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Premature atherosclerotic cardiovascular disease and systemic lupus erythematosus from bedside to bench Von Feldt JMBull NYU Hosp Jt Dis 2008[]; 66 (3): 184-7Cardiovascular morbidity and mortality in SLE is increased in patient with established disease, and SLE itself has been determined to be an independent risk factor for cardiovascular events. Autopsy studies have demonstrated that the coronary vessels of SLE patients have atherosclerotic plaque, and most cardiovascular events are not attributable to active vasculitis. It is believed that patients with inflammatory disease, including SLE, are more likely to have vulnerable plaque rupture, accounting for more frequent events. Elevated homocysteine levels have been associated with the presence and progression of atherosclerotic plaque. Enzyme polymorphisms involved in the folatehomocysteine pathway do not seem to contribute to differences in homocysteine concentration or atherosclerotic plaque. Recently, endothelial dysfunction has been identified as an early abnormality in ASCVD, and has been demonstrated in the vessels of SLE patients. Premature cardiovascular disease in SLE patients is likely attributable to the consequences of inflammation. There is preliminary evidence that type I interferons maybe the initial stimulation of the cascade of atherosclerotic development, starting with endothelial damage, and abnormal vascular repair.|Age of Onset[MESH]|Animals[MESH]|Atherosclerosis/*etiology/metabolism/pathology/physiopathology[MESH]|Biomarkers/blood[MESH]|Endothelium, Vascular/physiopathology[MESH]|Folic Acid/metabolism[MESH]|Homocysteine/blood[MESH]|Humans[MESH]|Lupus Erythematosus, Systemic/*complications/metabolism/pathology/physiopathology[MESH]|Rupture[MESH]|Up-Regulation[MESH] |