Accelerated Atherosclerosis in Patients with Systemic Autoimmune Diseases

Abstract

Systemic autoimmune diseases such as systemic lupus erythematosus and Wegener's granulomatosis are associated with a significantly increased prevalence of cardiovascular disease (CVD) compared with age- and sex-matched controls. Many risk factors are involved in the pathogenesis of atherosclerosis, the major underlying cause of CVD. In patients with systemic autoimmune diseases, it has been shown that traditional risk factors for CVD cannot completely explain the prevalence of atherosclerosis. Therefore, in addition to these traditional factors, nontraditional risk factors are suggested to contribute to atherogenesis. All risk factors, traditional and nontraditional, contribute to endothelial activation that, followed by endothelial dysfunction, is seen as one of the first steps in this process. This review updates information on the factors that contribute to accelerated atherosclerosis in patients with systemic autoimmune diseases, such as disease-related factors, inflammatory mediators, and advanced glycation end products.

Autoimmunity and heart diseases: pathogenesis and diagnostic criteria

“…This notion is supported by the presence of activated lymphocytes, macrophages, and immunoglobulins in the forming atherosclerotic plaque (Afek et al 2000;Sherer and Shoenfeld 2002). CRP is commonly high in autoimmune disease (de Leeuw et al 2005). There is a proven correlation between CRP levels and the risk of atherosclerosis and cardiovascular disease Singh et al2008).…”

“…Moreover, about 40% of individuals with cardiovascular morbidity have no conventional risk factor, indicating an alternative mechanism in the pathophysiology of atherosclerosis . Atherosclerosis is accelerated in several autoimmune and rheumatic diseases, such as rheumatoid arthritis (Szekanecz et al 2007), systemic lupus erythematosus, systemic sclerosis (Sherer et al 2007), Wegener's granulomatosis (de Leeuw et al 2005), and antiphospholipid syndrome (APS) (Belizna et al 2007). …”

Endothelial Progenitor Cells: New Targets to Control Autoimmune Disorders

“…This is mainly due to their differential effects on the immunopathogenesis of these diseases. Attempts to understand this field are further bedevilled by observations of patients with systemic lupus erythematosus (SLE) who exhibit a significant decrease in circulating EPCs as well as a striking increase in premature atherosclerosis of unclear aetiology (de Leeuw et al, 2005, Westerweel et al, 2007 demonstrating no significant difference in EPC number between SLE patients without and with advanced coronary artery calcification (Baker et al, 2011). As detailed above, the inflammatory milieu in autoimmune diseases is characterized by neo-angiogenesis and as such it would seem that increased EPCs might contribute to inflammation.…”

Non-Enzymatic Glycosylation and Deglycating Enzymes

“…AGe formation on the apoprotein component can lead to cross-linking of LDL to the collagen layer of the blood vessel wall thus leading to accelerated development of atherosclerosis (60). Moreover, high-density lipoproteins are expected, when subjected to glycation, to lose their anti-inflammatory and cytoprotective properties, which are suggested to play important protective role in the propagation of atherosclerosis and also in neurodegenerative diseases (40).…”