Activities of mitochondrial aspartate aminotransferase and creatine kinase isoenzyme MB in serum following coronary bypass surgery

The mitochondrial isoenzyme of aspartate aminotransferase showed only slight increases in serum of twenty-seven patients after uncomplicated coronary bypass surgery, which contrasted the rapid and substantial increases in creatine kinase MB. In seven patients suffering perioperative infarction or serious complications, substantial increases in mitochondrial aspartate aminotransferase were detected and the elevations in creatine kinase MB were prolonged. Mitochondrial aspartate aminotransferase may appear as a specific marker of myocardial necrosis following coronary bypass surgery. The elevations of creatine kinase and creatine kinase MB were detected as early as 5 minutes after onset of coronary reperfusion and slightly higher activities were measured in coronary sinus blood than in systemic blood sampled simultaneously. Increases in mitochondrial aspartate aminotransferase, however, could first be measured 8 hours after reperfusion.     

Systemic short-term fibrinolysis with high-dose streptokinase in acute myocardial infarction: time course of biochemical parameters

The course of plasma catalytic activities of total creatine kinase, creatine kinase isoenzyme MB, total, cytoplasmatic and mitochondrial aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, alpha-hydroxybutyrate dehydrogenase, glutamate dehydrogenase and concentrations of myoglobin, urea, acidic alpha 1-glycoprotein and creatinine were followed in 33 patients suffering from acute myocardial infarction. All patients were randomized in a double-blind, prospective study. One group (18 patients) was infused with streptokinase 1.5 X 10(6) units/90 minutes; the control group received routine continuous i.v. heparin treatment (1000 units/h). Ten hours after completion of the study protocol, treatment of both groups of patients was continued with heparin, 1000 units/h and Aspisol, 1 g/day2). Streptokinase treatment induced earlier wash-out and therefore earlier peak levels of several enzymes: total creatine kinase (11 hours), creatine kinase isoenzyme MB (6 hours), total and cytoplasmatic aspartate aminotransferase (6 hours) and lactate dehydrogenase (9 hours). Total creatine kinase peak catalytic activity and myoglobin peak concentration were higher in the group receiving thrombolytic therapy. A significantly different course of catalytic activity between both treatment groups was found for total creatine kinase and creatine kinase isoenzyme MB, total and cytosolic aspartate aminotransferase, lactate dehydrogenase and alpha-hydroxybutyrate dehydrogenase. The course of mitochondrial aspartate aminotransferase catalytic activity was different only 12 hours after the beginning of treatment. The shift of several catalytic activities to an earlier peak level in plasma may indicate reperfusion of ischaemic myocardium due to thrombolytic therapy.     

The serum selenium concentration of patients with acute myocardial infarction

Serum selenium concentration was determined in 49 patients with acute myocardial infarction within 4 hours after the beginning of the symptoms. The mean serum selenium concentration of the patients was significantly lower than that of healthy controls (55 +/- 15 micrograms/l vs. 78 +/- 11 micrograms/l). Among the 49 patients with acute myocardial infarction 20 (41%) had serum selenium concentration below the 95% percentile of the healthy control group. It is concluded that the low serum selenium concentration was present in these patients before the acute event and was not a consequence of the myocardial infarction. No relationship was found in this study between the serum selenium concentration and the severity of myocardial infarction if the number of coronary vessels occluded is taken as the criterion of severity. Serum selenium concentration was similar in patients with 1 or more coronary vessels occluded. Patients with anterior or posterior myocardial infarction had similar serum selenium concentrations. A positive correlation was observed between serum selenium concentration and total serum creatine kinase (CK) activity and serum myoglobin (MB). The serum selenium concentration correlated negatively with the ratio CK-MB/total CK activity, which can be interpreted as minor injury of mitochondria during infarction in patients with normal serum selenium concentration.     

Determination of creatine kinase isoenzyme MB activity in serum using immunological inhibition of creatine kinase M subunit activity. Activity kinetics and diagnostic significance in myocardial infarction.

This is a new method for the determination of creatine kinase isoenzyme MB activity in serum. The method uses direct activity measurement of creatine kinase B subunit activity after blocking of CK-M subunit activity by inhibiting antibodies. The test takes no longer than 15 min. The method yields an intra-serial C.V. of 2.0-12.9%, and a C.V. from day to day of 5.5%. The detection limit is 3.4 U/l creatine kinase MB. In the 95 cases with proven myocardial infarction several types of creatine kinase MB activity kinetics could be determined. The percentage of creatine kinase MB of peak CK-total is 6-25%, with a mean of 11.1%. The amount of creatine kinase MB with respect to total CK activity after reinfarction is higher than the amount after initial infarction.     

