group) as well as 26 healthy controls. The platelet count of CAP group was higher than the non-CAP group ( p = 0.015). Compared with the health control group, native T1 was higher in the CAP group ( p < 0.001) and the non-CAP group ( p = 0.002). ECV was higher in the CAP group ( p < 0.001) and the non-CAP group ( p = 0.002). The LV ejection fraction ( p = 0.049) and RV ejection fraction ( p = 0.026) of the CAP group was lower than that of the healthy control group, whereas no significant difference was observed between non-CAP and healthy control groups. Conclusions This is the first study that assesses the effects of CAP on MInj of SLE patients by CMRI T1 mapping. We highlight SLE patients with CAP who are at increased risk of MInj, manifesting as myocardial inflammation, diffuse myocardial fibrosis, and decreased ventricular function.