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Interleukin 6 Inhibition and Coronary Artery Disease in a High-Risk Population: A Prospective Community-Based
Bruno Cesar Bacchiega1, Ana Beatriz Bacchiega2, Magali Justina Gomez Usnayo2
1Department of Internal Medicine, Rio de Janeiro State University, Rio de Janeiro, Brazil brunobacchiega@gmail.com.
Insights
Tocilizumab improved endothelial function in rheumatoid arthritis patients, despite increasing cholesterol levels. This IL-6 blockade offers potential cardiovascular benefits, though lipid changes require monitoring.
Area of Science:
- Cardiovascular Medicine
- Rheumatology
- Immunology
Background:
- Atherosclerosis is a chronic inflammatory disease driven by interleukin-6 (IL-6).
- IL-6 blockade may reduce cardiovascular risk but can cause dyslipidemia.
- The prognostic implications of IL-6-induced dyslipidemia are unclear.
Purpose of the Study:
- To assess the impact of tocilizumab, an IL-6 inhibitor, on endothelial function in rheumatoid arthritis (RA) patients.
- To compare endothelial function changes with anti-tumor necrosis factor α (anti-TNFα) and conventional synthetic disease-modifying antirheumatic drugs (csDMARDs).
Main Methods:
- A 16-week prospective study involving 60 RA patients.
- Patients received tocilizumab (n=18), anti-TNFα (n=18), or csDMARDs (n=24).
- Endothelial function was measured by flow-mediated dilation (FMD) percentage variation pre- and post-therapy.
Main Results:
- Tocilizumab significantly improved FMD (3.43% to 5.96%, P=0.03).
- Anti-TNFα and csDMARDs did not show statistically significant improvements in FMD.
- Tocilizumab and csDMARDs increased total cholesterol, while only tocilizumab showed a significant increase in LDL.
Conclusions:
- Tocilizumab enhances endothelial function in RA patients, a high-risk population for cardiovascular events.
- Despite improvements in endothelial function, tocilizumab increases total cholesterol and low-density lipoprotein levels.
- The cardiovascular benefits of IL-6 blockade via tocilizumab warrant further investigation considering the associated lipid profile changes.
Background:
Atherosclerosis is a chronic inflammatory disease, with interleukin 6 (IL-6) as a major player in inflammation cascade. IL-6 blockade may reduce cardiovascular risk, but current treatments to block IL-6 also induce dyslipidemia, a finding with an uncertain prognosis.
Methods And Results:
We aimed to determine the endothelial function responses to the IL-6-blocking agent tocilizumab, anti-tumor necrosis factor α, and synthetic disease-modifying antirheumatic drug therapies in patients with rheumatoid arthritis in a 16-week prospective study. Sixty consecutive patients with rheumatoid arthritis were enrolled. Tocilizumab and anti-tumor necrosis factor α therapy were started in 18 patients each while 24 patients were treated with synthetic disease-modifying antirheumatic drugs. Forty patients completed the 16-week follow-up period. The main outcome was flow-mediated dilation percentage variation before and after therapy. In the tocilizumab group, flow-mediated dilation percentage variation increased statistically significantly from a pre-treatment mean of (3.43% [95% CI, 1.28-5.58] to 5.96% [95% CI, 3.95-7.97]; P=0.03). Corresponding changes were 4.78% (95% CI, 2.13-7.42) to 6.75% (95% CI, 4.10-9.39) (P=0.09) and 2.87% (95% CI, -2.17 to 7.91) to 4.84% (95% CI, 2.61-7.07) (P=0.21) in the anti-tumor necrosis factor α and the synthetic disease-modifying antirheumatic drug groups, respectively (both not statistically significant). Total cholesterol increased significantly in the tocilizumab group from 197.5 (95% CI, 177.59-217.36) to 232.3 (201.62-263.09) (P=0.003) and in the synthetic disease-modifying antirheumatic drug group from 185.8 (95% CI, 169.76-201.81) to 202.8 (95% CI, 176.81-228.76) (P=0.04), but not in the anti-tumor necrosis factor α group. High-density lipoprotein did not change significantly in any group.
Conclusions:
Endothelial function is improved by tocilizumab in a high-risk population, even as it increases total cholesterol and low-density lipoprotein levels.
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