Impact of Cumulative Inflammation, Cardiac Risk Factors, and Medication Exposure on Coronary Atherosclerosis Progression in Rheumatoid Arthritis

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.

Biologics May Prevent Cardiovascular Events in Rheumatoid Arthritis by Inhibiting Coronary Plaque Formation and Stabilizing High‐Risk Lesions

“…Emerging information supports similar effects for non-TNFi biologics (13,14). We recently reported that longer biologic DMARD exposure was associated with a lower likelihood of increase in noncalcified plaque burden in RA (6). Biologic DMARD use also predicted decreases in noncalcified plaque and necrotic core burden in patients with psoriasis (15).…”

“…We previously reported that RA disease activity was associated with greater coronary plaque burden and vulnerability (5). Cumulative inflammation also predicted coronary plaque progression in RA (6). Lastly, subclinical coronary plaque burden was associated with mid-term CVD events in RA above and beyond traditional risk factors or the Framingham-D'Agostino score of cardiovascular risk (7,8).…”

“…Multidetector CCTA. CCTA protocols for acquisition and processing have been described previously (6). Acquisition parameters (milliamperes and kilovoltage) and slice thickness (0.625 mm) were identical between baseline and follow-up scans.…”

Largely accelerated arterial aging in rheumatoid arthritis is associated with inflammatory activity and smoking in the early stage of the disease

“…According to recently published data, coronary artery calci cation increases with higher total prednisone dose, by contrast methotrexate and other csDMARDs do not in uence coronary plaque progression [33]. Furthermore, DMARD and TNF-α antagonists are associated with reduced risk of myocardial infarction, stroke and cardiovascular death [56,57].…”

“…The traditional cardiovascular risk scores underestimate the real cardiovascular risk in RA [29][30][31]. CCS is better in CV risk strati cation in RA than combinations of the traditional CV risk factors [32,33]. Here we investigated the baseline and follow-up CCS of RA patients and studied its progression over time.…”