Inflammatory markers in patients with coronary artery disease with and without inflammatory rheumatic disease

• Published in: Rheumatology (Oxford, England) Vol. 49; no. 6; pp. 1118 - 1127
• Main Authors: Breland, Unni M., Hollan, Ivana, Saatvedt, Kjell, Almdahl, Sven M., Damås, Jan K., Yndestad, Arne, Mikkelsen, Knut, Førre, Øystein T., Aukrust, Pål, Ueland, Thor
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01-06-2010
• Subjects: Aged; Biological and medical sciences; Biomarkers - metabolism; Cardiology. Vascular system; Case-Control Studies; Chemokines; Chemokines - metabolism; Coronary artery disease; Coronary Artery Disease - complications; Coronary Artery Disease - metabolism; Coronary heart disease; Diseases of the osteoarticular system; Female; Heart; Humans; Inflammation; Inflammatory joint diseases; Inflammatory rheumatic disease; Male; Medical sciences; Middle Aged; Models, Biological; Osteoprotegerin; Osteoprotegerin - metabolism; Regression Analysis; Rheumatic Diseases - complications; Rheumatic Diseases - metabolism; Risk Factors; Chemokine; Human; Diseases of the osteoarticular system; Rheumatology; Cardiovascular disease; Inflammation; Inflammatory joint disease; Inflammatory rheumatic disease; Coronary heart disease; Coronary artery disease; Chemokines; Osteoprotegerin
• ISSN: 1462-0324; 1462-0332
• DOI: 10.1093/rheumatology/keq005

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.