Objective: To examine and compare risk factors for various stages of subclinical vascular disease in different vascular beds (carotid and aorta) in women with systemic lupus erythematosus (SLE) who have not yet developed clinical cardiovascular disease.
Methods: This cross-sectional study was conducted in 214 women without clinical cardiovascular disease who were enrolled in the Pittsburgh Lupus Registry. B-mode ultrasound was used to measure carotid plaque and intima-media wall thickness (IMT). Doppler probes were used to collect pulse-wave velocity waveforms from the right carotid and femoral arteries as a measure of aortic stiffness. All risk factor data were collected on the day of the ultrasound examinations.
Results: The mean +/- SD age of the women was 45.2 +/- 10.5 years and the median SLE disease duration was approximately 9 years. Sixty-eight (32%) of the women had at least 1 focal plaque. The mean +/- SD IMT was 0.71 +/- 0.1 mm, and the mean +/- SD pulse-wave velocity was 5.96 +/- 1.6 meters/second. Using logistic regression, we found that determinants of plaque included older age, higher systolic blood pressure, lower levels of high-density lipoprotein 3, and antidepressant use. Determinants of plaque severity were older age, higher systolic blood pressure, lower levels of albumin, and smoking. Independent determinants of the highest quartile of IMT were older age, higher pulse pressure, lower levels of albumin, elevated C-reactive protein levels, high cholesterol, and higher levels of glucose. Higher aortic stiffness was associated with older age, higher systolic blood pressure, higher C3 levels, lower white blood cell count, higher insulin levels, and renal disease.
Conclusion: In women with SLE, the risk factors associated with carotid plaque and IMT are those typically associated with cardiovascular disease in the general population, whereas the risk factors associated with vascular stiffness include SLE-specific variables related to immune dysregulation and complement metabolism. The high prevalence of cardiovascular disease among lupus patients may result from both early adverse effects on vascular stiffening as well as later promotion of wall thickening and plaque through inflammatory-mediated processes. These observations provide clues for future mechanistic studies.