复苏犬心肌损伤的实验研究

目的：本实验通过研究复苏犬的心肌损伤，探讨心肌肌钙蛋白T对复苏犬心肌损伤的诊断价值。方法：利用犬室颤心跳呼吸骤停模型，进行标准心肺复苏，观察室颤前及复苏后犬血心肌肌钙蛋白T水平和心肌病理学变化。结果：在犬恢复自主循环1h后，血心肌肌钙蛋白T就明显升高，且其升高水平与病理学改变程度相对应。结论：（1）复苏犬存在急性心肌损伤；（2）心肌肌钙蛋白T血浓度能客观地反映心肌受损状态。     

复苏犬心肌损伤的实验研究

目的：本实验通过研究复苏犬的心理损伤，探讨心肌肌钙蛋白Ｔ对复苏犬心肌损伤的诊断价值。方法：利用犬室颤心跳呼吸骤停模型，进行标准心肺复苏，观察室颤前及复苏后犬血心肌肌钙蛋白Ｔ水平和心肌闰理学变化。结果：在犬恢复自主循环１ｈ后，血心肌肌钙蛋白Ｔ就明显升高，且其升高水平与病理学改变程度相对应。结论：（１）复苏犬存在急性心肌损伤；（２）心肌肌钙蛋白Ｔ血浓度能客观地反映心肌损伤状态。     

家兔心肺复苏后心肌肌钙蛋白T脱失的免疫组化研究

目的:观察家兔心肺复苏(CA-CPR)后心肌组织内心肌肌钙蛋白T(cTnT)的脱失情况,探讨心肌损伤的机制。方法:采用家兔缺氧型CA-CPR模型,于心肺复苏前后分时间点抽取动脉血,测血清cTnT值;自主循环恢复后4小时取心肌组织,应用免疫组化LSAB法显色观察cTnT表达的脱失情况。结果:自主循环恢复后血清cTnT明显升高。自主循环恢复后4小时心肌组织内cTnT明显脱失,图像分析显示心肺复苏后cTnT的脱失面积与正常家兔心肌之间存在显著性差异。结论:家兔心肺复苏后血清cTnT明显升高,心肌组织内cTnT的明显脱失,两者呈负相关。     

烧伤与心肌梗死患者血清TnT及心肌酶对比分析

目的 评估血清肌钙蛋白T(TnT)对烧伤后心肌损伤的诊断价值.方法 对86例烧伤患者及36例急性心肌梗死患者病后血清TnT及心肌酶比较.结果 TnT在重度烧伤组及电击伤组阳性率均大于50％,而急性心肌梗死组则100％.说明烧伤后血清TnT升高水平与烧伤面积有关,也与是否电烧伤有关.而心肌酶谱并非心肌损伤的特异性指标.结论 血清TnT测定对于烧伤后心肌损伤诊断的特异性明显优于心肌酶谱.     

参麦注射液对家兔自主循环复苏后心肌肌钙蛋白T的影响

目的 观察参麦注射液对家兔心肺复苏后血清心肌肌钙蛋白T(cTnT)和心肌组织内cTnT脱失的影响,探讨其对心肌保护作用的机制.方法 采用家兔缺氧型模型,随机分两组,心肺复苏前后分时间点分别注射参麦注射液、生理盐水,抽取动脉血,测血清cTnT值;自主循环恢复后4 h取心肌组织,应用免疫组化LSAB法显色观察cTnT表达的脱失情况.结果 两组自主循环恢复后血清cTnT均升高,但对应时间点比较无显著性差异;参麦组自主循环恢复后4 h心肌组织内cTnT表达部分脱失,对照组明显脱失,两组比较存在显著性差异.结论 家兔心肺复苏后血清cTnT明显升高,参麦注射液对血清cTnT升高无明显抑制作用,对心肌组织内cTnT的脱失有明显抑制作用,说明参麦注射液对心肌损伤有一定的保护作用.     

