The pathogenesis of atherosclerosis in autoimmune rheumatic diseases: roles of inflammation and dyslipidemia

Abstract

As patients with autoimmune rheumatic diseases live longer due to improved therapies and preventive measures, death and disability from atherosclerosis, particularly myocardial infarcts, are increasing. The relative risks for atherosclerosis vary from approximately 1.6 in ankylosing spondylitis and psoriatic arthritis to 3.0 in rheumatoid arthritis (RA), and 6.0 in systemic lupus erythematosus (SLE). Increased risks are found when analyzed by atherosclerotic events, causes of death, or surrogate measures of atherosclerosis, such as carotid artery plaque, intimal-media thickness, or coronary artery calcification. At all ages among adults, atherosclerosis is increased in patients with SLE or RA compared to healthy controls. For example, in women with SLE under the age of 40 years, approximately 13% have carotid plaque compared to 2% of controls; over age 59 the percentages are 71 and 45, respectively. For patients with RA, prevalence is 7% under the age of 40 in patients compared to zero in controls; over 59 years the prevalences are 80% and 44%, respectively. In this review we will discuss the mechanisms involved as well as an overview of the natural history in pathobiology.