ABSTRACT
The aim of this study was to evaluate the impact of soluble tumor necrosis factor receptor -2 in acute coronary heart diseases. This prospective study had been carried on 30 patients with acute coronary heart diseases [group I] admitted consecutively in the critical care medicine department at Alexandria main university hospital. Demographic data and medical history had been taken. Thorough clinical examination, Troponin, CKMB, ECG, x ray chest and echocardiography had been done for each patient on admission. In addition, samples of plasma had been taken from each patient and also, from 10 healthy volunteers of matched age and sex [control group] [group II] to determine plasma level of soluble tumor necrosis factor receptor -2 [sTNFR-2] by ELISA test. Plasma level of sTNFR-2 in group [I] was significantly higher than the group [II], [mean +/- SD was 15.315 +/- 8.909 versus 5.03 +/- 2.01ng/ml respectively, t=5.22. p = 0.0001*]. It was found non significant positive correlation between both ejection fraction [EF] and fraction shorting [FS] [left ventricular systolic function] and sTNFR-2, [r=0.121, p=0.526, r=0.293 and p=0.116 respectively]. Non significant, negative correlation was found between both early filling left ventricle/late filling left ventricle [E/A ratio] [left ventricular diastolic function] and mitral valve regurgitation [MR] and sTNFR-2 [r=- 0.108, p=0.569, r=-0.320 and p=0.085 respectively]. A negative significant correlation was found between wall motion score index [WMSI] and sTNFR-2 [r=-0.419, p=0.021*]. Measurement of sTNFR-2 may be of value in evaluation of the TNF system in acute coronary heart diseases. sTNFR-2 is increased in acute coronary heart diseases and may modulate the in vitro cytotoxicity of TNF. In this work, it is not clear whether the elevation of sTNFR-2 in acute coronary heart diseases is due to an actual increase or to a reduced breakdown or elimination of these receptors. Further explorations are needed to more precisely define the meaning, molecular basis, and interaction ofsTNFR-2 and TNF