A biomarker of inflammation in cardiovascular disease View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

2003

AUTHORS

Giora Z. Feuerstein , Ron Firestein , Peter Libby , Douglas L. Mann

ABSTRACT

First discovered in 1929 by Oswald Avery, C-reactive protein (CRP) is produced andreleased primarily by the liver and normally circulates at very low levels [1]. However, levels of CRP increase markedly in response to trauma or disease and closelytrack the inflammatory burden of disease. Synthesis and release of CRP appears tobe largely controlled by the cytokine IL-6. As the role of inflammation in cardiacdisease gains greater acceptance, the significance of biomarkers of the inflammatory burden gains recognition as well. In the past, scientists studied the potential roleof CRP as a biomarker in conjunction with clinical and other diagnostic measuresto assess cardiovascular disease severity. More recent data point to a role for CRPas a prospective marker of cardiovascular risk. These data have now generated theintriguing hypothesis that CRP reductions may serve as a surrogate marker of therapeutic efficacy of interventions aimed to reduce cardiovascular morbidity and mortality. Indeed, the efficacy of cholesterol-lowering drugs such as statins in loweringcardiovascular events may depend in part on anti-inflammatory effects reflected byreduced CRP due to either direct or low density lipoprotein (LDL)-lowering effectsof these drugs. Using robust correlation analyses of multiple inflammatory markers,CRP correlates excellently with heart diseases, exceeding other inflammatory markers such as IL-6 or adhesion molecules. Furthermore, CRP seems to predict risk forheart attacks and stroke in individuals with normal or low cholesterol levels as wellas in apparently healthy women. More... »

PAGES

9-20

References to SciGraph publications

Book

TITLE

Inflammation and Cardiac Diseases

ISBN

978-3-0348-9419-7
978-3-0348-8047-3

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-3-0348-8047-3_2

DOI

http://dx.doi.org/10.1007/978-3-0348-8047-3_2

DIMENSIONS

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55 schema:description First discovered in 1929 by Oswald Avery, C-reactive protein (CRP) is produced andreleased primarily by the liver and normally circulates at very low levels [1]. However, levels of CRP increase markedly in response to trauma or disease and closelytrack the inflammatory burden of disease. Synthesis and release of CRP appears tobe largely controlled by the cytokine IL-6. As the role of inflammation in cardiacdisease gains greater acceptance, the significance of biomarkers of the inflammatory burden gains recognition as well. In the past, scientists studied the potential roleof CRP as a biomarker in conjunction with clinical and other diagnostic measuresto assess cardiovascular disease severity. More recent data point to a role for CRPas a prospective marker of cardiovascular risk. These data have now generated theintriguing hypothesis that CRP reductions may serve as a surrogate marker of therapeutic efficacy of interventions aimed to reduce cardiovascular morbidity and mortality. Indeed, the efficacy of cholesterol-lowering drugs such as statins in loweringcardiovascular events may depend in part on anti-inflammatory effects reflected byreduced CRP due to either direct or low density lipoprotein (LDL)-lowering effectsof these drugs. Using robust correlation analyses of multiple inflammatory markers,CRP correlates excellently with heart diseases, exceeding other inflammatory markers such as IL-6 or adhesion molecules. Furthermore, CRP seems to predict risk forheart attacks and stroke in individuals with normal or low cholesterol levels as wellas in apparently healthy women.
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