停跳与非停跳冠脉搭桥术后心肌肌钙蛋白水平的变化及其临床意义探讨

目的 研究停跳与非停跳冠脉搭桥术后心肌肌钙蛋白水平的变化。方法 30例择期行冠脉搭桥术的患者根据手术方式分为不停跳组(n=15)和停跳组(n=15)。不停跳组采用Octopus组织固定器局部固定心肌后进行冠脉搭桥，而停跳组在体外循环心脏停跳下进行冠脉搭桥。分别于入手术室(T0)、麻醉诱导平稳后(T1)、手术结束即刻(TST)、术后4h(T4)、8h(T8)、12h(T12)、24h(T24)、36h(T36)、48h(T48)抽静脉血4ml测定心肌肌钙蛋白T(cTnT)和心肌肌钙蛋白Ⅰ(cTnI)。结果 两组患者T0和Tl时cTnT、cTnI正常，术后则显著性升高。两组之间，组2比组l术后各时间点cTnT和cTnI升高均有显著性差异。两组cTnT于术后8小时达到峰值，并一直保持较高水平；cTnI于术后12小时达高峰，不停跳组cTnI在术后36小时即恢复正常水平。结论 不停跳搭桥比体外循环搭桥手术对心肌细胞损伤轻，持续时间短。心肌损伤时，cTnT比cTnI峰值出现早，持续时间长，似乎更加灵敏。     

血清心肌肌钙蛋白在判断危重病合并心肌损伤中的应用价值

自1987年英国Cummins首先报道血清心肌肌钙蛋白测定用于急性心肌梗死（AMI）诊断以来，心肌肌钙蛋白已广泛用于临床AMI诊断，且被国内外专家公认为诊断AMI的金标准。近年来研究发现，在非冠状动脉综合征危重病中也有血清心肌肌钙蛋白升高，许多学者认为这种升高与危重病合并心肌损伤密切相关。危重病合并心肌损伤较隐匿，通过常规心电图和超声心动图诊断敏感性低，常被临床忽视，但当这种心肌损伤发展为严重心功能障碍或心衰时，临床采取措施已晚，大大增加了危重病患者的病死率。     

心肌肌钙蛋白T与慢性心力衰竭的相关研究

目的:探讨慢性心力衰竭患者血清心肌肌钙蛋白T水平与心脏功能及远期心脏事件的关系.方法:心力衰竭患者68例,按照纽约心脏协会(NYHA)心功能分级标准分为3组,测定心力衰竭患者血清心肌肌钙蛋白T水平,观察其与心脏功能及心力衰竭患者远期心脏事件的关系.并选取同期健康体检者作为对照组.结果:68例心力衰竭患者中31例血清心肌肌钙蛋白T升高,心功能Ⅲ级心肌肌钙蛋白T升高的检出率(66.7%)比心功能Ⅱ级检出率(8.6%)显著增高(P<0.05),心功能Ⅳ级心肌肌钙蛋白T升高的检出率(100%)比心功能Ⅲ级患者明显增高(P<0.05).68例心力衰竭患者远期随访,随访时间(14±6)个月,心肌肌钙蛋白T正常组远期心脏事件16例次,升高组远期心脏事件33例次(P<0.01).结论:心功能越差心肌肌钙蛋白T升高的检出率越大,血清心肌肌钙蛋白T不仅是心力衰竭患者心肌损伤的敏感标志物,而且是远期心脏事件的独立预测因子.     

心脏手术前后心肌肌钙蛋白T和心肌酶谱的变化

目的：探讨血清心肌肌钙蛋白T（cTnI）和心肌酶谱在心肌手术损伤前后的变化及其临床意义。方法：动态观察20例二尖瓣瓣膜置换术患手术前,术后2h及24h血清cTnI和心肌酶谱变化。另制备家兔心肌损伤模型,检测动物模型伤前和伤后4,8,24h血清cTnI的变化特点。结果：二尖瓣瓣膜置换术患血清cTnI含量,心肌酶谱尖性在术后2,24h较术前显升高（P＜0．01）,其中血清cTnI含量术后2h增加倍数高于其他指标。家兔心肌损伤模型伤后4,8,24h血清cTnI含量较伤前或高非常显（P＜0．01）,呈后期大峰值双基线。结论：血清cTnI含量及心肌酶谱活性均对心肌损伤的诊断有意义,但cTnI的心肌特异性及早期灵敏度更高,cTnI后期峰值对心肌损伤的预后判断有重要价值。     

