Schumacher M, Halwachs G, Tatzber F, Fruhwald F M, Zweiker R, Watzinger N, Eber B, Wilders-Truschnig M, Esterbauer H, Klein W
Department of Internal Medicine, Karl-Franzens-University, Graz, Austria.
J Am Coll Cardiol. 1997 Sep;30(3):703-7. doi: 10.1016/s0735-1097(97)00172-1.
The aim of our study was to determine neopterin levels in patients with chronic and acute coronary syndromes.
In chronic and acute coronary syndromes the release of different cytokines activates cellular defense. Infiltration of neutrophils and monocytes/macrophages is detected in the vessel wall as well as in the myocardium. Neopterin, which is a by-product of the guanosine triphosphate-biopterin pathway, is a marker for those activated macrophages.
We studied 123 subjects: 1) 21 consecutive patients (17 men, 4 women; mean age +/- SD 66 +/- 15 years, range 31 to 87) with acute myocardial infarction (AMI); 2) 62 consecutive patients (50 men, 12 women; mean age 61 +/- 8 years, range 43 to 81) with signs and symptoms of clinically stable coronary artery disease (CAD); and 3) 40 healthy blood donors (28 men, 12 women; mean age 35 +/- 13 years). Neopterin levels were determined with a commercially available enzyme-linked immunosorbent assay method.
In patients with AMI before thrombolytic therapy, neopterin levels were significantly higher than levels in patients with CAD and control subjects (13.7 vs. 8.6 and vs. 6.8 nmol/liter, p < 0.0001). Values also differed significantly between patients with CAD and control subjects (p < 0.0001). Neopterin levels in patients with AMI were measured seven times during a 72-h period. Within-group comparison showed significant differences over this period (p < 0.00001). The lowest value (11.4 nmol/liter) was observed after 4 h and differed significantly from the initial value and values after 24 and 72 h (p < 0.05). After 72 h, neopterin increased to 14.9 nmol/liter, a value significantly different from all values other than the initial one. There was no correlation between neopterin and creatine kinase (CK); CK, MB isoenzyme; or lactate dehydrogenase as markers for the extent of the myocardial infarction during the observation period.
Our data support the hypothesis of an activation of monocytes and macrophages in patients with an acute or chronic coronary syndrome. Neopterin as a marker for macrophage activation is significantly increased in patients with chronic CAD and more pronounced in patients with AMI shortly after the onset of symptoms.
我们研究的目的是测定慢性和急性冠状动脉综合征患者的蝶呤水平。
在慢性和急性冠状动脉综合征中，不同细胞因子的释放激活了细胞防御。在血管壁以及心肌中可检测到中性粒细胞和单核细胞/巨噬细胞的浸润。蝶呤是三磷酸鸟苷 - 生物蝶呤途径的副产物，是那些活化巨噬细胞的标志物。
我们研究了123名受试者：1）21例连续的急性心肌梗死（AMI）患者（17名男性，4名女性；平均年龄±标准差66±15岁，范围31至87岁）；2）62例连续的有临床稳定冠状动脉疾病（CAD）体征和症状的患者（50名男性，12名女性；平均年龄61±8岁，范围43至81岁）；3）40名健康献血者（28名男性，12名女性；平均年龄35±13岁）。采用市售的酶联免疫吸附测定法测定蝶呤水平。
在溶栓治疗前的AMI患者中，蝶呤水平显著高于CAD患者和对照组（13.7 vs. 8.6和vs. 6.8 nmol/升，p < 0.0001）。CAD患者和对照组之间的值也有显著差异（p < 0.0001）。在72小时内对AMI患者的蝶呤水平进行了7次测量。组内比较显示在此期间有显著差异（p < 0.00001）。最低值（11.4 nmol/升）在4小时后观察到，与初始值以及24小时和72小时后的数值有显著差异（p < 0.05）。72小时后，蝶呤升至14.9 nmol/升，该值与除初始值外的所有数值均有显著差异。在观察期内，蝶呤与肌酸激酶（CK）、CK的MB同工酶或乳酸脱氢酶作为心肌梗死范围的标志物之间无相关性。
我们的数据支持急性或慢性冠状动脉综合征患者单核细胞和巨噬细胞活化的假说。蝶呤作为巨噬细胞活化的标志物，在慢性CAD患者中显著升高，在症状发作后不久的AMI患者中更为明显。
