10 Managing lupus and cardiovascular disease

Case 1: A 20-year-old Caucasian female A 20-year-old Caucasian female presented with a malar rash, polyarthritis, Raynaud’s phenomenon, oral ulcers and pleurisy in November 1977. Serology revealed ANA +, anti-DNA (+) and normal C3/C4. She was treated with chloroquine 250 mg/day.Atherosclerotic risk factors included: BP: 130–139/80–89mmHg; Cholesterol: 220–240mg/dl; and Triglycerides: 250–350mg/dl. She was an ex-smoker (approximately 4–5 pack-years). She was not diabetic, obese and had no family history of premature coronary artery disease.In 1981 she had a healthy boy with C-section due to pre-eclampsia. In 1981–1984 she had relapsing-remitting disease, which was treated with prednisone 15–30mg/day consistently, and chloroquine 250 mg/day. Azathioprine was added in 1982 but discontinued later due to a hypersensitivity reaction. In February 1985 she developed intermittent claudication (left lower limb) when walking at 100 meters.In October 1985 her hypertension was noted for the first time in her clinical notes, with consistent readings of 130–140/95–105mmHg. Diltiazem 90 mg/day was prescribed. In February 1986 (age 29) she was admitted to hospital with unstable angina and underwent a triple coronary by-pass. She had no active disease (clinically and serologically) for the last 6 months before the surgery. Her hypertension was controlled with metoprolol, and nifedipine. Gemfibrozil 600mg/day was added for hyperlipidaemia.In August 1987 she had a second pregnancy, and a healthy baby girl was delivered by caesarean section. She remained clinically/serologically quiescent afterwards. Tapered prednisone was successfully and discontinued in 1990 and she continued chloroquine 250mg/day maintenance therapy. There were no other complications until 2007, when she died at the age of 50 (cause of death unknown).Learning Objectives At the end of this workshop participants will be able to:Discuss the early onset atherosclerotic cardiovascular risk factors specific to premenopausal patients with SLEEvaluate how current hypertension guidelines highlight an increased predisposition to atherosclerotic events in SLE patientsExplain the paradoxical occurrence of atherosclerotic cardiovascular events in clinically and serologically inactive SLE patientsApply the European Alliance of Associations for Rheumatology (EULAR) published recommendations for cardiovascular risk management in patients with SLEReferences Drosos GC, Vedder D, Houben E, et al. EULAR recommendations for cardiovascular risk management in rheumatic and musculoskeletal diseases, including systemic lupus erythematosus and antiphospholipid syndrome. Ann Rheum Dis. 2022;81(6):768–79. doi: 10.1136/annrheumdis-2021-221733Papazoglou N, Sfikakis PP, Tektonidou MG. Atherosclerotic plaque progression and incident cardiovascular events in a 10-year prospective study of patients with systemic lupus erythematosus: the impact of persistent cardiovascular risk factor target attainment and sustained doris remission. Arthritis Rheumatol. 2025;77(6):716–26. doi: 10.1002/art.43097Urowitz MB, Su J, Gladman DD. Atherosclerotic vascular events in systemic lupus erythematosus: an evolving story. J Rheumatol. 2020;47(1):66–71. doi: 10.3899/jrheum.180986Yazdany J, Pooley N, Langham J, et al. Systemic lupus erythematosus; stroke and myocardial infarction risk: a systematic review and meta-analysis. RMD Open. 2020;6(2). doi: 10.1136/rmdopen-2020-001247Case 2: A 20-year-old Caucasian female A 49-year-old woman with a 12-year history of systemic lupus erythematosus (SLE) presents with moderately controlled type 2 diabetes (HbA1c 72 mmol/mol), a history of treated hypertension, class I obesity (BMI 32.1), and evidence of non-alcoholic fatty liver disease without advanced fibrosis. Her lupus is clinically quiescent on weekly belimumab. She has not experienced any cardiovascular events to date but demonstrates multiple cardiovascular risk factors. Her LDL-C is 3.2 mmol/L, and she is not receiving lipid-lowering therapy. Despite structured dietary counselling, weight loss efforts have been largely unsuccessful due to caregiving responsibilities and financial strain. Given her high cumulative cardiometabolic risk, initiation of an SGLT2 inhibitor is being considered, in addition to optimising her glucose-lowering regimen.Learning Objectives At the end of this workshop participants will be able to:Describe the elevated cardiovascular risk in patients with SLEDiscuss the role of dyslipidemia, insulin resistance, and inflammation in SLE-related atherosclerosisRecognize the cardiovascular impact of antirheumatic treatmentsDiscuss cardiovascular risk management guidelines in SLEDescribe the role of SGLT2 inhibitors in SLE patients with comorbid diabetesReferences Bello N, Meyers KJ, Workman J, et al. Cardiovascular events and risk in patients with systemic lupus erythematosus: systematic literature review and meta-analysis. Lupus. 2023;32(3):325–41. doi: 10.1177/09612033221147471Drosos GC, Vedder D, Houben E, et al. EULAR recommendations for cardiovascular risk management in rheumatic and musculoskeletal diseases, including systemic lupus erythematosus and antiphospholipid syndrome. Ann Rheum Dis. 2022;81(6):768–79. doi: 10.1136/annrheumdis-2021-221733Ma KS, Lo JE, Kyttaris VC, et al. Efficacy and safety of sodium-glucose cotransporter 2 inhibitors for the primary prevention of cardiovascular, renal events, and safety outcomes in patients with systemic lupus erythematosus and comorbid type 2 diabetes: a population-based target trial emulation. Arthritis Rheumatol. 2025;77(4):414–22. doi: 10.1002/art.43037Oliveira G, Kaplan M. Atherosclerosis and cardiovascular disease in SLE: Immunopathogenic mechanisms. Semin Immunopathol. 2022;44(2):145–60.

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