title: High-sensitivity C-reactive protein and cardiovascular disease: a resolute belief or an elusive link?
abstract: The role of inflammation in the propagation of atherosclerosis and susceptibility to cardiovascular (CV) events is well established. Of the wide array of inflammatory biomarkers that have been studied, high-sensitivity C-reactive protein (hsCRP) has received the most attention for its use in screening and risk reclassification and as a predictor of clinical response to statin therapy. Although CRP is involved in the immunologic process that triggers vascular remodeling and plaque deposition and is associated with increased CV disease (CVD) risk, definitive randomized evidence for its role as a causative factor in atherothrombosis is lacking. Whether measurement of hsCRP levels provides consistent, clinically meaningful incremental predictive value in risk prediction and reclassification beyond conventional factors remains debated. Despite publication of guidelines on the use of hsCRP in CVD risk prediction by several leading professional organizations, there is a lack of clear consensus regarding the optimal clinical use of hsCRP. This article reviews 4 distinct points from the literature to better understand the current state and application of hsCRP in clinical practice: 1) the biology of hsCRP and its role in atherosclerosis; 2) the epidemiological association of hsCRP with CVD; 3) the quality of hsCRP as a biomarker of risk; and 4) the use of hsCRP as a tool to initiate or tailor statin therapy. Furthermore, we highlight recommendations from societies and important considerations when using hsCRP to guide treatment decisions in the primary prevention setting.
authors.affiliation: Johns Hopkins Ciccarone Center for Prevention of Heart Disease, Baltimore, Maryland 21287, USA. oyousuf1@jhmi.edu
authors.forename: Omair
authors.initials: O
authors.lastname: Yousuf
authors.forename: Bibhu D
authors.initials: BD
authors.lastname: Mohanty
authors.forename: Seth S
authors.initials: SS
authors.lastname: Martin
authors.forename: Parag H
authors.initials: PH
authors.lastname: Joshi
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Blaha
authors.forename: Khurram
authors.initials: K
authors.lastname: Nasir
authors.forename: Roger S
authors.initials: RS
authors.lastname: Blumenthal
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Budoff
mesh_terms: D000367:Age Factors; D050197:Atherosclerosis / Q000097:blood; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis* / Q000235:genetics; D002318:Cardiovascular Diseases / Q000097:blood* / Q000517:prevention & control; D008078:Cholesterol, LDL / Q000097:blood; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007249:Inflammation / Q000097:blood; D017410:Practice Guidelines as Topic; D011322:Primary Prevention; D016032:Randomized Controlled Trials as Topic; D018570:Risk Assessment; D012737:Sex Factors
chemical_list: D015415:Biomarkers; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D002097:C-Reactive Protein
keywords: CAC; CHD; CRP; CVD; FRS; Framingham risk score; LDL-C; MI; NRI; RRS; Reynolds risk score; atherosclerosis; cardiovascular disease; coronary artery calcium; coronary heart disease; high-sensitivity C-reactive protein; hsCRP; inflammation; low-density lipoprotein cholesterol; myocardial infarction; net reclassification improvement; prevention; statins