Progression of subclinical and clinical cardiovascular disease in a UK SLE cohort: the role of classic and SLE-related factors

Abstract

ObjectivesWe aimed to describe the rate and determinants of carotid plaque progression and the onset of clinical cardiovascular disease (CVD) in a UK SLE cohort.MethodsFemale patients with SLE of white British ancestry were recruited from clinics in the North-West of England and had a baseline clinical and CVD risk assessment including measurement of carotid intima–media thickness (CIMT) and plaque using B-mode Doppler ultrasound. Patients were followed up (>3.5 years after baseline visit) and had a repeat carotid Doppler to assess progression of plaque and CIMT. Clinical CVD events between visits were also noted.ResultsOf 200 patients with a baseline scan, 124 (62%) patients had a second assessment at a median (IQR) of 5.8 (5.2–6.3) years follow-up. New plaque developed in 32 (26%) (4.5% per annum) patients and plaque progression was observed in 52 (41%) patients. Factors associated with plaque progression were older age (OR 1.13; 95% CI 1.06 to 1.20), anticardiolipin (OR 3.36; 1.27 to 10.40) and anti-Ro (OR 0.31; 0.11 to 0.86) antibodies. CVD events occurred in 7.2% over 5.8 years compared with 1.0% predicted using the Framingham risk score (p<0.001). Higher triglycerides (OR 3.6; 1.23 to 10.56), cyclophosphamide exposure ‘ever’ (OR 16.7; 1.46 to 63.5) and baseline Systemic Lupus International Collaborating Clinics damage index score (OR 9.62; 1.46 to 123) independently predicted future CVD events.ConclusionAccelerated atherosclerosis remains a major challenge in SLE disease management. A more comprehensive approach to CVD risk management taking into account disease factors such as severity and anticardiolipin antibody status may be necessary to improve CVD outcomes in this high-risk population.

Asymptomatic Carotid Atherosclerosis Cardiovascular Risk Factors and Common Hypertriglyceridemia Genetic Variants in Patients with Systemic Erythematosus Lupus

“…In this sense, we only analyzed the data on the presence of carotid plaque. Our SLE population had a similar prevalence of carotid plaque (21.1% vs 16% to 37%) than what was reported in previous series of SLE patients (24,25). Patients with carotid plaque were more hypertensive and dyslipidemic than those without plaque.…”

Similar progression of carotid intima–media thickness in 7-year surveillance of patients with mild SLE and controls, but this progression is still promoted by dyslipidaemia, lower HDL levels, hypertension, history of lupus nephritis and a higher prednisolone usage in patients

“…Taking into consideration the high burden of CV risk factors in patients with SLE, this finding is of major importance because it suggests that excess progression of cIMT in SLE could be halted and argues for the concept of possibility to change the disease prognosis in SLE by applying improved monitoring, therapeutic and preventive strategies 21. It should be emphasised that the rate of antimalarial use in this cohort (about 90%) compares favourably with many other published cohort studies (35%–70%),22–25 which could account for some of the lower cIMT progression in the patients with SLE in this study. Further, frequent usage of preventive medication with antihypertensives, statins and low-dose aspirin may also contribute to favourable evolution of cIMT in these patients.…”

“…It is interesting to note that cIMT progression in this cohort was similar between the patients and the control population, yet the number of CV events during the 7-year follow-up was higher in the patients with SLE. In a study of 200 patients with SLE who were recruited from the clinics in England and had a baseline clinical and CV risk assessment including carotid ultrasound measures, neither presence of carotid plaque nor cIMT at baseline predicted future events after a median of 6 years, but higher triglycerides, ‘ever’ exposure to cyclophosphamide and the damage index independently predicted CV disease events 22. Possible explanations for this could be that in SLE, risk factors for the initiation of atherosclerosis may be different to those important for progression and severity of atherosclerosis.…”

Changes of NADH Fluorescence from the Skin of Patients with Systemic Lupus Erythematosus

“…In SLE, autoimmunity is perpetuated by defective clearance of apoptotic waste and immune complexes, along with disrupted lymphocyte biology and interferon pathways [3]. In addition, atherosclerosis has a great influence on morbidity and mortality in SLE [4]. Risk factors for the development of cardiovascular (CV) disease include both traditional risk factors, such as hyperlipidaemia, hypertension, diabetes, obesity, and smoking, together with SLEspecific factors, such as antiphospholipid antibodies and glucocorticoid therapy [4].…”

“…In addition, atherosclerosis has a great influence on morbidity and mortality in SLE [4]. Risk factors for the development of cardiovascular (CV) disease include both traditional risk factors, such as hyperlipidaemia, hypertension, diabetes, obesity, and smoking, together with SLEspecific factors, such as antiphospholipid antibodies and glucocorticoid therapy [4]. Endothelial function is also impaired: a recent study found that brachial artery endothelium-dependent flow-mediated dilation (baED-FMD), an example of a biophysical marker of endothelial function, was decreased in SLE patients without obvious cardiovascular disease [5].…”