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Published on: January 28, 2020
Inflammatory markers in patients with coronary artery disease with and without inflammatory rheumatic disease
Unni M Breland1, Ivana Hollan, Kjell Saatvedt
1Research Institute of Internal Medicine, Rikshospitalet University Hospital, Oslo, Norway.
Insights
Patients with inflammatory rheumatic diseases (IRDs) and coronary artery disease (CAD) exhibit a distinct inflammatory profile, characterized by increased endothelial cell activation and osteoprotegerin (OPG) levels, contributing to accelerated atherosclerosis.
Area of Science:
- Cardiovascular Medicine
- Rheumatology
- Immunology
Background:
- Patients with inflammatory rheumatic diseases (IRDs) face higher risks of accelerated atherosclerosis, leading to increased morbidity and mortality.
- The specific inflammatory phenotype in patients with both IRD and coronary artery disease (CAD) remains incompletely understood.
Purpose of the Study:
- To investigate the inflammatory phenotype in patients with the comorbidity of IRD and CAD compared to CAD patients without IRD.
- To identify specific inflammatory markers associated with accelerated atherosclerosis in the context of IRD.
Main Methods:
- A comparative study involving four patient groups: CAD with IRD (CAD-IRD), CAD without IRD, IRD without CAD, and healthy controls.
- Plasma levels of various inflammatory markers, including vascular cell adhesion molecule-1 (VCAM-1), von Willebrand factor, osteoprotegerin (OPG), and CCL21, were measured using enzyme immunoassays.
Main Results:
- CAD-IRD patients showed significantly elevated levels of VCAM-1, von Willebrand factor, and OPG, alongside decreased CCL21, compared to CAD patients without IRD.
- In CAD-IRD patients, acute coronary syndrome predicted OPG levels, indicating heightened inflammation during plaque destabilization.
- VCAM-1, OPG, and CCL21 levels were significant predictors distinguishing CAD-IRD from CAD, independent of lipid parameters and other inflammatory markers like C-reactive protein (CRP).
Conclusions:
- Inflammation plays a crucial role in the accelerated atherosclerosis observed in IRD patients.
- Specific inflammatory pathways, including enhanced endothelial cell activation and the RANK ligand/RANK/OPG system, are likely key contributors to this process.
Objectives:
Patients with inflammatory rheumatic diseases (IRDs) have a higher morbidity and mortality from accelerated atherosclerosis than the general population. We hypothesized that patients with the combination of IRD and coronary artery disease (CAD) would have a certain inflammatory phenotype compared with CAD patients without this comorbidity.
Methods:
Four groups of patients were included: patients with IRD, referred to coronary artery bypass grafting (CABG) (CAD-IRD, n = 67), patients without IRD, referred to CABG (CAD, n = 52), patients with IRD without CAD (IRD, n = 32) and healthy controls (n = 30). Plasma levels of several inflammatory markers were analysed by enzyme immunoassays.
Results:
(i) Plasma levels of markers of endothelial cell activation [i.e. vascular cell adhesion molecule-1 (VCAM-1) and von Willebrand factor] and osteoprotegerin (OPG) were significantly increased and plasma levels of CCL21 significantly decreased in CAD-IRD patients as compared with CAD patients without IRD. (ii) Within the CAD-IRD group, acute coronary syndrome was a significant predictor of OPG, suggesting an enhanced inflammatory response during plaque destabilization in CAD-IRD patients. (iii) Plasma levels of VCAM-1, OPG and CCL21, but not lipid parameters, IRD characteristics and several other inflammatory markers (e.g. CRP), were significant predictors of CAD-IRD as opposed to CAD in two logistic regression models.
Conclusion:
Our findings further support a role for inflammation in the accelerated form of atherosclerosis in IRD patients, and suggest that certain inflammatory pathways, such as the enhanced endothelial cell activation and the RANK ligand/RANK/OPG system, may be of particular importance.
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