title: Clinical implications of circulating soluble Fas and Fas ligand in patients with acute myocardial infarction.
abstract: BACKGROUND
  Apoptotic cell death is the major form of myocardial damage produced by coronary ischemic events.
  
  
  OBJECTIVE
  To assess whether circulating levels of soluble Fas (sFas), an inhibitor of apoptosis, and sFas ligand, an inducer of apoptosis, in patients with coronary artery disease are greater than normal.
  
  
  METHODS
  Forty-seven patients [acute myocardial infarction (AMI) in 17, old myocardial infarction (OMI) in 15, stable angina in 15] and 10 normal control subjects participated in this study. Serum levels of sFas and sFas ligand in all patients were measured, and cardiac catheterizations were performed.
  
  
  RESULTS
  Serum levels of sFas were greater than normal only in patients with AMI (4.6 +/- 1.6 ng/ml); the levels were significantly higher than those in patients with OMI (2.1 +/- 0.6 ng/ml) and stable angina (2.2 +/- 0.5 ng/ml), and in normal subjects (2.0 +/- 0.6 ng/ml; P < 0.0001). However, there was no difference among serum levels of sFas ligand for all groups. For patients with AMI, there was no significant correlation between serum levels of sFas and peak levels both of plasma creatine phosphokinase and of plasma myosin light chain type I as clinical indexes of infarct size. However, there were significant correlations between serum levels of sFas and both pulmonary artery wedge pressure (r = 0.767, P = 0.0003) and left ventricular end-diastolic pressure (r = 0.629, P = 0.03).
  
  
  CONCLUSIONS
  Circulating sFas increases in concentration in relation to the severity of hemodynamic conditions in patients with AMI, but it is independent from size of infarct. Therefore, circulating sFas could play an important role as the marker of pathophysiologic conditions associated with cardiomyocyte apoptosis in AMI.
authors.affiliation: Second Department of Internal Medicine, Ehime University School of Medicine, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Ohtsuka
authors.forename: M
authors.initials: M
authors.lastname: Hamada
authors.forename: O
authors.initials: O
authors.lastname: Sasaki
authors.forename: M
authors.initials: M
authors.lastname: Suzuki
authors.forename: Y
authors.initials: Y
authors.lastname: Hara
authors.forename: Y
authors.initials: Y
authors.lastname: Shigematsu
authors.forename: T
authors.initials: T
authors.lastname: Ohtani
authors.forename: T
authors.initials: T
authors.lastname: Honda
authors.forename: K
authors.initials: K
authors.lastname: Hiwada
mesh_terms: D000368:Aged; D053222:Fas Ligand Protein; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000473:pathology / Q000503:physiopathology; D011669:Pulmonary Wedge Pressure; D012995:Solubility; D013223:Statistics as Topic; D013318:Stroke Volume; D016277:Ventricular Function, Left; D019014:fas Receptor / Q000097:blood*
chemical_list: C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D019014:fas Receptor