title: Changes in fractalkine in patients with ST-elevation myocardial infarction.
abstract: BACKGROUND
  Fractalkine (FKN) was recently shown to play an important role in atherosclerotic plaque rupture and cardiac remodeling and dysfunction. We evaluated the changes in serum FKN (sFKN) in patients with acute ST-elevation myocardial infarction (STEMI) and the influence of a percutaneous coronary intervention (PCI) on the levels of sFKN.
  
  
  METHODS
  The study population included 40 patients with acute STEMI [acute myocardial infarction (AMI)+PCI: 20 underwent primary PCI; AMI: 20 without PCI] and 40 patients with symptomatic stable angina pectoris (SAP+PCI: 20 underwent PCI; SAP: 20 without PCI). sFKN were measured at different time points by ELIZA. The gene expression of heart FKN was assessed by real-time reverse transcription-PCR in a model of myocardial infarction mice.
  
  
  RESULTS
  We found that the baseline level of sFKN in patients with acute STEMI was significantly higher than that of patients with SAP. Primary PCI in STEMI resulted in a rapid decrease within 24 h and to a similar level after 48 h as in the SAP and SAP+PCI patients, whereas in the AMI group, the sFKN level showed a slight decrease from 6 to 24 h (from 1307.6±368.9 to 1092.7±258.1 pg/ml, P=0.036) and remained significantly higher at all later time points (P<0.001 for all). The sFKN level at 30 days was correlated positively with the NT-proBNP level (r=0.490, P=0.014). The time course of myocardial FKN gene expression in mice has a pattern similar to sFKN change in AMI patients.
  
  
  CONCLUSIONS
  Our study suggested that STEMI had a higher sFKN level and correlated positively with the NT-proBNP level at 1 month. PCI could lead to a rapid decrease in the sFKN level.
authors.affiliation: aDepartment of Cardiology, Zhongshan Hospital, Shanghai Institute of Cardiovascular Diseases bDepartment of Immunology cInstitutes of Biomedical Science, Fudan University, Shanghai, China.
authors.forename: Kang
authors.initials: K
authors.lastname: Yao
authors.forename: Shuning
authors.initials: S
authors.lastname: Zhang
authors.forename: Hao
authors.initials: H
authors.lastname: Lu
authors.forename: Xiaowu
authors.initials: X
authors.lastname: Hong
authors.forename: Juying
authors.initials: J
authors.lastname: Qian
authors.forename: Aijun
authors.initials: A
authors.lastname: Sun
authors.forename: Yunzeng
authors.initials: Y
authors.lastname: Zou
authors.forename: Junbo
authors.initials: J
authors.lastname: Ge
mesh_terms: D000368:Aged; D060050:Angina, Stable / Q000097:blood* / Q000175:diagnosis; D000818:Animals; D015415:Biomarkers / Q000097:blood; D054428:Chemokine CX3CL1 / Q000097:blood* / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D008297:Male; D008810:Mice, Inbred C57BL; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000175:diagnosis / Q000235:genetics / Q000628:therapy; D009206:Myocardium / Q000378:metabolism*; D020097:Natriuretic Peptide, Brain / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D062645:Percutaneous Coronary Intervention; D012333:RNA, Messenger / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; C515538:CX3CL1 protein, human; D054428:Chemokine CX3CL1; C515539:Cx3cl1 protein, mouse; D010446:Peptide Fragments; D012333:RNA, Messenger; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain