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Systemic inflammation and cardiovascular risk factors predict rapid progression of atherosclerosis in rheumatoid
Inmaculada del Rincón1, Joseph F Polak2, Daniel H O'Leary2
1Division of Rheumatology and Clinical Immunology, Department of Medicine, The University of Texas Health Science Center at San Antonio, Texas, USA.
Insights
Systemic inflammation and cardiovascular risk factors accelerate atherosclerosis in rheumatoid arthritis patients. Treatments like methotrexate may mitigate this progression by reducing inflammation.
Area of Science:
- Rheumatology
- Cardiology
- Vascular Biology
Background:
- Rheumatoid arthritis (RA) is linked to increased cardiovascular disease risk.
- Atherosclerosis, a key contributor to cardiovascular events, may be accelerated in RA patients.
- Understanding factors influencing atherosclerosis progression in RA is crucial for risk management.
Purpose of the Study:
- To quantify the rate of atherosclerosis progression in rheumatoid arthritis patients.
- To identify baseline factors, including cardiovascular risk factors and inflammation markers, associated with accelerated atherosclerosis.
- To explore potential interactions between inflammation, cardiovascular risk factors, and medication use in influencing atherosclerosis progression.
Main Methods:
- Carotid intima-media thickness (IMT) was measured using ultrasound at baseline and approximately 3 years later in 487 RA patients.
- Cardiovascular risk factors, inflammation markers (erythrocyte sedimentation rate - ESR), and medication use were recorded.
- Logistic regression analysis identified predictors of rapid IMT progression, with tests for interactions involving ESR.
Main Results:
- Atherosclerosis progression (IMT increase) was observed in RA patients at a mean rate of 0.018 mm/year.
- Higher numbers of cardiovascular risk factors and elevated ESR at baseline were significantly associated with rapid IMT progression.
- Significant interactions indicated that cardiovascular risk factors and medication use modify the impact of ESR on IMT progression.
Conclusions:
- Both systemic inflammation (indicated by ESR) and the burden of cardiovascular risk factors are associated with accelerated atherosclerosis in RA.
- Cardiovascular risk factors may modulate how systemic inflammation contributes to atherosclerosis progression over time.
- Disease-modifying antirheumatic drugs, specifically methotrexate and anti-tumour necrosis factor agents, may attenuate IMT progression by reducing inflammation's effect.
Objective:
To estimate atherosclerosis progression and identify influencing factors in rheumatoid arthritis (RA).
Methods:
We used carotid ultrasound to measure intima-media thickness (IMT) in RA patients, and ascertained cardiovascular (CV) risk factors, inflammation markers and medications. A second ultrasound was performed approximately 3 years later. We calculated the progression rate by subtracting the baseline from the follow-up IMT, divided by the time between the two scans. We used logistic regression to identify baseline factors predictive of rapid progression. We tested for interactions of erythrocyte sedimentation rate (ESR) with CV risk factors and medication use.
Results:
Results were available for 487 RA patients. The mean (SD) common carotid IMT at baseline was 0.571 mm (0.151). After a mean of 2.8 years, the IMT increased by 0.050 mm (0.055), p≤0.001, a progression rate of 0.018 mm/year (95% CI 0.016 to 0.020). Baseline factors associated with rapid progression included the number of CV risk factors (OR 1.27 per risk factor, 95% CI 1.01 to 1.61), and the ESR (OR 1.12 per 10 mm/h, 95% CI 1.02 to 1.23). The ESR×CV risk factor and ESR×medication product terms were significant, suggesting these variables modify the association between the ESR and IMT progression.
Conclusions:
Systemic inflammation and CV risk factors were associated with rapid IMT progression. CV risk factors may modify the role of systemic inflammation in determining IMT progression over time. Methotrexate and antitumour necrosis factor agents may influence IMT progression by reducing the effect of the systemic inflammation on the IMT.
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