Date: Sunday, November 8, 2015
Session Type: ACR Poster Session A
Session Time: 9:00AM-11:00AM
Background/Purpose: Abatacept (ABT) is very effective in treating rheumatoid arthritis(RA)1. Patients with RA have an increased risk of cardiovascular disease (CVD), and rheumatologists need to develop primary prevention strategies for CVD in RA patients2, 3. For example, some biologics used to treat RA also reduce subclinical atherosclerosis and may improve morbidity in CVD4, 5. There is no evidence that ABT effect subclinical atherosclerosis. To examine the effect on subclinical atherosclerosis in disease modified anti-rheumatic-drugs (DMARDs) resistant RA patients in a cohort study design.
Methods: 75 RA patients with moderate to severe active disease despite DMARDs treatment (disease activity score: DAS28>3.2) were received ABT (125mg every week subcutaneously). Subclinical atherosclerosis was assessed with cardio-ankle vascular index (CAVI) and augmentation index corrected for a heart rate of 75 beats per minute (AIx@75) at baseline and 24 weeks follow-up. Clinical data were collected at regular visits. CAVI is combined pulse wave velocity (PWV) and flow mediated dilation, and CAVI measures arterial wall stiffness independent of blood pressure and it is superior to brachial ankle PWV as an index of atherosclerosis. No new all treatments (stating, low lipids drug, and etc.) were allowed.
Results: 65 patients completed this study. There were no changes in CAVI(12.68 ± 1.76 and 12.71± 2.11; p = 0.96) and AIx@75(32.45 ± 9.8, 33.21 ± 12.6; p = 0.87) from baseline to 24 weeks follow up.DAS 28-ESR score improved significantly from baseline to 24 weeks(5.87±2.15, 2.57±1.32: p=0.01). There were no There was no change in systolic and diastolic blood pressure Total cholesterol/LDL cholesterol ratio, atherogenic index and triglycerides. Changes of CAVI and AIx@75 were not correlated with changes of disease activity from baseline to 24 weeks follow up. (CAVI: p=0.75, AIx@75: p=0.81).No patients suffered from new CV disease.
Conclusion: These findings suggest that ABT did not improve subclinical atherosclerosis after 24 weeks follow up despite good control of disease activity in rheumatoid arthritis.
1. Schiff M, et al. Subcutaneous abatacept for the treatment of rheumatoid arthritis.Rheumatology (Oxford). 2013 Jun; 52(6):986-97. doi: 10.1093/rheumatology/ket018.
2.van Halm VP, et al. Rheumatoid arthritis versus diabetes as a risk factor for cardiovascular disease: a cross-sectional study, the CARRE Investigation. Ann Rheum Dis 2009; 68:1395–400.
3.del Rincon ID, et al. High incidence of cardiovascular events in a rheumatoid arthritis cohort not explained by traditional cardiac risk factors. Arthritis Rheum 2001; 44:2737–45.
5. Greenberg JD, et al. Tumor necrosis factor antagonist use and associated risk reduction of cardiovascular events among patients with rheumatoid arthritis. Ann Rheum Dis. 2011; 70:576-82
To cite this abstract in AMA style:Kume K, Amano K, Yamada S, Kanazawa T, Hatta K, Amano K, Kuwaba N. Abatacept Does Not Improve Subclinical Atherosclerosis Despite Good Response in Rheumatoid Arthritis: A Cohort Study [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). https://acrabstracts.org/abstract/abatacept-does-not-improve-subclinical-atherosclerosis-despite-good-response-in-rheumatoid-arthritis-a-cohort-study/. Accessed January 19, 2020.
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ACR Meeting Abstracts - https://acrabstracts.org/abstract/abatacept-does-not-improve-subclinical-atherosclerosis-despite-good-response-in-rheumatoid-arthritis-a-cohort-study/