1346226 - Subclinical cardiovascular disease in South African systemic lupus erythematosus patients is a common finding

Cardiovascular disease (CVD) is a leading cause of morbidity and mortality in systemic lupus erythematosus (SLE); however data from Africa are lacking. We aimed to characterise cardiovascular (CV) involvement in a South African SLE cohort, without known CVD, using cardiovascular magnetic resonance (CMR). 



Methods:

SLE patients, without known CVD, were recruited from rheumatology clinics at a tertiary academic hospital in Cape Town and compared to matched controls. All participants underwent multiparametric CMR at 3T, including cine, T2-weighted, late gadolinium enhancement (LGE), native and postcontrast T1 mapping, ECV quantification and strain imaging. Clinical data, including disease activity and damage scores, were recorded.



Results:

49 SLE patients (mean age 35 ± 9 years) were enrolled; 90% were women, and majority were of mixed (69%) or black African (27%) ancestry. Median SLE disease duration was 5 (IQR 3-8) years. 73% of SLE patients had mild-moderate disease activity (median SLEDIA-2K score = 7 [IQR 4-11]) and 78% had low damage scores of 0 or 1 (median SLICC-DI = 1 [IQR 0-1]). Traditional CV risk factors, such as hypertension, smoking, and dyslipidaemia were present in 29%, 23% and 8%, respectively. 48% were on corticosteroid treatment, 43% were on methotrexate, and none were on biological antirheumatic drugs. Of the 49 patients with SLE, 42 (86%) patients had evidence of subclinical CVD on CMR. Myocardial involvement was the predominant manifestation seen in 38 (78%) SLE patients and pericardial effusions were observed in 13 (27%) patients. Mean LVEF was 57 ± 7 %, however, 21 (43%) SLE patients had evidence of mild systolic dysfunction (LVEF 47-56%). T2 time was similar between groups; SLE patients had significantly increased native myocardial T1 values (1269 ± 47 vs. 1220 ± 37 ms, p < 0.001, Figure 1a.) and ECV fraction (31 ± 4.3 vs. 28 ± 1.6 %, p < 0.001, Figure 1b.) indicative of myocardial fibrosis. Focal fibrosis detected by LGE imaging was present in 37 (79%) SLE patients with variable patterns; linear (43%), diffuse/patchy (32%), infarct-like pattern (4%). Myocardial strain was significantly impaired in SLE patients (peak longitudinal strain in SLE -15.4 vs. -17.4 in controls; p < 0.001) and correlated with LVEF and tissue characteristics.



Conclusion:

We demonstrate a high prevalence of subclinical CV involvement in a cohort of young ethnically diverse SLE patients in South Africa, in the setting of mild-moderate SLE disease activity indices. Myocardial involvement was frequently observed in SLE compared to controls, including significant differences in structural and functional parameters, tissue characteristics, and myocardial strain.