Increased arterial stiffness is independently associated with metabolic syndrome and damage index in systemic lupus erythematosus patients

Abstract

Objectives: We evaluated whether traditional or non-traditional cardiovascular (CV) risk factors and systemic lupus erythematosus (SLE)-related risk factors were associated with pathological arterial stiffness measured by pulse wave velocity (PWV) adjusted for patients’ age and blood pressure.

Method: CV risk factors were measured in the 46 SLE female patients studied. Activity and organ damage were assessed by the SLE Disease Activity Index (SLEDAI) and the Systemic Lupus International Collaborative Clinics/American College of Rheumatology (SLICC/ACR) Damage Index, respectively. Other lupus-related parameters and information concerning treatment were recorded. Subclinical atherosclerosis was assessed by PWV calculated from pulse wave recording by Doppler, a non-invasive method to measure arterial stiffness. Multivariate logistic regression analysis was used to identify independent determinants of increased PWV.

Results: PWV was categorized as normal or pathological arterial stiffness following the reference values adjusted by age and blood pressure recently published by the European Society of Cardiology. Pathological PWV was associated with CV risk factors including homocysteine (p = 0.01), high-sensitivity C-reactive protein (hs-CRP; p = 0.03), uric acid (p = 0.01), and metabolic syndrome (p = 0.007). With regard to SLE-specific risk factors, a significant association was found between PWV and SLICC/ACR score (p = 0.006). Multivariate analysis showed that increased PWV was independently associated with metabolic syndrome [odds ratio (OR) 6.6, 95% confidence interval (CI) 1.2–38, p = 0.03] and SLICC/ACR score (OR 1.5, 95% CI 1–2.32, p = 0.05).

Conclusions: We have found a close link between metabolic syndrome and SLICC/ACR score with increased aortic stiffness. These variables might be an indicator of subclinical atherosclerosis in SLE women without clinical evidence of atherosclerotic cardiovascular disease (CVD).

Acknowledgements

We thank Isabel Millan at the Department of Biostatistics for data analysis support. This work was supported by grants from the Health Institute Carlos III, Spain (grant PI10/01029) and the Foundation for Biomedical Research at the University Hospital Puerta de Hierro Majadahonda, Spain.