Role of inflammation in cardiovascular disease: how to use C-reactive protein in clinical practice.
Acute coronary syndromes, stroke, and sudden death are common complications of a disrupted atherosclerotic plaque. Unstable plaque is a result of multiple factors but is commonly characterized by an infiltrate of inflammatory cells. Medical research strongly supports a role for inflammation in the pathogenesis, progression, and disruption of atherosclerotic plaque. Medical science also has improved our understanding of the complex interactions between our environment and our immune, coagulation, and cardiovascular systems. Clinical studies have demonstrated systemic markers of inflammation to be strong predictors of clinical events, and specific treatments of atherosclerosis and its risk factors have been associated with reductions in inflammatory markers. The authors review the current understanding of the role of inflammation in the pathogenesis of atherosclerosis, the common inflammatory markers, and potential anti-inflammatory therapy. Among several potential circulating markers of vascular inflammation, high sensitivity C-reactive protein is best validated and standardized as a marker for cardiovascular risk assessment. Nevertheless, there remain many uncertainties in utilizing C-reactive protein in clinical practice. Here, the authors describe the central role of C-reactive protein in atherosclerosis, review the studies demonstrating predictive value of C-reactive protein, describe the factors requiring consideration when utilizing C-reactive protein, discuss clinical scenarios in which measurement of C-reactive protein may be helpful, and suggest ways to interpret and treat elevated C-reactive protein levels. Finally, the authors summarize future expectations for assessing and modulating the vascular inflammation to inhibit initiation and progression of the atherosclerotic process.
Zebrack
James S
JS
University of Utah School of Medicine, Department of Internal Medicine, Division of Cardiology, Salt Lake City, UT, USA. mmzebrack@pol.net
Anderson
Jeffrey L
JL
D000367:Age Factors; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D001161:Arteriosclerosis / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis* / Q000502:physiology; D003324:Coronary Artery Disease / Q000097:blood / Q000175:diagnosis* / Q000517:prevention & control; D006801:Humans; D007249:Inflammation / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology; D017035:Pravastatin / Q000627:therapeutic use; D012307:Risk Factors; D012680:Sensitivity and Specificity
D000924:Anticholesteremic Agents; D015415:Biomarkers; D002097:C-Reactive Protein; D017035:Pravastatin