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Ohtsuka Tomoaki; Hamada, Mareomi; Sasaki, Osamu; Suzuki, Makoto; Hara, Yuji; Shigematsu, Yuji; Ohtani, Takashi; Honda, Toshio; Hiwada, Kunio
Coronary Artery Disease: 1999
PATHOPHYSIOLOGY AND NATURAL HISTORY: PDF Only
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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 ± 1.6ng/ml); the levels were significantly higher than those in patients with OMI (2.1 ± 0.6ng/ml) and stable angina (2.2 + 0.5 ng/ml), and in normal subjects (2.0±0.6ng/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.

© 1999 Lippincott Williams & Wilkins, Inc.