Background RA patients have a higher risk of vascular events, especially cardiac ones. Besides, mortality in these patients is 54% higher than the general population. Nowadays, we have non-invasive techniques that allow us to detect subclinical vascular damage.

Objectives To describe subclinical vascular affection in a sample of RA patients and to explore its relationship with mortality and with the development of vascular events.

Methods Ambispective observational study with analytical components. We included, consecutively, RA patients controlled in a tertiary hospital. We gathered demographic (sex, age, body mass index [BMI]), clinical (traditional vascular risk factors, previous vascular events), and analytical variables (atherogenic index, glomerular filtration [GF] [MDRD], CRP, ESR). Other variables were collected retrospectively from the electronic medical record. We estimated the modified SCORE. We explored the extracranial branches of the carotid artery with an Esaote MyLab70XVG ultrasound device with a linear probe (7–12mHz) and an automated program measuring intima media thickness (IMT) by radiofrequency (“Quality intima media thickness in real-time, QIMT”), and the presence of atheroma plaques, as per the Mannheim consensus, was registered. We also determined pulse wave velocity (PWV) by a validated MobilOGraph® device. We considered an IMT>900 μand a PWV≥10m/s as pathologic values. We prospectively collected mortality and the development of new vascular events over three years. Statistical analysis was performed using SPSS 17.0 software.

Results We included 198 patients, excluding 13 because of previous vascular events. The mean age was 65,8 years (DE 13,3) and most of them were women (76,2%). The mean BMI was 27,29 (DE 4,84). 27% were smokers, 42,7% hypertensive, 46,7% dyslipemic and 10,8% were diabetic. The mean duration of RA was 17,37 years. 74,6% of patients were seropositive (RF and/or ACPA) and 75, 5% had erosions. 74,6% received glucocorticoids, 58,4% NSAIDs, 98,9% DMARDs and 35,7% biologic therapies. The mean CRP and ESR were 9,45mg/L (DE: 32,2) and 14,04mm/h (DE:14,46), respectively. The mean modified SCORE was 1,81 (DE: 1,79).

Regarding the vascular study, 48,6% of the patients had atheroma plaques, 31,7% had a pathologic PWV with a mean value of 9,13 (DE 2,12), and 16,7% had a pathologic IMT with a mean value of 754 μ(DE 168,52).

During 3 years of follow up, we registered 26 (14,1%) vascular events: 9,7% cardiac, 2,1% cerebral and 2,2% peripheral. There were 5 deaths: 3 vascular, 1 infectious and 1 respiratory. The development of vascular events was related with the presence of atheroma plaques (p 0,008) and with pathologic PWV (p 0,028), as well as with the presence of erosions, GF, HTA and dyslipidemia. The appearance of cardiac events was related, also, with the use of NSAID (p 0,041). The presence of a pathologic IMT (p 0,032) and HTA (p 0,044) were the only variables related with death from any cause.

Conclusions A combination of carotid ultrasonography and arterial stiffness study can help us to best identify patients with RA who have an increased risk of dying or developing a vascular event.

Disclosure of Interest None declared