Inflammatory markers predict late cardiac events in patients who are exhausted after percutaneous coronary intervention.
Chronic inflammation is one of the main underlying mechanisms in the development of coronary artery disease (CAD). We investigated the prognostic value of inflammatory markers for cardiac events occurring more than 6 months after percutaneous coronary intervention (PCI), i.e. late cardiac events, furthermore we investigated the temporal stability of these markers. Exhausted patients (234) recently treated by successful PCI were studied. Serum samples collected about 6 weeks after PCI (baseline), 6 and 18 months after baseline were analyzed for CRP, IL-6, tumour necrosis factor (TNF-alpha), IL-10, IL-1ra, IL-8 and neopterin. In the mean cardiac follow-up of 24 months, 25 late cardiac events occurred. Cox proportional hazards analysis was used to determine the prognostic value. Elevated concentrations of IL-6 at baseline and 6 months later increased the risk of late cardiac events (RR 3.9, CI 1.7-9.0, p 0.00 and RR 3.6, CI 1.6-8.5, p 0.00). Elevated concentrations of CRP and IL-10 at baseline also increased the risk of late cardiac events (RR 2.5, CI 1.1-5.7, p 0.04 and RR 2.5, CI 1.1-5.6, p 0.03) as did IL-1 receptor antagonist at 6 months (RR 2.6, CI 1.1-6.1, p 0.04). Temporal stability was high for most markers, but highest for IL-6. These results support the assumption that chronic inflammation is a pathophysiological mechanism in the development of CAD.
Kwaijtaal
Martijn
M
Department of Medical Microbiology, University Hospital Maastricht, P. Debeyeplein 25, P.O. Box 5800, 6202 AZ, Maastricht, Limburg, The Netherlands. mkw@lmib.azm.nl
van Diest
Rob
R
Bär
Frits W
FW
van der Ven
André J
AJ
Bruggeman
Cathrien A
CA
de Baets
Marc H
MH
Appels
Ad
A
D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000097:blood*; D002097:C-Reactive Protein / Q000276:immunology / Q000378:metabolism; D003324:Coronary Artery Disease / Q000150:complications / Q000276:immunology* / Q000628:therapy*; D005221:Fatigue / Q000175:diagnosis / Q000209:etiology / Q000276:immunology*; D005500:Follow-Up Studies; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D016753:Interleukin-10 / Q000097:blood / Q000276:immunology; D015850:Interleukin-6 / Q000097:blood / Q000276:immunology; D016209:Interleukin-8 / Q000097:blood / Q000276:immunology; D008875:Middle Aged; D019798:Neopterin / Q000097:blood / Q000276:immunology; D011183:Postoperative Complications / Q000175:diagnosis / Q000276:immunology; D011237:Predictive Value of Tests; D012795:Sialoglycoproteins / Q000097:blood / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000378:metabolism
D015415:Biomarkers; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6; D016209:Interleukin-8; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D019798:Neopterin; D002097:C-Reactive Protein