Mass concentration of creatine kinase MB isoenzyme and lactate dehydrogenase isoenzyme 1 in diagnosis of perioperative myocardial infarction after coronary bypass surgery

Recent advances in methodology allow the mass concentration of creatine kinase MB isoenzyme (CK-MB), and of lactate dehydrogenase isoenzyme 1 (LD1) to be determined quickly and easily as routine, emergency tests. We evaluated these tests as diagnostic criteria of perioperative myocardial infarction (PMI) after coronary bypass surgery. These tests were compared with the usual measurements of CK-MB activity by immunoinhibition and LD1 by electrophoresis and with other biological markers of myocardial infarction such as total CK, total LD, and aspartate aminotransferase. Sixty-one patients who underwent coronary bypass grafting were followed pre- and postoperatively by enzyme determinations and electrocardiography; a subgroup was monitored by myocardial scintigraphy. CK-MB mass appeared to be the best marker of PMI during the first 48 h, although LD1 was the marker of choice from days 2 to 4.     

Secretion of creatine kinase MB isoenzyme by an immature teratoma with predominant rhabdomyosarcomatous elements

A 37-year-old man with metastatic immature (malignant) teratoma with prominent rhabdomyosarcomatous elements had markedly increased activity of creatine kinase (EC 2.7.3.2) MB in serum. There was no electrocardiographic evidence of infarction or ischemia, and autopsy revealed no myocardial infarction, significant coronary atherosclerosis, myocarditis, or invasion of the heart by tumor. A high proportion of the creatine kinase activity in a homogenate of the tumor was attributable to the MB isoenzyme. Persistent increases of creatine kinase-MB and an unusually high MB isoenzyme activity, out of proportion to total creatine kinase activity, may indicate a nonmyocardial origin of this isoenzyme.     

Use of creatine kinase MB isoenzyme for diagnosing myocardial infarction when total creatine kinase activity is high

The usefulness of measuring creatine kinase MB isoenzyme for diagnosing myocardial infarction when activities of total creatine kinase are very high is unclear. We conducted a retrospective study in an urban hospital that serves a largely indigent population. We concentrated on 146 patients whose creatine kinase activity was greater than 1000 U/L (upper limit of normal: 165 U/L for women and 225 U/L for men), with MB isoenzyme greater than 10 U/L and less than 5% of total creatine kinase. The positive predictive value of MB isoenzyme (isoimmune method) values greater than 10 U/L was between 11.6% and 56.8% when the value for total creatine kinase exceeded 1000 U/L. Using different values (MB greater than 4% of total creatine kinase) as positive for myocardial infarction would have resulted in far fewer false-positives, but 10 cases of myocardial infarction would have been missed. The most appropriate cutoff value for MB isoenzyme in this population (total creatine kinase greater than 1000 U/L) was found to be greater than 2% of total creatine kinase.     

Creatine kinase isoforms in ischemic heart disease

The MM and MB isoenzymes of creatine kinase exist in serum as a collection of at least three major MM and two major MB isoforms. Each of these are derived from single tissue MM and MB isoforms, which are converted to these other forms by carboxypeptidase N after their release from necrotic skeletal and myocardial tissue. Measurement of the MM isoforms in ischemic heart disease is useful for early diagnosis of acute myocardial infarction and for the noninvasive determination of coronary artery reperfusion for infarction patients receiving thrombolytic therapy. Because MM is also released in acute skeletal-muscle disease, MB isoform measurements may have the highest clinical sensitivity. These determinations are important for providing objective information to cardiologists who need to make critical decisions concerning the management of these patients. I review the procedures for treating patients with myocardial infarction, the potential role of CK isoforms, and the methods currently available for isoform analysis, including high-resolution electrophoresis, isoelectric and chromatofocusing, and liquid chromatography. Rapid and highly sensitive methods are needed for implementation of CK-MM and MB isoforms for prospective emergency determinations for patients with acute myocardial infarction.     

