Krüger D, Giannitsis E, Sheikhzadeh A, Stierle U
Department of Cardiology, University Hospital Lübeck, Germany.
Am J Cardiol. 1998 Jun 15;81(12):1421-6. doi: 10.1016/s0002-9149(98)00203-3.
This study was designed to assess the release kinetics of endothelin after percutaneous transluminal coronary angioplasty (PTCA) and to prove the coronary endothelium as the source of the endothelin release. Twenty-seven patients with single-vessel coronary artery disease underwent PTCA. Endothelin, troponin T, myoglobin, and creatine phosphokinase paired blood samples were withdrawn from the coronary sinus and a peripheral vein before the balloon maneuver and at 1, 5, 10, 30, 45 minute(s), and at 1, 2, 3, 6, 12, and 24 hour(s) after the last balloon maneuver. Myocardial ischemia was monitored by means of cardiac lactate metabolism and 12-lead electrocardiogram. Thirteen patients who underwent a diagnostic cardiac catheterization served as a control group. In the left coronary artery, PTCA (n = 19) endothelin concentrations increased from 4.1 pg/ml as a common mean baseline level before intervention to 13.9 +/- 2.6 pg/ml (mean +/- SD) in the coronary sinus and 7.9 +/- 2.2 pg/ml (mean +/- SD) in the peripheral vein at 1 minute after the intervention (p <0.001). The levels remained elevated for 3 hours with higher coronary sinus than peripheral venous concentrations due to persistent cardiac endothelin release. PTCA of the right coronary artery (n = 8) also led to an instantaneous endothelin increase from a mean concentration of 4.4 before intervention to 8.3 pg/ml after intervention with identical coronary sinus and peripheral venous levels (p <0.001). Endothelin levels gradually decreased to normal within 6 hours. No patient developed a measurable myocardial ischemia or a myocardial infarction. In the control group all parameters remained unchanged. Uncomplicated PTCA was followed by a significant cardiac endothelin release that seems to indicate endothelial injury and not myocardial ischemia.
本研究旨在评估经皮腔内冠状动脉成形术（PTCA）后内皮素的释放动力学，并证明冠状动脉内皮是内皮素释放的来源。27例单支冠状动脉疾病患者接受了PTCA。在球囊操作前以及最后一次球囊操作后1、5、10、30、45分钟以及1、2、3、6、12和24小时，从冠状窦和外周静脉采集内皮素、肌钙蛋白T、肌红蛋白和肌酸磷酸激酶的配对血样。通过心脏乳酸代谢和12导联心电图监测心肌缺血情况。13例接受诊断性心导管检查的患者作为对照组。在左冠状动脉，PTCA（n = 19）后，内皮素浓度从干预前的平均基线水平4.1 pg/ml增加到干预后1分钟时冠状窦的13.9±2.6 pg/ml（平均值±标准差）和外周静脉的7.9±2.2 pg/ml（平均值±标准差）（p<0.001）。由于心脏内皮素持续释放，这些水平在3小时内一直升高，冠状窦浓度高于外周静脉浓度。右冠状动脉PTCA（n = 8）也导致内皮素瞬间增加，从干预前的平均浓度4.4增加到干预后的8.3 pg/ml，冠状窦和外周静脉水平相同（p<0.001）。内皮素水平在6小时内逐渐降至正常。没有患者发生可测量的心肌缺血或心肌梗死。在对照组中，所有参数均保持不变。无并发症的PTCA后会出现明显的心脏内皮素释放，这似乎表明是内皮损伤而非心肌缺血。
