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SAT0088 Hdl cholesterol efflux capacity in rheumatoid arthritis patients: contributing factors and relationship with subclinical atherosclerosis
  1. B Tejera Segura1,
  2. M Macía-Díaz2,
  3. JDM Machado2,
  4. A Vera-González de3,
  5. A González-Delgado3,
  6. JM Olmos4,
  7. JL Hernández4,
  8. F Díaz-González1,
  9. MA González-Gay5,
  10. I Ferraz-Amaro1
  1. 1Division of Rheumatology
  2. 2Pharmacology Department
  3. 3Central Laboratory Division, Hospital Universitario de Canarias, Tenerife
  4. 4Division of Internal Medicine
  5. 5Rheumatology Department, Hospital Universitario Marqués de Valdecilla-IDIVAL, Santander, Spain

Abstract

Background Lipid profiles appear to be altered in rheumatoid arthritis (RA) patients due to disease activity and inflammation. Cholesterol efflux capacity (CEC) has not only been linked to cardiovascular events in the general population, but also to be impaired in RA patients.

Objectives To analyze whether CEC is related to subclinical atherosclerosis, as determined by the presence of carotid plaque or increased levels of carotid intima-media thickness (cIMT) in RA patients. Secondarily, we aimed to describe the disease-contributing factors that are related to CEC as an expression of the abnormalities in the lipid profile associated with the disease.

Methods Cross-sectional study that encompassed 401 individuals; 178 patients with RA and 223 sex-matched controls. CEC was measured using an in vitro assay, lipoproteins serum concentrations, and standard lipid profile were assessed in patients and controls. Carotid intima-media thickness and carotid plaques were assessed in RA patients. A multivariable analysis was performed to evaluate the relation of CEC with RA-related data, lipid profile and subclinical carotid atherosclerosis.

Results Mean CEC was not significantly different between RA patients (18.9 ± SD 9.0%) and controls (16.9±10.4%), p=0.11. Demographic variables were not associated with CEC except for a correlation with male gender that was only found in RA patients, but not in controls. Systolic blood pressure inversely correlated with CEC in controls (beta coefficient -0.1 [-0.2–0.0] %, p=0.025). In RA patients, a similar trend was found although a statistically significant difference was not reached. Neither the traditional cardiovascular risk factors nor the cardiovascular co-morbidity-related data were associated with CEC. Similarly, lipid profile did not show any relationship with CEC in patients or controls. ESR tended to be associated with a lower CEC although it did not reach statistical significance. RA patients with low (beta coef. -5.2 [-10.0–0.3] %, p=0.039) and moderate disease activity (beta coef. -4.6 [-8.5–0.7] %, p=0.020) were associated with inferior levels of CEC when compared to patients in remission. CEC was not found to be associated with cIMT in RA patients. However, higher CEC was associated with a protective effect for the presence of carotid plaque in RA patients. This relationship was maintained even after multivariate analysis (OR 0.94 [0.89–0.98], p=0.015).

Conclusions Our study, which includes the largest series of RA patients ever assessed for CEC, reveals for the first time that CEC is related to subclinical atherosclerosis in RA patients. The fact that CEC is also associated with disease activity reinforces the idea that CEC may be a mediator between disease activity and subclinical atherosclerosis.

Disclosure of Interest None declared

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