Pichon H, Chocron S, Alwan K, Toubin G, Kaili D, Falcoz P, Latini L, Clement F, Viel J F, Etievent J P
Department of Thoracic, Saint-Jacques Hospital, Besancon, France.
Circulation. 1997 Jul 1;96(1):316-20.
Cardiac troponin I (CTnI) has been shown to be a marker of myocardial injury. The aim of this study was to compare antegrade crystalloid cardioplegia with antegrade cold blood cardioplegia with warm reperfusion using CTnI release as the criteria for evaluating the adequacy of myocardial protection.
Seventy patients were randomly assigned to receive crystalloid or blood cardioplegia. CTnI concentrations were measured in serial venous blood samples drawn just before cardiopulmonary bypass and after aortic unclamping at 6, 9, 12, and 24 hours and daily thereafter for 5 days. ANOVA with repeated measures was performed to test the effect of the type of cardioplegia on CTnI release. The total amount of CTnI released was higher in the crystalloid cardioplegia group than in the blood cardioplegia group (11.2 +/- 8.9 versus 7.8 +/- 8.6 micrograms, P < .02). CTnI concentration was significantly higher in the crystalloid group than in the blood group in the samples drawn at hours 9 and 12. Three patients in each group had ECG evidence of perioperative myocardial infarction. Eight patients in the crystalloid group and five patients in the blood group had CTnI evidence of perioperative myocardial infarction. CTnI release was significantly lower in patients requiring no electrical defibrillation after aortic unclamping.
Cold blood cardioplegia followed by warm reperfusion is beneficial in an unselected group of patients with a preserved left ventricular function undergoing an elective first coronary artery bypass grafting. CTnI allowed the diagnosis of small perioperative necrotic myocardial areas. The need for electrical defibrillation after aortic unclamping was related to a higher release of CTnI. A further study is necessary to determine whether this technique was beneficial because of cold blood cardioplegia, warm reperfusion, or both.
心肌肌钙蛋白I(CTnI)已被证明是心肌损伤的标志物。本研究的目的是使用CTnI释放作为评估心肌保护充分性的标准,比较顺行晶体心脏停搏液与顺行冷血心脏停搏液加温暖再灌注的效果。
70例患者被随机分配接受晶体或血液心脏停搏液。在体外循环前以及主动脉开放后6、9、12和24小时及之后5天每天采集系列静脉血样本,测量CTnI浓度。采用重复测量方差分析来检验心脏停搏液类型对CTnI释放的影响。晶体心脏停搏液组释放的CTnI总量高于血液心脏停搏液组(11.2±8.9对7.8±8.6微克,P<.02)。在9小时和12小时采集的样本中,晶体组的CTnI浓度显著高于血液组。每组有3例患者有围手术期心肌梗死的心电图证据。晶体组有8例患者和血液组有5例患者有围手术期心肌梗死的CTnI证据。主动脉开放后无需电除颤的患者CTnI释放显著较低。
对于一组未选择的左心室功能保留且接受择期首次冠状动脉旁路移植术的患者,冷血心脏停搏液加温暖再灌注是有益的。CTnI有助于诊断围手术期小面积坏死心肌区域。主动脉开放后需要电除颤与较高的CTnI释放有关。有必要进一步研究确定该技术有益是因为冷血心脏停搏液、温暖再灌注还是两者皆有。