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CLINICAL STUDY: MYOCARDIAL INFARCTION

Increased plasma levels of the soluble form of fas ligand in patients with acute myocardial infarction and unstable angina pectoris

Masumi Shimizu, MD^*, Keisuke Fukuo, MD^*,*, Shigekazu Nagata, PhD, Toshimitsu Suhara, MD^*, Masashi Okuro, MD^*, Kenshi Fujii, MD, Yorihiko Higashino, MD, Masaki Mogi, MD^*, Yasuko Hatanaka, MD^* and Toshio Ogihara, MD^*

^* Department of Geriatric Medicine, Osaka University Medical School, Suita, Japan
Department of Genetics, Osaka University Medical School, Suita, Japan
Sakurabashi-Watanabe Hospital, Sakurabashi, Osaka, Japan

Manuscript received September 29, 2000; revised manuscript received November 7, 2001, accepted November 29, 2001.

^* Reprint requests and correspondence: Dr. Keisuke Fukuo, Department of Geriatric Medicine, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
fukuo{at}geriat.med.osaka-u.ac.jp

OBJECTIVES: To examine whether the Fas/Fas ligand system is involved in the pathogenesis of acute myocardial infarction (AMI), we measured the levels of the soluble form of the Fas ligand (sFasL) in the plasma of patients with AMI and stable or unstable angina pectoris (AP).

BACKGROUND: The Fas ligand (FasL) is rapidly cleaved off by a metalloproteinase from the cell membrane to become a soluble form as a cytokine. Fas is expressed in most cells, including cardiomyocytes, whereas FasL is mainly expressed in inflammatory cells such as macrophages, which are greatly accumulated in unstable plaque.

METHODS: Thirty patients with AMI, 10 patients with unstable AP, 10 patients with stable AP and 30 control subjects were enrolled in the present study.

RESULTS: Plasma sFasL levels were significantly elevated on hospital admission in patients with AMI and unstable AP, compared with control subjects. Time-course studies revealed that plasma sFasL levels rapidly decreased within 3 h and then increased again after percutaneous transluminal coronary angioplasty in patients with AMI, but not in patients with stable AP. Importantly, the sFasL levels were higher in the coronary sinus than in the circulation. In addition, in vitro studies showed that the expression of FasL messenger ribonucleic acid was upregulated in mononuclear cells isolated from patients with AMI and that hypoxia stimulated the release of sFasL from isolated mononuclear cells.

CONCLUSIONS: This demonstration of elevated levels of sFasL in patients with AMI and unstable AP suggests that activation of the Fas/FasL system may play a pathogenic role in AMI and acute coronary syndromes.

Abbreviations and Acronyms   CK-MB   AMI   acute myocardial infarction   AP   angina pectoris   CHF   congestive heart failure   CK-MB   creatine kinase-MB isoenzyme   ELISA   enzyme-linked immunosorbent assay   mFasL   membrane-bound Fas ligand   sFasL   soluble Fas ligand   PBMCs   peripheral blood mononuclear cells   PCR   polymerase chain reaction   PTCA   percutaneous transluminal coronary angioplasty   TNF-   tumor necrosis factor-

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