Serial determinations of serum enzymes following aorta-coronary bypass surgery and acute myocardial infarction

Serial determinations of serum creatine kinase (CK), cardio-specific isoenzyme of CK (CK-MB), glutamic oxaloacetic transaminase (GOT) and alpha-hydroxybutylate dehydrogenase (HBD) were made in 29 consecutive patients undergoing aorta-coronary (AC) bypass grafting, and the results were compared with those in 31 patients with acute myocardial infarction (AMI). Postoperatively, all patients had an uneventful postoperative course and there was no evidence of AMI. The time course of enzyme activity following surgery was characterized by 1) shortening of peak activity time of all enzymes except CK, 2) rapid disappearance of CK-MB, 3) prolonged normalization of GOT and HBD. Peak activities of CK, CK-MB, GOT and HBD in AC bypass patients were 801 +/- 77, 46 +/- 6, 100 +/- 9 and 718 +/- 32 IU (mean +/- SEM), respectively, which were equivalent to 46%, 12%, 22% and 47% of those in AMI. The degree of postoperative CK-MB elevation was influenced by the duration of the operation and the extracorporeal circulation, and the number of grafts bypassed. The peak CK-MB activity did not correlate with the CK peak. The ratio of CK-MB to CK was much smaller in AC bypass than in AMI (6.5 +/- 1.8 vs. 20.1 +/- 1.4%). It was concluded that serum enzyme elevations after AC bypass surgery largely reflected enzyme release from the skeletal muscle rather than the myocardium.     

The inflammatory response in myocardial infarction.

One of the major therapeutic goals of modern cardiology is to design strategies aimed at minimizing myocardial necrosis and optimizing cardiac repair following myocardial infarction. However, a sound understanding of the biology is necessary before a specific intervention is pursued on a therapeutic basis. This review summarizes our current understanding of the cellular and molecular mechanisms regulating the inflammatory response following myocardial ischemia and reperfusion. Myocardial necrosis induces complement activation and free radical generation, triggering a cytokine cascade initiated by Tumor Necrosis Factor (TNF)-alpha release. If reperfusion of the infarcted area is initiated, it is attended by an intense inflammatory reaction. Interleukin (IL)-8 synthesis and C5a activation have a crucial role in recruiting neutrophils in the ischemic and reperfused myocardium. Neutrophil infiltration is regulated through a complex sequence of molecular steps involving the selectins and the integrins, which mediate leukocyte rolling and adhesion to the endothelium. Marginated neutrophils exert potent cytotoxic effects through the release of proteolytic enzymes and the adhesion with Intercellular Adhesion Molecule (ICAM)-1 expressing cardiomyocytes. Despite this potential injury, substantial evidence suggests that reperfusion enhances cardiac repair improving patient survival; this effect may be in part related to the inflammatory response. Monocyte Chemoattractant Protein (MCP)-1 is also markedly upregulated in the infarcted myocardium inducing recruitment of mononuclear cells in the injured areas. Monocyte-derived macrophages and mast cells may produce cytokines and growth factors necessary for fibroblast proliferation and neovascularization, leading to effective repair and scar formation. At this stage expression of inhibitory cytokines such as IL-10 may have a role in suppressing the acute inflammatory response and in regulating extracellular matrix metabolism. Fibroblasts in the healing scar undergo phenotypic changes expressing smooth muscle cell markers. Our previous review in this journal focused almost exclusively on reduction of the inflammatory injury. The current update is prompted by the potential therapeutic opportunity that the open vessel offers. By promoting more effective tissue repair, it may be possible to reduce the deleterious remodeling, that is the leading cause of heart failure and death. Elucidating the complex interactions and regulatory mechanisms responsible for cardiac repair may allow us to design effective inflammation-related interventions for the treatment of myocardial infarction.     

急性心肌梗死溶栓疗效判断中血清酶测定时间的合理选择

目的　适时合理选择急性心肌梗死 (AMI)溶栓疗效判断中血清酶学指标。方法　回顾性分析 145例AMI溶栓患者血清酶学及心肌肌钙蛋白T(TnT)资料 ,其中男 10 7例 ,女 38例 ,平均年龄 (6 1 9± 9 3)岁。以无创指标判断溶栓成功者 110例 ,未成功者 35例。 6 5例行冠脉造影 ,梗死相关血管 (IRA)开通者 44例 ,未开通者2 1例。 5 9例同时测定TnT。结果　 (1)TnT首次异常检出率 84 7% ,高于肌酸磷酸激酶 (CK)同功酶 (CK -MB)(4 9 2 % ) (P <0 0 5 )。 (2 )溶栓成功、IRA开通者与溶栓未成功、IRA未开通者间CK/CK -MB峰值无显著性差异 (P >0 0 5 )。结论　 (1)TnT用于AMI心肌损伤早期诊断优于CK -MB。 (2 )CK/CK -MB峰值前移与溶栓成功与否、IRA开通与否有关 ,而CK/CK -MB峰绝对值与此无直接关系。对早期溶栓的AMI患者不必过早取血测定CK/CK -MB ,而在发病后 16～ 2 0h间取血测定即可满足判断酶峰是否前移的需要 ,从而减轻病人痛苦和经济负担。