Cremer J, Steinhoff G, Karck M, Ahnsell T, Brandt M, Teebken O E, Hollander D, Haverich A
Department of Cardiovascular Surgery, Christian-Albrechts-University, Kiel, Germany.
Eur J Cardiothorac Surg. 1997 Nov;12(5):753-8. doi: 10.1016/s1010-7940(97)00255-8.
Encouraging results on myocardial preconditioning in experimental models of infarction, stunning or prolonged ischemia raise the question whether preconditioning techniques may enhance conventional cardioplegic protection used for routine coronary surgery.
A prospective clinical trial was conducted to investigate the effect of additional ischemic normothermic preconditioning prior to cardioplegic arrest applying cold blood cardioplegia in patients scheduled for routine coronary surgery (3 vessel disease, left ventricular ejection fraction > 50%). Two cross clamp periods of 5 min with the hearts beating in sinus rhythm were applied followed by 10 min of reperfusion, each (n = 7, group I). Inducing moderate hypothermia cold blood cardioplegia was delivered antegradely. In control groups, cold intermittent blood cardioplegia (n = 7, group II) was used alone. Coronary sinus effluents were analyzed for release of creatine kinase (CK), CK-MB, lactate, and troponin T at 1, 3, 6, 9, and 12 h. In addition, postoperative catecholamine requirements were monitored.
The procedure was tolerated well, and no perioperative myocardial infarction in any of the groups studied occurred. Concentrations of lactate tended to be higher in group I, but this difference was not significant. In addition, no significant differences for concentrations of CK, CK-MB, and troponin T were found. Following ischemic preconditioning an increased dosage of dopamine was required within the first 12 h postoperatively (group I: 2.63 +/- 1.44 microg/kg/min, group II: 0.89 +/- 1.06 microg/kg/min).
Combining ischemic preconditioning and cardioplegic protection with cold blood cardioplegia does not appear to ameliorate myocardial protection when compared to cardioplegic protection applying cold blood cardioplegia alone. Inversely, contractile function seemed to be impaired when applying this protocol of ischemic preconditioning.
在梗死、心肌顿抑或长时间缺血的实验模型中,心肌预处理取得了令人鼓舞的结果,这引发了一个问题,即预处理技术是否可以增强用于常规冠状动脉手术的传统心脏停搏保护。
进行了一项前瞻性临床试验,以研究在计划进行常规冠状动脉手术(三支血管病变,左心室射血分数>50%)的患者中,在心脏停搏前应用冷血心脏停搏液时额外进行缺血性常温预处理的效果。在窦性心律下心脏跳动时进行两个5分钟的交叉夹闭期,随后各进行10分钟的再灌注(n = 7,第一组)。诱导中度低温,冷血心脏停搏液顺行灌注。在对照组中,单独使用冷间歇性血液心脏停搏液(n = 7,第二组)。在1、3、6、9和12小时分析冠状窦流出液中肌酸激酶(CK)、CK-MB、乳酸和肌钙蛋白T的释放情况。此外,监测术后儿茶酚胺的需求量。
该手术耐受性良好,所研究的任何一组均未发生围手术期心肌梗死。第一组乳酸浓度有升高趋势,但差异无统计学意义。此外,CK、CK-MB和肌钙蛋白T浓度无显著差异。缺血预处理后,术后最初12小时内多巴胺的用量增加(第一组:2.63±1.44微克/千克/分钟,第二组:0.89±1.06微克/千克/分钟)。
与单独应用冷血心脏停搏液进行心脏停搏保护相比,将缺血预处理与冷血心脏停搏液的心脏停搏保护相结合似乎并不能改善心肌保护。相反,应用这种缺血预处理方案时收缩功能似乎受到了损害。