Mass concentration and activity concentration of creatine kinase isoenzyme MB compared in serum after acute myocardial infarction

We compared three current methods (immunoinhibition, "Isomune-CK" immunoprecipitation, and the Tandem-E CKMB II immunoenzymometric assay) for determination of creatine kinase (CK; EC 2.7.3.2) isoenzyme MB in serum. Although results inter-correlated well, the immunoinhibition assay gave higher activity values. Atypical CK forms did not interfere with the immunoprecipitation and immunoenzymometric methods. In acute myocardial infarction the catalytic properties of CK decreased with the enzyme's age, as reflected by a steady increase in activation energy of the catalyzed reaction. In septicemia patients with very low CK and CK-MB catalytic activity, mean CK-MB mass concentration exceeded the upper reference limit, suggesting an increased rate of loss of activity concentration in these patients' sera. Because of the assay's lesser susceptibility to conformational changes at the active site of the enzyme, we suggest that measurement of CK-MB mass concentration is better suited for infarct sizing than measurement of catalytic activity.     

院前一氧化氮吸入加静脉溶栓对急性心肌梗死再通率的影响

目的　观察急性心肌梗死 (AMI)早期吸入一氧化氮 (NO)加静脉溶栓治疗的再通率。方法　采用随机方法将 6 0例 AMI患者分为 NO吸入加静脉溶栓组 30例 (治疗组 ,30例 )和单用静脉溶栓组 (对照组 ,30例 )。治疗组在院前现场立刻吸入浓度为 (2 0± 1) mg/ L 的 NO30 m in,并同时给予质量分数为 0 .9%的氯化钠10 0 m l加尿激酶 15 0× 10 4 U于 30 min内静脉滴入。对照组除不吸入 NO外 ,溶栓方法与治疗组相同。两组溶栓后的治疗方法一致。结果　治疗组中再通者 2 5例 ,再通率为 83.3% ;未通者 5例。对照组中再通者 19例 ,再通率为 6 3.3% ;未通者 11例。治疗组再通率明显优于对照组 (P<0 .0 5 )。治疗组乳酸脱氢酶 (L DH)、肌酸磷酸激酶 (CPK)没有出现明显的高峰期 ,与对照组相比有显著差异 (P<0 .0 5 )。结论　 NO吸入同时进行静脉溶栓疗效确切 ,可以提高静脉溶栓时闭塞血管的再通率 ,为后期的治疗奠定了基础 ,且方法简单易行 ,安全可靠 ,有利于院前急救。     

Detection of cardiac-specific creatine kinase isoenzyme in sera with normal or slightly increased total creatine kinase activity.

We describe a spectrophotometric kinetic assay for detecting creatine kinase MB isoenzyme activity in the 1 to 10 U/liter range. The MB isoenzyme was isolated [Clin. Chem. 20, 36 (1974)] and assayed (Rosalki method) with an Abbott ABA-100. Good reproducibility was demonstrated for MB isoenzyme activities near 1 U/liter (CV = 2.6%). Sera with normal or slightly increased total creatine kinase activity were evaluated. Sera of 14 patients with acute myocardial infarction contained, per liter, 84 to 236 U of total creatine kinase activity and 4.6 to 28.0 U of isoenzyme MB activity; corresponding ranges for sera from healthy lab technicians and patients with noncardiac disease were 36 to 277 and 0 to 2.6 U. MB isoenzyme activity for infarction patients rose and fell sharply within three days after the infarction. Atypical time-course patterns, MB isoenzyme activity remaining abnormally great for five days, were observed in serum from patients with prolonged atrial fibrillation and congestive heart failure or cardiomyopathy; the BB isoenzyme (1 to 5 U/liter) was also detected in sera of such patients but was absent in sera from infarcation patients. Quantification of column-isolated MB by the assay described is rapid, easy, specific, and extremely sensitive for measuring MB in the 1 to 10 U/liter range.     

Concordance of creatine kinase-MB activity and mass

The recent availability of monoclonal antibodies that are highly specific for creatine kinase (CK; EC 2.7.3.2) MB isoenzyme should allow for the development of rapid, sensitive, and specific assays of CK-MB mass and activity. However, the relationship between the mass concentration of CK-MB and its activity in plasma has previously been thought by some to be variable. To determine the extent to which discrepancies of potential clinical significance might arise between measurements of activity and mass in plasma, we compared CK-MB activity and concentration in 1298 samples obtained from 226 patients admitted to the cardiac-care unit. CK-MB activity concentration was determined with an immunoadsorption assay, and mass concentration was measured by an automated "sandwich" assay (Magic Lite; Ciba Corning Diagnostics). Both of these assays are based on specific monoclonal antibodies for CK-MB. Values obtained with these assays correlated well (r = 0.94). Normal and abnormal values with the two assays were concordant in 96% of the samples. In all but three instances, differences occurred late after myocardial infarction and were characterized by minimal increases as determined by one method vs values at the upper limit of normal as determined with the other. Thus, measurements of CK-MB mass and activity concentrations in plasma with assays based on these specific monoclonal antibodies are comparable for the detection or exclusion of acute myocardial infarction.     

