AB0371 The effect of cumulative exposure to cigarette smoking on vascular damage in patients with rheumatoid arthritis

2018 
Background Smoking is described as a classic cardiovascular (CV) risk factor and we also know the beneficial effect on the CV system of smoking cessation. However, there is contradictory data about its effect in patients with rheumatoid arthritis (RA). It is possible that the measure of cumulative exposure to tobacco expressed in pack-year gives us more information than the smoking status. Objectives To explore the relation between smoking exposure, measured in pack-year, and subclinical vascular damage, mortality and vascular events in patients with RA. Methods Observational ambispective study. We included, consecutively, RA patients controlled in a tertiary hospital. We gathered demographic (sex, age, body mass index [BMI]), clinical (characteristics of RA, classic CV risk factors and history of vascular events) and analytical variables (CRP, ESR). 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 registered the presence of atheroma plaques (per Mannheim consensus). We determined pulse wave velocity (PWV) by a validated MobilOGraph device. We considered as pathological an IMT >900 μ and a PWV ≥10 m/s and the presence of plaque and/or pathological IMT. We prospectively collected mortality and the development of new vascular events over four years and the current smoking status and exposure calculated in pack-year. Statistical analysis was performed using SPSS 17.0 software. Results We included 198 patients, excluding 15 because of previous CV events. The mean age was 66,5 years (SD 13,44) 76% were women and the mean BMI was 27,35 (SD 4,82). 31,1% were smokers, 43,2% hypertensive, 47,5% dyslipemic and 10,4% were diabetic. The mean duration of RA was 19,95 years (SD 11,88). 76,5% of patients were seropositive and 75,4% had erosions. The mean CRP and ESR were 9,51 mg/L (SD: 32,29) and 13,83 mm/h (SD:14,26), respectively. The mean modified SCORE was 1,81 (SD: 1,81). Regarding the vascular study, 48,1% had atheroma plaques, 32,2% a pathologic PWV [mean value of 9,13 (SD 2,12)], and 16,7% had a pathologic IMT [mean value of 748 μ(DE 168,73)]. 31.1% of the patients (57) were smokers or former smokers. The average pack-year was 24.17 (SD: 21.37). No relation was found between current or previous use of tobacco and any of the outcome measures described. However, when considering cumulative exposure to tobacco, there was a trend to correlate with higher values of PWV (p=0.07) and a higher plaque presence (p=0.089) was detected. After 4 years of follow-up, 3 deaths were recorded among smoking patients, but a higher incidence of CV events was not detected in relation to cumulative exposure to tobacco (p=0.99). Conclusions The quantification of the exposure by pack-year of cigarette smoked could give us more information about vascular damage in patients with RA. The limitation of our study is the small number of smokers in the time they were followed. Disclosure of Interest None declared
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