Increased arterial stiffness is independently associated with metabolic syndrome and damage index in systemic lupus erythematosus patients: comment on the article by Valero-Gonzalez et al

We read with a great interest the article titled ‘Increased arterial stiffness is independently associated with metabolic syndrome and damage index in systemic lupus erythematosus patients’ by Valero-Gonzalez et al (1). The authors investigated the relationship between traditional cardiovascular (CV) risk factors, non-traditional CV risk factors, systemic lupus erythematosus (SLE)related risk factors, and arterial stiffness. They found a close link between metabolic syndrome and Systemic Lupus International Collaborative Clinics/American College of Rheumatology (SLICC/ACR) score with increased aortic stiffness. These variables might be an indicator of subclinical atherosclerosis in SLE women without clinical evidence of atherosclerotic CV disease. We suggest that these findings will provide guides for further studies about the effect of inflammation on arterial stiffness parameters (ASPs) in patients with SLE. ASPs provide information about endothelial function. Increased arterial stiffness is an indicator of coronary artery disease, cerebrovascular disease, and peripheral arterial disease based on endothelial dysfunction (2). ASPs may also increase the known atherosclerotic risk factors such as hypertension, smoking, hypercholesterolaemia, diabetes mellitus (DM), renal disease, alcohol consumption, hypothyroidism, and older age (3). We previously investigated the relationship between increased arterial stiffness in patients with Behçet’s disease (BD) without CV involvement and known CV risk factors. We concluded that ASPs were associated with BD without significant CV involvement (4). We also reported that arterial stiffness was significantly higher in psoriasis patients compared to a control group (5). We suggest that Valero-Gonzalez et al should have mentioned this association between some inflammatory diseases, such as psoriasis, and the ASPs. In addition, no mention was made of the affecting factors, and information about these factors would have been appropriate. Furthermore, the use of some medications such as antihypertensive treatment, including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and statins, may influence ASPs. Again, the authors did not mention any of these factors in their paper. ASPs have high CV predictive value, reproducibility, cost-effectiveness, and availability in many patients. These parameters are important for both research and clinical use. In clinical practice, interand intra-observer variability of the non-invasive devices used to measure arterial stiffness may be different in many studies. It might have been useful to give values for the interand intraobserver variability for ASPs in the study considered here. Because ASPs provide a non-invasive method to assess endothelial dysfunction in clinical practice and, without other inflammatory markers, ASPs alone may not provide sufficient information to clinicians about the prognosis in patients with SLE (6), it would have been better if these factors had been included in the paper.