Key result
Missing cardiovascular risk targets is linked to greater plaque progression in SLE patients.
Why the study?
Does attaining cardiovascular risk targets reduce the progression of subclinical atherosclerosis in patients with systemic lupus erythematosus?
Cohort (n=69)
Does attaining cardiovascular risk targets reduce the progression of subclinical atherosclerosis in patients with systemic lupus erythematosus?
Better control of cardiovascular risk targets is associated with reduced progression of subclinical atherosclerotic plaque in patients with systemic lupus erythematosus.
Background/Aims Patients with systemic lupus erythematosus (SLE) have increased risk of both clinical cardiovascular disease (CVD) and subclinical atherosclerosis. Reports from a mono-ethnic population in Greece have shown that controlling CVD risk factors reduces subclinical plaque progression in patients with SLE. We investigated whether this finding also holds in our ethnically diverse cohort of patients, measuring total plaque area (TPA) as well as number of plaques. Methods Sixty-nine patients with SLE but with no previous history of clinical CVD underwent ultrasound scans of both carotid and both common femoral artery bifurcations (four sites in all) on two occasions, a mean of 63 months apart. Clinical, demographic, CVD risk and treatment factors were recorded for each patient. We assessed use of medications and time in low disease activity state or remission between scans. We enumerated the number of CVD risk targets (BMI, blood pressure, smoking cessation and low density lipoprotein) achieved for each patient. Targets were as defined in the 2021 European Society for Cardiology guidelines for prevention of CVD. The outcome measures were change in number of sites with plaque (range 0-4) and total plaque area (TPA) between scans. We carried out statistical analysis to identify factors that were significantly associated with an increase in plaque number and/or with increased TPA. Results Thirty-one of 69 patients had plaque at the second scan, of whom 18 had an increased number of plaque sites since the first scan, while 13 had an unchanged plaque number. TPA had increased in all 31 patients with a median increase of 4.59mm2/year. Increased plaque number was associated with increased age at baseline (p < 0.001), positive lupus anticoagulant (p = 0.006), negative anti-La (p = 0.027) and failure to attain at least three CVD risk targets by the time of the second scan (p < 0.005). Increased TPA was also associated with increased age at baseline (p < 0.001), positive lupus anticoagulant (p = 0.018), negative anti-La (p = 0.023) and failure to attain at least three CVD risk targets by the time of the second scan (p < 0.001). We found no associations of either outcome with cumulative steroid dose between scans, use of immunosuppressants or time in remission/low activity state. Conclusion In this ethnically diverse (40% non-Caucasian) population, we confirmed earlier findings that better control of CVD risk targets reduces progression of atherosclerotic plaque. Anti-La positivity was associated with less plaque progression, which was unexpected. Lupus anticoagulant positivity was associated with increased plaque progression, consistent with previous reports.
No takes yet. Share an insight, caveat, or question.
Bakshi et al. (2026) conducted a cohort in systemic lupus erythematosus (n=69). Failure to attain at least three CVD risk targets vs. Attaining at least three CVD risk targets was evaluated on change in number of sites with plaque and total plaque area (TPA) between scans (p=<0.005). Failure to attain at least three cardiovascular risk targets was significantly associated with increased plaque number (p<0.005) and total plaque area (p<0.001) in patients with SLE.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: