Chapter 29 - Atherosclerosis and Tissue Injury in Systemic Lupus Erythematosus

Abstract

Systemic lupus erythematosus (SLE) can cause tissue damage in many organs. Damage affecting organs such as the kidneys is most clinically obvious and causes substantial morbidity and mortality. As the treatment of renal and other complications of lupus has improved, the mortality associated with acute lupus has decreased and survival has improved. With this increased long term survival has come a clearer recognition of tissue damage affecting the vasculature, particularly the coronary vasculature, and the impact of coronary heart disease (CHD) on long-term morbidity and mortality in lupus. Studies have led to efforts to quantify the morbidity and mortality due to CHD in SLE, use noninvasive measures to identify atherosclerosis in SLE, understand the relationship between traditional cardiovascular risk factors and increased CHD, and characterize the factors specific to patients with lupus that increase CHD risk and identify their underlying mechanisms. There have been significant advances in the diagnosis of early atherosclerosis in SLE and in defining the contribution of both traditional and nontraditional cardiovascular risk factors to accelerated atherosclerosis in lupus. A better understanding of the mechanisms underlying vascular damage, plaque formation and stability, and thrombosis, and an improved ability to accurately identify and intervene in patients at highest cardiovascular risk, is greatly banked upon to facilitate the long-term care of patients with lupus.