聚合血红蛋白对活体大鼠心肌缺血再灌注的保护作用

目的 通过建立活体大鼠心肌缺血再灌注模型,模拟人类冠心病,研究聚合血红蛋白(PolyHb)在心肌缺血再灌注中的保护作用,探究PolyHb在冠心病领域中的保护和治疗作用.方法 将45只Sprague-Dawley(SD)大鼠随机分成3组:实验组(15只)、对照组(15只)、假手术组(15只),建立大鼠心肌缺血模型.实验组...     

Serum release of the creatine kinase tissue-specific isoforms MM3 and MB2 is simultaneous during myocardial reperfusion

The release sequence of the creatine kinase MM and MB tissue-specific subforms after myocardial reperfusion was elucidated by computer-fitting serial enzyme data from 6 humans in whom coronary flow in the infarct-related artery was angiographically documented as initially zero, opening to normal after angioplasty. The model equation used demonstrated acceptable performance according to standard criteria including visual examination and statistical parameters. The model successfully described the sequential conversion of the MM3 and MB2 tissue isoforms to their respective MM2 and MM1, and MB1 isoforms. Release of MM3 and MB2 was simultaneous, differing in calculated release times by 0.2 to 10%, median 3%. Since MB2 release is not retarded after myocardial reperfusion compared to the more clinically established CK-MM3 isoform, assays for sensitive and rapid measurement of MB2 should be the focus for the non-invasive assessment of myocardial reperfusion due to its higher cardiospecificity.     

冠心病患者分泌型磷脂酶A2与高敏C反应蛋白、肌酸激酶的检测及其临床价值

【目的】观察分泌型磷脂酶A2(sPLA2)与高敏C反应蛋白(hs-CRP)、肌酸激酶(CK-MB)在冠心病中的变化情况并分析其相关性,评价其在冠心病诊疗方面的价值。【方法】测定28例稳定型心绞痛(SA)、54例不稳定型心绞痛(UA)、22例急性心梗患者(AMI)、20例非冠心病患者(NS)血浆sPLA2、hs-CRP和CK-MB的浓度变化情况,并进行统计学分析。【结果】sPLA2和hs-CRP在AMI组升高最明显,UA组和SA组次之;CK-MB在AMI组升高最明显,而SA组以及UA组两组间比较无显著性差异,但较对照组有显著升高。【结论】冠心病患者sPLA2与hs-CRP、CK-MB呈现正相关,三者显著升高可辅助临床诊断急性心梗、sPLA2和hs-CRP升高可用以鉴别SA和UA。     

用心肌钙蛋白T判断急性心肌梗塞溶栓疗效的观察

目的动态观察急性心肌梗塞（AMI）患者溶栓治疗后肌酸激酶（CK）,肌酸激酶MB同功酶（CK－MB）活性及心肌肌钙蛋白T（cTnT）浓度变化规律,探讨cTnT对判断冠脉再通的临床价值。方法选择AMI并接受溶栓治疗患者37例,将其分为再灌注组与未再灌注组,于溶栓前和发病后间隔一定时间分别采血。同时检测CK、CK－MB、cTnT,并绘制曲线加以分析比较。结果再灌注组CK、CK－MB、cTnT峰值出现时间提前,与未再灌注组之间有显著性差异。AMI发病12小时（h）以内再灌注组的CK、CK－MB、cTnT浓度分别大于未再灌注组,尤以发病后10h,12h为著。cTnT峰值浓度的升高明显高于CK、CK－MB者。结论动态观察cTnT浓度曲线变化显示与CK、CK－MB浓度曲线变化相似,且更特异、更灵敏,可作为判断溶栓再灌注的又一重要参考指标。     

