Cardiovascular diseases secondary to accelerated
atherosclerosis are now accepted as a cause of mortality and morbidity in patients suffering from
systemic lupus erythematosus and
rheumatoid arthritis. More recently,
atherosclerosis is emerging as one of the most serious complications in the
anti-phospholipid syndrome, although large epidemiological studies, such as those performed in lupus and
rheumatoid arthritis patients, have not been performed up to now. Classical risk factors (dislipidemia,
hypertension, diabetes, smoking, etc.) and
steroid therapy cannot completely explain the high prevalence of cardiovascular complications in systemic
autoimmune diseases. Since the modern view defines
atherosclerosis as a chronic inflammatory disorder, it has been suggested that systemic
inflammation and soluble immune mediators (circulating
autoantibodies,
immune-complexes, complement activation products) might play a role in accelerating vessel pathology. The main target appears to be the endothelium because of its ability to switch to a pro-adhesive, pro-inflammatory and pro-
coagulant surface in response to these mediators. Recent advances in the knowledge of the pharmacology of
statins have indicated that these drugs rather than to be simple
cholesterol lowering molecules display a pleiotropic effects on several mechanisms involved in the
atherosclerotic plaque formation. Their anti-inflammatory activity and particularly their ability to downregulate endothelial cell activation induced by different stimuli strongly suggest their possible use in conditions in which the systemic
inflammation and the endothelial activation/damage are thought to represent key pathogenic mechanisms.