Impact of Cumulative Inflammation, Cardiac Risk Factors, and Medication Exposure on Coronary Atherosclerosis Progression in Rheumatoid Arthritis. Issue 3 (22nd January 2020)

• Record Type: Journal Article
• Authors: Karpouzas, George A.; Ormseth, Sarah R.; Hernandez, Elizabeth; Budoff, Matthew J.
• Is Part Of: Arthritis & rheumatology. Volume 72:Issue 3(2020)
• Page Start: 400
• Page End: 408
• Publication Date: 2020-01-22
• Subjects: Arthritis -- Periodicals; Rheumatism -- Periodicals; 616.72
• DOI: 10.1002/art.41122
• Languages: English
• ISSNs: 2326-5191

Abstract

Abstract : Objective: To explore incidence and progression of coronary atherosclerosis and identify determinants in patients with rheumatoid arthritis (RA). We specifically evaluated the impact of inflammation, cardiac risk factors, duration of medication exposure, and their interactions on coronary plaque progression. Methods: One hundred one participants with baseline coronary computed tomography angiography findings underwent follow‐up assessment a mean ± SD of 83 ± 3.6 months after baseline. Plaque burden was reported as the segment involvement score (describing the number of coronary segments with plaque) and the segment stenosis score (characterizing the cumulative plaque stenosis over all evaluable segments). Plaque composition was classified as noncalcified, mixed, or calcified. Coronary artery calcium (CAC) was quantified using the Agatston method. Results: Total plaque increased in 48% of patients, and progression was predicted by older age, higher cumulative inflammation, and total prednisone dose ( P < 0.05). CAC progressors were older, more obese, hypertensive, and had higher cumulative inflammation compared to nonprogressors ( P < 0.05). Longer exposure to biologics was associated with lower likelihood of noncalcified plaque progression, lesion remodeling, and constrained CAC change in patients without baseline calcification, independent of inflammation, prednisone dose, or statin exposure (all P < 0.05). Longer statin treatment further restricted noncalcified plaque progression and attenuated the effect of inflammation on increased plaque and CAC ( P < 0.05). Stringent systolic blood pressure (BP) control further weakened the effect of inflammation on total plaque progression. Conclusion: Inflammation was a consistent and independent predictor of coronary atherosclerosis progression in RA. It should therefore be specifically targeted toward mitigating cardiovascular risk. Biologic disease‐modifying antirheumatic drugs, statins, and BP control may further constrain plaque progression directly or indirectly.