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Pål Aukrust1,2, Arne Yndestad1, Camilla Smith1, Thor Ueland1,3, Lars Gullestad4, Jan K. Damås1,2
1Research Institute for Internal Medicine, 2Section of Clinical Immunology and Infectious Diseases, 3Section of Endocrinology, and 4Department of Cardiology, Rikshospitalet-Radiumhospitalet, Medical Center, University of Oslo, Oslo, Norway
In consideration of the important role of inflammation in plaque progression and stability, recent work has focused on whether plasma markers of inflammation can non-invasively diagnose and predict coronary artery disease (CAD) and other forms of atherosclerotic disorders. Although several studies support an important pathogenic role of chemokines in atherogenesis and plaque destabilization, potentially representing attractive therapeutic targets in atherosclerotic disorders,this does not necessarily mean that chemokines are suitable parameters for risk prediction. In fact, the ability to reflect up-stream inflammatory activity, stable levels in individuals and high stability of the actual protein (e.g. long half-life and negligible circadian variation), are additional important criteria for an ideal biomarker in cardiovascular disease. Although plasma/serum levels of certain chemokines (e.g. interleukin 8 and monocyte chemoattractant protein- 1) have been shown to be predictive for future cardiac events in some studies, independent of traditional cardiovascular risk factors and C-reactive protein,and although certain gene polymorphisms of chemokines/chemokine receptors (e.g. fractalkine receptor) have been shown to be predictive of future atherosclerotic disease, further prospective studies, including a larger number patients,are needed to make any firm conclusion. While the demonstrations of an association between chemokines and CAD are a necessary first step, such studies do not establish the full clinical utility of a biomarker, which is a more demanding process that requires validation in multiple cohorts, and clear demonstration of incremental prognostic value over traditional risk models. If successful, such new biomarker will be a useful indicator for better risk assessment,diagnosis,and prognosis, as well as monitoring pharmacological treatments for atherosclerosis.
Atherosclerosis, inflammation, gene polymorphism, biomarkers, Chemokines
| 1. | ||
Vincent Braunersreuther, François Mach, Sabine Steffens Thrombosis and Haemostasis 2007 97 5: 714-721 http://dx.doi.org/10.1160/TH07-01-0036 | ||
| 2. | ||
Didier Hanriot1,2*, Gaëlle Bello1,2*, Armelle Ropars1,2, Carole Seguin-Devaux5, Gaël Poitevin1,2, Sandrine Grosjean3, Véronique Latger-Cannard2,3,4, Yvan Devaux1,2,5, Faiez Zannad1,2, Véronique Regnault2,4, Patrick Lacolley1,2, Paul-Michel Mertes1,2, Ketsia Hess*1,2, Dan Longrois*1,2 Thrombosis and Haemostasis 2008 99 3: 558-569 http://dx.doi.org/10.1160/TH07-06-0410 | ||
| 3. | ||
Bruce S. Sachais1, Tiffany Turrentine1, Jennine M. Dawicki McKenna1, Ann H. Rux1, Daniel Rader2, M. Anna Kowalska3,4 Thrombosis and Haemostasis 2007 98 5: 1108-1113 http://dx.doi.org/10.1160/TH07-04-0271 | ||