Abstract
Atherosclerosis is a chronic inflammatory disorder characterized by immune cell activation, inflammation driven plaque formation and subsequent destabilization. In other disorders of an inflammatory nature, the chronic inflammatory state per se has been linked to acceleration of the atherosclerotic process which is underlined by an increased incidence of cardiovascular disease (CVD) in disorders such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and antiphopholipid (Hughes) syndrome (APS). SLE is an autoimmune disease that may affect any organ. Premature coronary heart disease has emerged as a major cause of morbidity and mortality in SLE. In addition to mortality, cardiovascular morbidity is also markedly increased in these patients, compared with the general population. The increased cardiovascular risk can be explained only partially by an increased prevalence of classical risk factors for cardiovascular disease; it also appears to be related to inflammation. Inflammation is increasingly being considered central to the pathogenesis of atherosclerosis and an important risk factor for vascular disease. Recent epidemiologic and pathogenesis studies have suggested a great deal in common between the pathogenesis of prototypic autoimmune disease such as SLE and that of atherosclerosis.We will review traditional risk factors for CVD in SLE. We will also discuss the role of inflammation in atherosclerosis, as well as possible treatment strategies in these patients.
Highlights
Systemic lupus erythematosus (SLE) is an autoimmune disease that primarily affects young women
Systemic inflammation may be regarded as accelerating the atherosclerotic process, in especially C reactive protein (CRP) has been associated with cardiovascular disease (CVD) risk in the general population
Antiphospholipid antibodies are a heterogeneous group of autoantibodies, including, anticardiolipin antibody and lupus anticoagulant (LA), generally directed to phospholipid binding proteins; in this regard, 2GPI represents the major antigenic target [21]. 2GPI can be found in human atherosclerotic lesions obtained from carotid endarterectomies, it is abundantly expressed within the subendothelial regions and the intimal-medial border of human atherosclerotic plaques, and it colocalizes with CD4_ lymphocytes [22, 35]
Summary
Systemic lupus erythematosus (SLE) is an autoimmune disease that primarily affects young women. Coronary artery disease (CAD) in SLE was described much later than the other cardiovascular manifestations. The clinical manifestations of CAD in SLE can result from several pathophysiologic mechanisms, including atherosclerosis, arteritis, thrombosis, embolization, spasm, and abnormal coronary flow [2]. The striking clinical characteristic of most patients with SLE who have a myocardial infarction is their young age. Recent case- control series have confirmed that the risk of myocardial infarction in patients with SLE is increased between 9- and 50-fold over that in the general population [1,2,3]. Clinical epidemiological observations strongly suggest that, together with classical conventional risk factors, other mechanisms (non-conventional/disease-specific factors) promote accelerated atherosclerosis in diseases like SLE and other rheumatic diseases [3,4,5,6,7]. We further will review the presence of traditional and nontraditional risk factors in SLE patients
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