生物化学和分子生物学检验与临床

心肌肌钙蛋白Ⅰ和肌钙蛋白T对急性缺血性心脏病预后相关性分析，高原红细胞增多症患者血清肌钙蛋白Ⅰ含量测定，心脏肌钙蛋白Ⅰ与抗心肌抗体对川崎病早期的临床意义，中国肝病患者血清铜蓝蛋白水平的研究，妊娠期糖尿病视网膜病变患者血中糖基化血红蛋白和果糖胺的水平及其临床意义……     

Cardiac troponin T for prediction of short- and long-term morbidity and mortality after elective open heart surgery

BACKGROUND: Increased cardiac troponins in blood are observed after virtually every open heart surgery, indicating perioperative myocardial cell injury. We sought to determine the optimum time point for blood sampling and the respective cutoff value of cardiac troponin T (cTnT) for risk assessment in patients undergoing cardiac surgery. METHODS: In a series of 204 patients undergoing scheduled open heart surgery, mainly for coronary artery bypass grafting (n = 132) or valve repair (n = 27), cTnT concentrations were measured before and 4 and 8 h after cross-clamping and then daily for 7 days. Individual risk was assessed by use of the Cleveland Clinic Foundation Risk score and intraoperative risk indicators such as duration of cardiopulmonary bypass, cross-clamping, and perioperative release of cardiac markers. Patients were followed for 28 months. RESULTS: Cardiac mortality, all-cause mortality rates, and rates of nonfatal acute myocardial infarction (AMI) at 28 months were 6.9%, 8.8%, and 6.8%, respectively. cTnT was higher in patients with Q-wave AMI or postoperative heart failure requiring inotropic support, and in nonsurvivors. The ROC curve revealed a cTnT > or = 0.46 microg/L at 48 h as the optimum discriminator for long-term cardiac mortality. Stepwise logistic regression identified higher Cleveland Clinic Risk Score [odds ratio (OR) = 2.6 per point], cross-clamp time >65 min (OR = 6.6), and cTnT (OR = 4.9) as significant and independent predictors of long-term cardiac mortality. CONCLUSIONS: A single postoperative cTnT measurement can be used to estimate myocardial cell injury that impacts long-term survival after open heart surgery. It adds independently to established risk indicators.     

Serum cardiac troponin T levels as an indicator of myocardial injury in ischemic and hemorrhagic stroke patients

Many studies in the literature have clearly shown the increase in creatine kinase-myocardial subfraction (CK-MB) levels and changes in electrocardiography (ECG) after stroke. However, the studies on cardiac troponin T (cTnT) which is more sensitive and specific to myocardium after stroke are relatively scarce. Moreover, its associations with volume of stroke lesions and type of stroke have not been investigated thoroughly. Thus, the aims of this study were to investigate a predictive value of cTnT in assessing myocardial injury and cardiac dysfunction in different types of stroke (hemorrhagic or ischemic stroke) and its relationship with stroke size and volume. This study included 62 patients (30 males and 32 females) with acute stroke confirmed by computed tomography (CT). Blood samples were obtained within 24 hours of stroke onset to measure the serum levels of creatin kinase (CK), CK-MB, lactate dehydrogenate (LDH), and cTnT. ECG and echocardiography were performed to assess myocardial function and left ventricular ejection fraction (LVEF). Of all patients included in the study, 20 patients (32%) demonstrated elevations in cTnT, while 28 patients (45%) had increased CK-MB levels. Serum levels of cTnT were positively correlated with stroke volume (r = 0.65, p < 0.0001), while inversely correlated with LVEF (r = -0.53, p < 0001). Serum levels of both CK-MB and cTnT were higher in patients with hemorrhagic stroke than those with ischemic stroke but this difference was not significant (p > 0.05). As a conclusion, cTnT has a higher specificity and sensitivity in detecting myocardial injury after stroke of both ischemic and hemorrhagic origins. Measurement of the serum levels of cTnT is of clinical importance in evaluating myocardial injury and provides a useful aid in estimating the volume of stroke lesions.     

