Update on vascular disease in systemic lupus erythematosus.

PURPOSE OF REVIEW

Young women with systemic lupus erythematosus have strikingly high rates of coronary heart disease. Current knowledge indicates that atherosclerosis is an active inflammatory and immune-mediated process. Therefore, the chronic inflammation and immune dysregulation characteristic of systemic lupus erythematosus undoubtedly contribute to the accelerated vascular disease seen in these patients. Carefully considering what is known about atherogenesis in the general population will provide clues to unraveling the complexity of why systemic lupus erythematosus and atherosclerosis are linked so frequently.

RECENT FINDINGS

Inflammation is involved in all aspects of atherogenesis from the initial endothelial "response to injury," to foam cell formation leading to the atherosclerotic lesion, to the rupture of the "vulnerable" fibrous cap, resulting in the acute coronary syndrome and potentially in death. The authors review how factors commonly seen in systemic lupus erythematosus or inherent to the underlying disease mechanism may contribute to each of the stages of atherogenesis.

SUMMARY

Our focus on the causes of vascular disease in systemic lupus erythematosus must now include nontraditional risk factors such as immune and inflammatory mediators. With the advent of noninvasive screening tools for atherosclerosis, we are better equipped to measure subclinical vascular disease and associated risk factors, including immune and inflammatory mediators. When considering strategies for preventing premature cardiovascular disease in systemic lupus erythematosus, modifying immune and inflammatory risk factors will likely become a major component of the program in addition to modifying the current traditional risk factors.