Hirschl M M, Gwechenberger M, Binder T, Binder M, Graf S, Stefenelli T, Rauscha F, Laggner A N, Sochor H
Department of Emergency Medicine, University of Vienna, Austria.
Eur Heart J. 1996 Dec;17(12):1852-9. doi: 10.1093/oxfordjournals.eurheartj.a014803.
Clinical and experimental data have shown that after acute myocardial infarction there is a significant release of tumour necrosis factor alpha. Therefore, an attempt was made to correlate changes in serum tumour necrosis factor alpha concentrations with indices of infarct extent in patients with acute myocardial infarction. In 50 patients with acute myocardial infarction, blood samples for evaluation of tumour necrosis factor alpha and alpha-hydroxybutyrate-dehydrogenase were collected every 6 h until 120 h after admission. Infarct extent was estimated by clinical parameters such as the occurrence of heart failure and rhythm disturbances, by enzymatic methods such as cumulative release of alpha-hydroxybutyrate-dehydrogenase and imaging techniques, by late resting single photon emission tomography--201 thallium scintigraphy--using an extent score and by echocardiography using a wall motion index. The maximum change in serum tumour necrosis factor alpha after infarction (delta TNF) was calculated by subtracting tumour necrosis factor alpha concentration on admission from peak tumour necrosis factor alpha concentration. The average peak tumour necrosis factor alpha level was observed 84 h after admission (median: 12 pg.ml-1). Between the 72nd and the 96th h no significant changes in tumour necrosis factor alpha values were observed. Analysis of the data showed that larger delta (TNF) values were found to be associated significantly with signs of heart failure (P = 0.003), the presence of rhythm disturbances (P = 0.001), increased enzymatic infarct extent indicated by cumulative release of alpha-hydroxybutyrate-dehydrogenase (r = 0.74; P < 0.001), large myocardial perfusion defects measured with 201 thallium scintigraphy (r = 0.80; P < 0.001), and a considerable number of left ventricular wall motion abnormalities (r = 0.57; P < 0.001). In conclusion, delta (TNF) is a reliable method of assessing damage severity in the myocardium after acute myocardial infarction. As only two blood samples are necessary within 84 h, the method may be one of the more convenient for the assessment of infarct size in clinical practice.
临床和实验数据表明,急性心肌梗死后肿瘤坏死因子α会大量释放。因此,人们试图将急性心肌梗死患者血清肿瘤坏死因子α浓度的变化与梗死范围指标联系起来。对50例急性心肌梗死患者,在入院后每6小时采集一次血样,用于评估肿瘤坏死因子α和α-羟丁酸脱氢酶,直至120小时。通过临床参数如心力衰竭和心律失常的发生情况、酶学方法如α-羟丁酸脱氢酶的累积释放以及成像技术、通过晚期静息单光子发射断层扫描——铊-201闪烁扫描——使用范围评分以及通过超声心动图使用壁运动指数来估计梗死范围。梗死发生后血清肿瘤坏死因子α的最大变化量(ΔTNF)通过将入院时肿瘤坏死因子α浓度从肿瘤坏死因子α峰值浓度中减去来计算。入院后84小时观察到血清肿瘤坏死因子α平均峰值水平(中位数:12 pg/ml)。在第72小时至第96小时之间,肿瘤坏死因子α值未观察到显著变化。数据分析表明,较大的Δ(TNF)值与心力衰竭体征显著相关(P = 0.003)、心律失常的存在(P = 0.001)、α-羟丁酸脱氢酶累积释放所表明的酶学梗死范围增加(r = 0.74;P < 0.001)、铊-201闪烁扫描测量的大面积心肌灌注缺损(r = 0.80;P < 0.001)以及相当数量的左心室壁运动异常(r = 0.57;P < 0.001)。总之,Δ(TNF)是评估急性心肌梗死后心肌损伤严重程度的可靠方法。由于在84小时内仅需采集两份血样,该方法可能是临床实践中评估梗死大小较为方便的方法之一。