内源性白介素-10在心肌缺血-再灌注损伤中的作用

目的　探讨大鼠心肌缺血 再灌注过程中血清白介素 10 (IL 10 )浓度的变化 ,以及甲泼尼龙对内源性IL 10产生的影响。方法　将 6 3只大鼠随机分成假手术组、缺血 再灌注 (对照 )组、甲泼尼龙(药物 )组。分别测定缺血 0 5h、再灌注 0 5h及 2h时血清中IL 10、磷酸肌酸激酶同功酶 (CK MB)的含量和心肌梗死面积。结果　对照组与药物组IL 10和CK MB含量自缺血 0 5h、再灌注 0 5h至 2h均呈逐渐升高趋势 ,再灌注 2h与再灌注前相比具有统计学差异 (P <0 0 5 )。再灌注后相应时段内 ,药物组较对照组IL 10明显升高 (P <0 0 5 ) ,心肌梗死面积减少 (P <0 0 5 ) ,CK MB降低且升高延迟。结论　在大鼠心肌缺血 再灌注中 ,甲泼尼龙可促进内源性IL 10大量释放。IL 10通过减轻心肌缺血 再灌注损伤发挥保护作用     

强化他汀类药物治疗对不稳定型心绞痛合并糖尿病患者经皮冠状动脉介入术后冠状动脉血流的影响

目的 探讨阿托伐他汀强化治疗对不稳定型心绞痛合并糖尿病患者经皮冠状动脉介入（PCI）治疗术后冠状动脉血流灌注及安全性的影响.方法 对我院2011年7月至2013年7月收治的合并糖尿病的不稳定型心绞痛患者137例行PCI治疗,随机分为强化组78例和常规组59例;两组患者入院后常规给予阿托伐他汀20 mg/d口服,强化组术前2h口服阿托伐他汀80 mg,常规组术前未用阿托伐他汀预处理.观察主要终点即术后即刻冠状动脉血流灌注及围手术期心肌梗死情况;安全终点即出院前肝功能、肌酸激酶及肾功能变化.结果 强化组患者术后无复流、慢血流及围手术期心肌梗死总体发生率5.1％ （4/78）较常规组17.0％ （10/59）相比减少,差异有统计学意义（x2=5.44,P=0.02）;而出院前,两组患者的肝功能、肌酸激酶及肾功能水平差异无统计学意义（P均＞0.05）.在多因素相关分析后发现,校正性别、年龄、吸烟、高脂血症、病变累及重要分支及后扩张等因素后,强化阿托伐他汀治疗仍是避免发生无复流、慢血流及围手术期心肌梗死的独立预测因子（OR =0.21,95％ CI为0.07 ～0.91,P=0.04）.结论 阿托伐他汀强化治疗可以改善合并糖尿病的不稳定型心绞痛患者PCI后冠状动脉血流灌注情况,且不增加不良反应的发生.     

Using troponin T to diagnose acute coronary syndromes

Elevated troponin T is a useful marker for acute myocardial infarction: it is more specific than is elevated creatine kinase MB isoenzyme, and it remains elevated for many days after creatine kinase levels have returned to normal, providing a useful indicator for late presentations. Nevertheless, creatine kinase MB still has many important roles, including providing estimates of infarct size and diagnosing acute myocardial infarction in patients with renal failure. Often, measuring both markers provides additional information. This article provides a diagnostic algorithm for using both markers.     

急性心肌梗死患者血清肌红蛋白水平在早期冠脉再灌流中的意义

目的　探讨急性心肌梗死患者尿激酶溶栓治疗过程中血清肌红蛋白 (Mb)的变化 ,判断其是否可以作为早期、非侵入性判断冠脉再灌流的指标。方法　对 2 2例尿激酶溶栓治疗和2 2例保守治疗的AMI患者治疗前后的 1h、2h、4h、8h、12h、14h、15h、18h和 2 4h的血清Mb进行测定 ,同时测定血清磷酸肌酸激酶同工酶 (CK MB) ,比较再灌流组和未再灌流组血清Mb的峰浓度和达峰时间 ,并同CK MB进行比较。结果　再灌流组血清Mb和CK MB的峰浓度分别为 6 19 5 9±198 5 5ng/ml和 15 7 10± 36 19u/L ,均显著高于未再灌流组 (487 31± 6 0 87ng/ml和 141 80± 2 2 18u/L) ;再灌流组较未再灌流组血清Mb达峰时间明显提前 (192min对 480min ,P <0 0 1) ,再灌流组血清Mb达峰时间显著早于血清CK MB达峰时间 (192min对 72 0min ,P <0 0 1) ,而且Mb的 2h出现率 (Mb2 /Mb0 )较未再灌流组也显著增高 (4 2 4对 2 12 ,P <0 0 1)。结论　血清Mb值早期上升、快速达峰是一种可靠、简便的非侵入性判断AMI再灌流治疗成功与否的指标。