Predictors of arterial stiffness in systemic lupus erythematosus patients

Abstract Patients with systemic lupus erythematosus (SLE) have increased cardiovascular risk and develop early atherosclerosis, further leading to end-organ damage and increased morbi-mortality. Quantifiable markers of subclinical disease are of utmost importance for timely diagnosis and adequate preventive management. The cardio-ankle vascular index (CAVI) is a noninvasive, quantitative measure of arterial stiffness The aim of this study was to identify the clinical and paraclinical predictors of elevated CAVI in SLE patients. Methods This observational prospective cohort study included consecutive adult SLE patients evaluated between August 2021 and May 2024. Patients with a history of either acute myocardial infarction or stroke were excluded. Vascular stiffness was evaluated using CAVI measured using a Fukuda Denshi device. The values of CAVI range from ≤ 8.0 (normal CAVI), to borderline (8.0 < CAVI ≤ 9.0), and to abnormal (CAVI > 9.0). We defined arterial stiffness (AS) for CAVI > 9.0. The data analysis was performed with JASP 0.95.4. Results We included 77 SLE patients, with a mean age of 53 ± 12 years; 71 were women. The mean duration of SLE in the cohort was 14 years. 30 patients had more than one autoimmune disease. Arterial stiffness was associated with a longer disease duration (p = 0.35), the presence of overlap autoimmune diseases (CAVI (χ² = 4.03, p = 0.045), positive anti-dsDNA antibodies (χ² = 5.1, p = 0.024). When analyzing the impact of traditional cardiovascular risk factors (TCVRF), we found a normal CAVI in patients without TCVRF (mean CAVI 7.46), compared with those presenting at least one TCVRF, who had a mean CAVI of 8.77 (borderline value), with a statistically significant correlation (p = 0.006). Among TCVRF, arterial hypertension (HT) and dyslipidemia (D) showed the strongest associations with AS (mean CAVI 8.11 in patients without HT vs. 8.97 in those with HT, p = 0.011; and mean CAVI 7.93 in patients without dyslipidemia vs. 8.75 in those with dyslipidemia, p = 0.48). In addition, cardiac involvement was significantly correlated with AS (χ² = 6.23, p = 0.044), as were pulmonary and cutaneous involvement. Based on these findings, we developed a prediction model for AS. The coexistence of multiple autoimmune diseases, hypertension, pulmonary and cutaneous involvement, and a history of positive anti-dsDNA antibodies generated a strong predictive model for AS, with an AUC = 0.909, p < 0.001. Conclusions Predictors of arterial stiffness in SLE patients include traditional cardiovascular risk factors—particularly hypertension and dyslipidemia—as well as disease-related parameters such as overlap autoimmune diseases, organ involvement, and a history of positive anti-dsDNA antibodies. A multivariable model incorporating these factors demonstrated strong predictive performance, suggesting that targeted screening of high-risk patients may improve early identification of subclinical vascular damage.