心肌钙蛋白T定性在急性冠状动脉综合征诊断上的应用

目的　评价心肌钙蛋白T (cTnT)在急性冠状动脉综合征的诊断价值。方法　收入急诊ICU的急性冠状动脉综合征病人分为 :AMI组和UAP组 ,抽取肘部静脉血 1ml立即注入肝素抗凝试管中 ,混匀。用德国宝灵曼中国有限公司提供的肌钙蛋白T灵敏检测试纸条进行定性检查。同时用放免分析方法测定血清CK、CK MB及AST。结果　AMI组cTnT阳性率为 70 6 % ,UAP组阳性率 16 7% ,两组阳性率对比有显著性差异性 (P <0 0 1)。结论　cTnT是反映心肌细胞损伤的灵敏性、特异性均较好的生化指标 ,cTnT定性检测可用于ACS早期鉴别诊断 ,其临床意义优于血清CK、CK MB及AST。     

Myoglobin stratifies short-term risk in acute major pulmonary embolism

BACKGROUND: Concentrations of cardiac troponins can be elevated in acute pulmonary embolism (APE) indicating myocardial injury. Although concentration of myoglobin (MYO) increases after myocardial damage, even before detectable rise of cardiac troponin levels occurs, MYO was not evaluated in APE. Therefore, we assessed prevalence and prognostic significance of myoglobin in major APE. METHODS: We studied 46 patients (30 women, aged 61.9+/-17.8 years) with major APE defined with right ventricular dilatation. On admission serum myoglobin, and cardiac troponin T (cTnT) were measured. Serum MYO concentrations >58 ng/ml for women, and >72 ng/ml for men were considered abnormal. CTnT>0.01 ng/ml was regarded to indicate myocardial injury. RESULTS: MYO levels exceeding sex specific norms were found in 21/46 (45.7%) of patients, while detectable cTnT was found in 24/46 (52.1%) of patients. Seven patients died during hospitalization. Elevated MYO significantly predicted in-hospital mortality (OR 25, 95% CI 1.3-474.2), while increased cTnT concentration did not affect the survival. Among clinical and echocardiographic variables only older age indicated worse prognosis (OR 1.6, 95% CI 1.06-2.41). CONCLUSIONS: Myoglobin levels are elevated in serum on admission in almost half of patients with major APE. Elevated myoglobin level, marker of myocardial injury, is a powerful predictor of increased risk of fatal outcome in major pulmonary embolism.     

心肌肌钙蛋白Ⅰ和肌钙蛋白T对急性缺血性心脏病预后相关性分析

目的探讨心肌肌钙蛋白I(cTnI)和肌钙蛋白T(cTnT)对急性缺血性心脏病转归的影响。方法对就诊的急性缺血性心脏病患者定性测定入院时及距胸痛发作间隔10h的cTnI和定量测定相同时点的cTnT。同时随访患者发病后1、3、6、12个月的疾病转归,以心绞痛、心肌梗死、心力衰竭、心源性猝死为终点评价指标。结果cTnI或cTnT异常患者与正常者相比较,不稳定型心绞痛、心肌梗死、心力衰竭、心源性猝死的发生率具有显著性差异(P<0.01)。cTnI或cTnT异常与终点事件(不稳定型心绞痛、心肌梗死、心力衰竭、心源性心源性猝死)发生率呈正相关。结论cTnI或cTnT对急性心肌梗死,尤其是微小心肌坏死诊断具有高度的敏感性和特异性,并与急性缺血性心脏病的预后密切相关。     

Lack of association between cardiac troponin T and D-dimer in the evaluation of myocardial damage

Acute myocardial infarction (AMI) disrupts cardiac cell membranes, releasing intracellular cardiac proteins into the vascular system. Some of these proteins, including the cardiac troponin subunits T and I, have proven useful for diagnosing myocardial damage. Intracoronary thrombosis plays a key role in the pathogenesis of AMI, and the formation of an occlusive thrombus usually precedes the development of myocardial damage. To evaluate whether there is an association between the size of intracoronary thrombosis and myocardial damage, we analyzed D-dimer and cTnT levels in blood samples from patients suspected to have myocardial damage. We investigated 102 patients who were admitted to emergency service for suspected myocardial damage. D-dimer was assessed with the use of the immunoassay Liatest D-dimer, and cTnT levels were measured with an electrochemiluminescence immunoassay (Troponin T STAT). D-dimer levels were lower in patients with cTnT < 0.01 than in patients presenting cTnT > 0.01 ng/mL. We investigated the relationship between D-dimer and cTnT levels in the patients with cTnT > 0.01 ng/mL (0.40 +/- 0.10 ng/mL), and no significant agreement (r = 0.20, P > 0.05) was observed. The levels of D-dimer were not associated with the levels of cTnT in patients with cTnT > 0.01 ng/mL.     

