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The Relationship between the complement system and subclinical carotid atherosclerosis in patients with rheumatoid
Marta Hernández-Díaz1, Dara Rodríguez-González2, Elena Heras-Recuero3
1Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, Santander, Spain.
Insights
The complement system is linked to carotid atherosclerosis in rheumatoid arthritis (RA) patients. Specific complement factors like C3a and C5a correlate with carotid intima media thickness and plaque presence in RA.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Rheumatology
Background:
- Rheumatoid arthritis (RA) patients face elevated cardiovascular (CV) event and mortality risks.
- Subclinical carotid atherosclerosis is a known predictor of CV events in RA.
- The complement system plays a role in both RA and CV disease pathogenesis.
Purpose of the Study:
- To investigate the association between complement system activation and subclinical carotid atherosclerosis in RA patients.
- To explore the relationship between specific complement components and carotid intima media thickness and plaque.
Main Methods:
- Recruited 430 RA patients for the study.
- Assessed functional assays of the three complement pathways and measured serum levels of individual complement components.
- Evaluated subclinical carotid atherosclerosis using ultrasonography and performed multivariable linear regression analysis.
Main Results:
- C3a and C5a showed significant positive correlations with carotid intima media thickness after multivariable adjustment.
- Higher levels of C1-inhibitor, properdin, C3, C5, and C5a were independently associated with the presence of carotid plaque.
Conclusions:
- The study establishes a link between the complement system and subclinical carotid atherosclerosis in RA patients.
- Complement system activation may contribute to the development of atherosclerosis in RA.
Background:
Patients with rheumatoid arthritis (RA) have an increased risk of cardiovascular (CV) events and CV mortality. Subclinical carotid atherosclerosis is independently associated with rates of incident CV events among patients with RA. The complement system has been related to both the etiopathogenesis of RA and CV disease. In this study, we aimed to evaluate the association between a comprehensive assessment of the complement system and carotid intima media thickness and carotid plaque in patients with RA.
Methods:
430 patients with RA were recruited. Functional assays of the three pathways of the complement system, utilizing new-generation techniques, were assessed. Additionally, serum levels of individual components of the complement system belonging to the three pathways were measured: C1q (classical), lectin (lectin), C2, C4, and C4b (classical and lectin), factor D and properdin (alternative), C3 and C3a (common), C5, C5a, and C9 (terminal), as well as regulators factor I and C1-inhibitor. Subclinical carotid atherosclerosis was evaluated by ultrasonography. Multivariable linear regression analysis was conducted to investigate the association between the complement system and carotid intima media thickness and carotid plaque.
Results:
After multivariable adjustment, which included traditional CV risk factors and disease-related data, C3a and C5a exhibited significant positive correlations with carotid intima media thickness. Additionally, higher values of C1-inhibitor, properdin, C3, C5, and C5a were independently associated with the presence of carotid plaque.
Conclusion:
The complement system and subclinical carotid atherosclerosis are linked in patients with RA.
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