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From the Journals

Cholesterol's Role in RA Atherosclerosis

Study links changes in cholesterol loading capacity to coronary atherosclerosis progression in rheumatoid arthritis, highlighting therapy impacts.

Conexiant

Changes in serum cholesterol loading capacity were significantly associated with coronary atherosclerosis progression, including high-risk plaque features, in patients with rheumatoid arthritis, according to a recent study.

Researchers conducted a prospective observational study involving 100 patients with rheumatoid arthritis (RA) without prior cardiovascular disease. Patients underwent coronary computed tomography angiography (CCTA) at baseline and after an average follow-up of 6.9 ± 0.4 years. Serum cholesterol loading capacity (CLC), which reflects cholesterol uptake by macrophages, was measured using a fluorometric assay.

The study, published in RMD Open, aimed to examine whether changes in serum CLC correlated with progression in coronary plaques—non-calcified, partially calcified, and fully calcified plaques—and the impact of medications such as prednisone, biologic disease-modifying antirheumatic drugs (bDMARDs), and statins.

Results showed that mean CLC increased by 1.54 ± 3.69 μg cholesterol/mg protein, significantly associated with progression in:

  • Non-calcified plaques (odds ratio [OR] 2.55, 95% confidence interval [CI] 1.22–5.35),

  • Fully calcified plaques (OR 3.10, 95% CI 1.67–5.76),

  • Coronary artery calcium (CAC) scores (OR 1.80, 95% CI 1.18–2.74).

Prednisone use was linked to progression of partially calcified plaques, while bDMARDs and statins reduced progression of high-risk lipid-rich non-calcified plaques and extensive or obstructive disease. The study highlighted that fully calcified plaques are generally more stable than lipid-rich non-calcified plaques, which pose higher cardiovascular risk.

In addition, the study observed that CLC decreased in 68% of patients over time, potentially due to improvements in systemic inflammation, oxidation, or the use of immunomodulators. Reductions in CLC were associated with lower cumulative inflammation, as measured by time-averaged erythrocyte sedimentation rate (ESR).

These findings indicate the role of macrophage cholesterol loading in RA-related cardiovascular risk and suggest that therapies targeting cholesterol uptake and processing by macrophages could complement existing anti-inflammatory and lipid-lowering strategies. The study also emphasizes the complex interplay between inflammation, lipid metabolism, and medication effects in managing atherosclerosis in this high-risk population.

Full disclosures and funding details, including support from the American Heart Association and Pfizer, can be found in the published study.