C-reactive protein for diagnosis and screening of coronary artery disease

Health Technology Advisory Committee
Record ID 32003000446
Authors' objectives:

This report aims to assess the effectiveness of measuring C-reactive protein in the diagnosis and screening of coronary artery disease.

Authors' recommendations: Coronary artery disease (CAD), the leading cause of death in the United States, resulted in 459,841 deaths in 1998 and accounted for one of every five deaths. CAD is the leading cause of premature and permanent disability in the United States and in 1997, $10.8 billion was paid by Medicare for CAD. Numerous studies suggest that inflammatory changes in the vessel walls initiate atherosclerosis. As the disease progresses, the atherosclerotic plaques erode, become unstable, and eventually rupture. Plaque rupture causes thrombosis and the acute coronary syndromes, unstable angina (UA) and acute myocardial infarction (MI). Due to this link between chronic, low-grade inflammation and CAD, researchers have investigated serum inflammatory markers, particularly, acute-phase reactants, to determine if their appearance correlates with the presence or extent of CAD. C-Reactive protein (CRP) is the classic acute-phase reactant. Researchers have hypothesized that CRP may provide an adjunctive method for assessment of cardiovascular risk. Several studies indicate that plasma levels of CRP are a strong independent risk predictor of future (MI), stroke, and vascular death among individuals without clinically recognized cardiovascular disease. Serum levels of this sensitive but nonspecific acute-phase reactant can increase by as much as 10,000-fold in response to tissue injury. Studies have shown that slight elevations in baseline serum levels of CRP have a significant, dose-dependent association with increased risks for CAD morbidity and mortality in individuals with and without symptomatic CAD. Nevertheless, CRP is a nonspecific marker of inflammation, and it remains unclear whether CRP is a risk factor for CAD and a potential target for intervention, whether increased levels indicate the presence of an atherosclerotic plaque at high risk for rupture leading to thrombosis and acute MI, or whether this inflammatory marker is increased due to conditions unrelated to atherosclerosis, ie, the coexistence of a disorder associated with the acute-phase response. The results of CRP testing must be analyzed in conjunction with the results of standard diagnostic tests, medical history, and clinical findings. Its efficacy as a stand-alone test has not been proven. There is some evidence from epidemiological studies demonstrating that serum levels of CRP are increased in patients with MI, stable or unstable angina. Nevertheless, it remains unclear whether CRP itself is a risk factor for CAD or whether it simply reflects the extent of the acute-phase response to arterial inflammation or inflammation elsewhere in the body, or whether it is a marker of other classic CAD risk factors such as obesity or smoking. The CRP test is a promising avenue of research but at the present time, there is no solid proof that CRP testing is superior to standard methods of risk stratification, that reducing serum CRP levels improves health outcomes or quality of life, or that CRP testing is cost-effective. Thus, the available evidence does not support the routine use of the CRP test for the diagnosis, management, or screening of patients with diagnosed disease, or in asymptomatic, healthy subjects.
Authors' methods: Review
Project Status: Completed
Year Published: 2002
English language abstract: An English language summary is available
Publication Type: Not Assigned
Country: United States
MeSH Terms
  • Costs and Cost Analysis
  • C-Reactive Protein
  • Coronary Disease
Organisation Name: Health Technology Advisory Committee
Contact Address: Queries should be referred to the Minnesota Department of Health (http://www.health.state.mn.us/)
Copyright: Health Technology Advisory Committee
This is a bibliographic record of a published health technology assessment from a member of INAHTA or other HTA producer. No evaluation of the quality of this assessment has been made for the HTA database.