AB0677 C-REACTIVE PROTEIN AT RHEUMATOID ARTHRITIS ONSET IS THE FOREMOST CAUSE FOR A CONTINUING SUBCLINICAL ATHEROSCLEROSIS PROGRESSION
Authors: H. Hannawi, S. Hannawi, M. Al-Salmi
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Rheumatoid arthritis (RA) patients are at higher risk of cardiovascular diseases (CVD) of which carotid intima-media thickness (cIMT) serves as a non-invasive surrogate marker. Previously, we published that our RA patients have more sub-clinical atherosclerosis with thicker cIMT, and more carotid atherosclerotic plaque compared to their age, sex, and traditional CVD risk factors matched controls. <h3>Objectives:</h3> To investigate the determinants of subclinical atherosclerosis progression (cIMT as a marker) in early RA patients who started their RA treatment early at RA diagnosis. <h3>Methods:</h3> A total of 31 adult (&gt;18 years old), early RA patients who met the ACR-EULAR 2010 classification criteria for RA were recruited through a specialized early RA clinic. cIMT was recorded at baseline-week (wk0) (at the diagnosis of RA; within 6 months of RA symptoms onset, and before starting anti-rheumatic therapy), and again after one year of diagnosis (wk52), and starting DMARD treatment, with EULAR remission criteria as the target for treatment. Inclusion criteria included early RA patients with no history of traditional CVD (diabetes mellitus, hypertension, thyroid disturbance, atherosclerosis (cardiac/central nervous system), dyslipidemia, current/history of smoking, and alcohol consumption) risk factors. Patients with concomitant autoimmune disease or any other chronic diseases, and pregnant women were excluded. RA disease activity assessment, physical examination, laboratory investigations (at fasting status), and cIMT sonographic measurement were obtained within the same week of RA diagnosis, in two different sessions. cIMT progression was calculated by subtracting the average of cIMT at week 0 from the average of cIMT at week 52. The correlation between cIMT progression and the explanatory variables (CVD risk factors; (traditional and non-traditional) obtained at wk0 (baseline), investigated using linear regression analysis. Variables with continuous variables were reported as mean ± standard deviations, and the categorical variables as percentages. <h3>Results:</h3> The mean age of the RA participants was 50±13 (min 24, max 87) years. The mean cIMT at baseline (wk0) was 0.58±0.10 mm. The mean cIMT at one year (wk52) was 0.61± 0.13 mm. cIMT progression over a year (wk52) was found in 18 (58%) of RA patients, with an average of cIMT progression 0.05±0.08 mm. Univariate analysis demonstrated a positive correlation between cIMT progression and each of, age at RA onset (p=0.03, CI: 0.00,0.00), inflammatory activity at wk0; erythrocyte sedimentation rate (ESR) (p=0.03, CI 0.00,0.00), C-reactive protein (p=0.00, CI: 0.00, 0.01), and ferritin level (p=0.00, CI: 0.00,0.00). Out of blood rheology, there was a positive linear correlation between cIMT progression and each of the total white cell count (p=0.00, CI:0.01,0.02), and neutrophil absolute count (p=0.03, CI:0.00, 0.02), and a negative association with red blood cell count (p=0.03, CI: -0.12,-0.01). There was no correlation between the cIMT progression and other parameters obtained at baseline (wk0), including body mass index, systolic and diastolic blood pressure, triglycerides, high-density lipoprotein, low-density lipoprotein, and total cholesterol. Multiple linear regression analysis, including all the factors that showed significant association in the univariate linear regression as explanatory variables yield, a positive correlation between cIMT and CRP level at WK0 (p=0.00, CI: 0.00, 0.00) with adjusted R2 of 63. <h3>Conclusion:</h3> In addition to the known role of CRP in the onset of atherosclerosis, the CRP level at RA onset is most responsible determinant for continuing atherosclerosis progression and CVD complications in RA. Early diagnosis and early suppression of inflammation activity would be of help to hinder the progression of subclinical atherosclerosis. <h3>REFERENCES:</h3> [1] Hannawi SM, et al. Saudi Med J. 2020 Sep;41(9):1022-1025. [2] Hannawi S, et al. Hypertens Res. 2020 Sep;43(9):982-984. [3] Hannawi S, et al. Arthritis Res Ther. 2007;9(6):R116. <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> Haifa Hannawi: None declared, Suad Hannawi the "paid instructor" is not related to the abstract. have served as an instructor for internal workshops for Janssen, Amgen, AstraZeneca, and Lilly, I have paid as a speaker for Abbvie, Lilly, Novartis, Amgen, AstraZeneca, Bhorengher, and Janssen, Maria Al-Salmi: None declared.