Cardiac troponin I and troponin T: recent players in the field of myocardial markers.

The troponin (Tn) complex consists of three subunits referred to as TnT, TnI and TnC. Myocardium contains TnT and TnI isoforms which are not present in skeletal muscles and which can be separated from the muscular isoforms by immunological techniques. Using commercially available immunoassays, clinical laboratories are able to determine cardiac TnT and TnI (cTnT and cTnI) quickly and reliably as classical cardiac markers. After acute myocardial infarction, cTnT and cTnI concentrations start to increase in serum in a rather similar way than CK-MB, but return to normal after longer periods of time (approximately one week). Because of their excellent cardiac specificity, Tn subunits appear ideally suited for the differential diagnosis of myocardial and muscular damage, for example in noncardiac surgery patients, in patients with muscular trauma or with chronic muscular diseases, or after intense physical exercise. cTnT and cTnI may also be used for detecting evidence of minor myocardial damage: therefore they have found new clinical applications, in particular risk stratification in patients with unstable angina. In spite of the possible reexpression of cTnT in human skeletal muscles, and of the lack of standardization of cTnI assays, Tn subunits are not far to meet the criteria of ideal markers for acute myocardial injury. Only an insufficient sensitivity in the first hours following the acute coronary syndroms requiries to maintain an early myocardial marker in the cardiac panel for routine laboratory testing.     

Cardiac troponin T and I in end-stage renal failure

BACKGROUND: In patients suffering from end-stage renal failure, cardiac troponin T (cTnT) and I (cTnI) may be increased in serum without other signs of acute myocardial damage. Whether these increases are specific to myocardial injury or nonspecific is not completely clear. METHODS: We investigated time courses of cTnT and cTnI over 1 year and the clinical outcome over 2 years in 59 patients with end-stage renal failure undergoing chronic hemodialysis. At the start of the study, we divided the patients into two groups, group 1, without history of cardiac failure, and group 2, with history of cardiac failure, and looked for differences between the groups in later adverse outcome. cTnT was measured using the Enzymun((R)) troponin T assay on an ES 700 analyzer (Roche). cTnI was measured on a Stratus((R)) II analyzer (Dade Behring). Creatinine and blood urea nitrogen were measured on a Vitros((R)) 950 IRC (Ortho). RESULTS: Dialysis acutely increased cTnT (P: <0.01) and decreased cTnI (P: <0.001) regardless of the dialysis membrane used. Although statistically not significant, cTnT but not cTnI was increased more frequently in group 2 than in group 1, in some cases over the whole study period. Five patients (8.5%) died of cardiac complications within 2 years; all of them had mostly increased cTnT and, in one or more samples, increased cTnI. CONCLUSIONS: Dialysis alters measured cTnT and cTnI concentrations in serum. In patients suffering from end-stage renal failure, sporadic or persistently increased cTnT and cTnI appear to predict cardiac complications. Because of the effects of the dialysis procedure on troponin values, we recommend that blood be collected before dialysis.     

The specificity of biochemical markers of cardiac damage: a problem solved.

This paper reviews the tissue specificity of cardiac troponin I (cTnl), cardiac troponin T (cTnT) and creatine kinase (CK) MB in human and animal heart and skeletal muscles. Studies reveal that CK-MB can be expressed up to 20% of total CK activity in human skeletal muscle; and therefore is not 100% specific for the heart. One cTnl isoform has been described and shown to be 100% specific for the heart. While one to four cTnT isoforms are expressed in diseased and regenerating human skeletal muscle, these isoforms are not the same as the cTnT isoforms expressed in the human heart and are not detected by the cTnT diagnostic assays used in clinical practice. Representative cases are described demonstrating the role of monitoring cardiac troponins in blood for differentiating false positive CK-MB increases due to skeletal muscle injury. Further, sufficient reactivity and tissue specificity of cTnl and cTnT assays are demonstrated for use as markers of myocardial injury in laboratory animals. Monitoring cTnl and cTnT concentrations in the circulation appears poised as the new standards for detection of myocardial injury.