Abstract

Over the last 40 years, it has become established that patients with Systemic Lupus Erythematosus (SLE) have a greater risk of atherosclerosis and related events compared with the general population of similar age and sex. While the precise mechanisms that cause accelerated atherosclerosis in SLE remain undetermined, much evidence from inceptional and prospective longitudinal studies suggests a role for traditional cardiovascular disease and lupusspecific risk factors, systemic inflammation and lupus-directed therapies. This review will summarize much of the important knowledge available in the medical literature on this topic.

Highlights

  • Systemic Lupus Erythematosus (SLE) is a chronic, multi-system autoimmune disease with a predilection for females, with a female-tomale ratio of between 4.3 and 13.6 [1], and a mean age at diagnosis of 34.3 years [2].Atherosclerosis is a pathological inflammatory process of the artery, primarily affecting the intima, involving a complex interplay of endothelial dysfunction, monocyte and T-lymphocyte intimal invasion and inflammatory cytokine production, producing lesions known as atheromata that are responsible for infarction of target organs, through occlusion of the affected vessel [3]

  • This group found no difference in the incidence of atherosclerotic vascular events after baseline entry into the cohort among the 3 ethnicities [21]; they found that the C-Reactive Protein (CRP) gene variant, GT20, was more prevalent in African American and Hispanic patients and that carriers of this polymorphism have greater risk for developing Cardiovascular Disease (CVD) events [22] and that a mannose-binding lectin-deficient genotype was associated with cerebrovascular events in Caucasians only [23]

  • At the University of Toronto Lupus Clinic (UTLC), we have found that the total carotid plaque area is a much stronger predictor of coronary artery disease (CAD) compared with CIMT in a cross-sectional study comparing SLE patients with (N=27) and without (N=76) a history of CAD

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Summary

Introduction

Systemic Lupus Erythematosus (SLE) is a chronic, multi-system autoimmune disease with a predilection for females, with a female-tomale ratio of between 4.3 and 13.6 [1], and a mean age at diagnosis of 34.3 years [2]. The ‘traditional risk factors’ for CVD have been identified from longitudinal studies on a population from Framingham in the USA, and include increasing age, male sex, hypertension, smoking, dyslipidemia and diabetes mellitus [4]. Despite their relative youth and the predominance of the female sex, patients with SLE have a pronounced risk for accelerated atherosclerosis. The precise mechanisms for the development of premature atherosclerosis remain elusive but an increasing volume of evidence suggests that combinations of traditional CVD risk factors with lupus-specific and treatment-related variables are important contributors to this process. The UTLC has the largest, longest-followed single-centre cohort of SLE patients which has allowed detailed examination of CVD in lupus. This review will summarize much of the important evidence available, from the UTLC and other international centres, with the intent of stimulating interest and hypothesis-generation in the advancement of knowledge in this field

Epidemiology of Atherosclerosis is SLE
Atherosclerosis and Rheumatic Diseases
Racial differences in atherosclerotic risk in SLE
Endothelial cell dysfunction
Coronary artery calcification
Myocardial perfusion
The University of Toronto Lupus Clinic
The SLICC registry for atherosclerosis
Metabolic syndrome
Autoantibodies including antiphospholipid antibodies
Disease activity
Inflammatory Risk Factors
Role of Medications
Antimalarial medication
Findings
Conclusions
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