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Relation between circulating soluble Fas ligand and subsequent ventricular remodelling following myocardial infarction
  1. T Soeki,
  2. Y Tamura,
  3. H Shinohara,
  4. K Sakabe,
  5. Y Onose,
  6. N Fukuda
  1. Department of Cardiology and Clinical Research, National Zentsuji Hospital, Senyu-cho 2-1-1, Zentsuji City, Kagawa, 765-8507, Japan
  1. Correspondence to:
    Takeshi Soeki, MD, Department of Biochemistry, National Cardiovascular Center Research Institute, 5-7-1, Fujishirodai, Suita, Osaka, 565-8565, Japan;

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The Fas/Fas ligand (Fas-L) system has been established as one of the regulatory pathways of apoptotic cell death. Fas is a type I membrane protein which belongs to the tumour necrosis factor/nerve growth factor receptor family and mediates apoptosis.1 A soluble form of Fas (sFas) found in sera of human subjects is thought to block apoptosis by inhibition of binding between Fas and the antibody to Fas on the cell membrane. Fas-L is a type II membrane protein in the tumour necrosis factor family, and human soluble Fas-L (sFas-L) apparently induces apoptosis of Fas expressing cells.1 Recently, the occurrence of apoptotic death of cardiomyocytes has been demonstrated experimentally after injury caused by hypoxia, reperfusion, myocardial infarction, and coronary embolism. However, only two clinical reports assessing the concentrations of circulating sFas and sFas-L in patients with acute myocardial infarction (AMI) have been published.2,3 No study has evaluated the relation between these concentrations and left ventricular (LV) remodelling following AMI. Thus, in this study we measured the circulating concentrations of sFas and sFas-L in patients with AMI. We also investigated the relation of sFas and sFas-L to LV remodelling after AMI.


Fifty two consecutive patients (41 men; mean age 64 years) who presented with their first episode of AMI within 24 hours of symptom onset and who underwent successful coronary angioplasty were studied. Patients with significant concomitant diseases, such as malignancy, pulmonary disease, autoimmune disease, thyroid disease, or concurrent viral infection were excluded from this study. The control …

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