LAUSR

Background Patients with psoriatic arthritis (PsA) have a higher prevalence of classical vascular risk factors (CVRF) and early atherosclerosis determined by chronic inflammation. Objectives To study the evolution over time of different vascular damage evaluation measures in patients with PsA and investigate the factors related to these changes. Methods Pre-post longitudinal study with analytical components. PsA patients with peripheral joint involvement were included. Demographic (sex, age), clinical [duration of the disease, DAS28, current treatment, body mass index (BMI), CVRF, vascular events] and analytical variables [atherogenic index, glomerular filtration (GF-MDRD), fibrinogen, glycosylated hemoglobin (HbA1c), CRP, ESR, ultrasensitive CRP, Apolipoprotein A1, apolipoprotein B] were collected. Other variables were collected from the clinical history retrospectively. Basal vascular risk was estimated through SCORE tool. Extracranial carotid artery was explored with an Esaote MyLab70XVG ultrasound with linear probe (7-12mHz) and an automated program that measures intima media thickness (IMT) by radiofrequency (“Quality intima media thickness in real-time), and the presence of ateroma plaques was evaluated following Mannheim consensus. Pulse wave velocity (PWV) was measured through Mobil o graph® dispositive. We repeat vascular study 3 years later. IMT≥900 μ and PWV≥ 10m/s were considered as pathological values. Statistical analysis were performed using SPSS 22.0 program. Results 108 patients were included. Twelve patients excluded due to high vascular risk [previous event and/or diabetes type II or type I with target organ injury]. Repeated VOP measurement was only available in 49 patients. 64.2% of patients were women and the mean age was 54.2 (SD 1,3) years. Mean disease duration was 93.1 (SD 12.7) months and mean DAS28 was 1.7 (SD 0.1). 22.4% of patients received glucocorticoids, 47.8% NSAIDs, 83.6% DMARDs and 37.3% biological drugs. Mean BMI was 26.5 (SD 0.5) kg/m2. 38.8%, 28.4% and 43.3% of patients were smokers, hypertensive (11.9% on ARA2, 3% on IECA, 1.5% on calcium channel blockers, 10.4% on combined treatment) and 43.3% dyslipidemic [most of them (38.8%) on statins]. Mean CRP and ESR were 6.2 (SD 0.4) mg/l and 9.9 (SD 1) mm/h, respectively. Mean SCORE was 1.06 (SD 0.1). Baseline, 23.9% of patients had atheromatous plaques, and 13.4% and 20.4% had a pathological IMT or PWV, respectively. Three years later, we detected new and/or atheromatous plaques rises in 19.4% of patients and PWV and IMT worsening in 10.2% and 1.5% of patients, respectively. As per logistic regression analysis, high baseline SCORE (16.9%), high systolic blood pressure (8.6%), GF-MDRD (8.2%), fibrinogen (6.8%) and the presence of dyslipidemia were the factors that most contributed to the progression of vascular damage, with independence of the therapeutic objective used for their treatment. Conclusion Progression of vascular damage is mainly related to CVRF in patients with PsA, therefore it is essential to intervene on CVRF early. Disclosure of Interests None declared