Endothelial dysfunction and increased carotid intima-media thickness in patients with spondyloarthritis without traditional cardiovascular risk factors

Background The aim of our study was to assess subclinical atherosclerosis in spondyloarthritis (SpA) by combining three ultrasound methods (flow-mediated dilation (FMD), carotid intima-media thickness (cIMT) and Ankle Brachial Index (ABI)) and to determine the predictive factors of theses parameters. Methods This was a case control study conducted over 12 months including 47 patients with SpA-free-cardiovascular (CV) disease in comparison with age and sex matched 47 healthy controls. Sociodemographic, clinical and biological features as well as therapeutic modalities were recorded in our patients. All subjects had Doppler ultrasound with measurement of cIMT, FMD and ABI. Ultrasound measurements were compared between patients and controls. Linear regression was performed and assessed by machine learning to determine the predictive models of markers of subclinical atherosclerosis. Results We found higher cIMT (p<0.0001), lower FMD (p=0.008) and higher left ABI (0.048) in patients with SpA compared with controls. cIMT was positively correlated to patient-related parameters (age, systolic blood pressure) and disease parameters (age at onset of SpA, disease duration and renal involvement). Biologically, cIMT was positively correlated with creatinine, blood-glocose, total cholesterol (CT) and CT/cholesterol-high density lipoprotein ratio. FMD was negatively correlated with male gender, age, systolic blood pressure, creatinine, blood glucose and Left Lequesne Index. ABI was significantly associated with diastolic blood pressure. Multiple regression analysis identified age, CT and creatinine as independents predictive factors for increased cIMT. Regarding endothelial dysfunction, blood glucose and Left Lequesne Index were the independents predictive factors of decreased FMD. Conclusion Our study supported the accelerated subclinical atherosclerosis in patients with SpA. This subclinical atherosclerosis was mainly mediated by traditional CV risk factors.