心肌肌钙蛋白I、肌钙蛋白T、肌酸激酶同工酶MB早期诊断 急性心肌梗死敏感性及特异性比较分析

目的 探讨心肌肌钙蛋白Ⅰ（cTnI)、 肌钙蛋白T（cTnT)、 肌酸激酶同工酶MB（CK－MB）早期诊断急性心肌梗死的临床应用价值。方法 对60例急性心肌梗死（AMI）和40例不稳定型心绞痛（UA）患者的同一血样标本检测cTnI、cTnT、CK－MB3项指标,分别进行两组间比较,并对 AMI组和UA组各指标作对比分析。结果 cTnI、cTnT早期诊断急性心肌梗死灵敏度高于CK－MB,阳性率分别为63.3%、46.7%、18.3％,P＜0.01;cTnI和cTnT无显著差别,P＞0.05;cTnI、cTnT、CK－MB特异性相当。结论 心肌肌钙蛋白I和肌钙蛋白T对于AMI的早期诊断具有较高灵敏度和较强特异性,是心肌损伤特异笥标志物,cTnI检测方便、快捷、准确,具有较好的临床价值。     

肌钙蛋白T、肌红蛋白、肌酸激酶同工酶诊断心肌损伤的灵敏度及特异性比较分析

人心肌肌钙蛋白T（cardiac troponin T,cTnT）、肌酸激酶同工酶MB（CK—MB）、肌红蛋白（myoglobin,Mb）是急性心肌梗死早期诊断灵敏度高、特异性强的血清标志物。本组对急性心肌梗死（AMI）、不稳定性心绞痛（UAP）患者和健康人群进行cTnT、Mb和CK—MB的联合检测,对cTnT、Mb和CK—MB在诊断心肌损伤的灵敏度及特异性进行比较分析。     

心肌肌钙蛋白Ⅰ定性在急性冠状动脉综合征诊断中的意义

目的：评价心肌肌钙蛋白Ⅰ（cTnI）在急性冠状动脉综合征的诊断价值。方法：将急性冠脉综合征的病人分为AM1组和UA组，抽取静脉血进行cTnI的定性检测，同时测定血清CK、CK－MB及AST。结果：AMI组cTnI阳性率为85．9％，UA组阳性率为17．0％，两组相比有显著性差异（P＜0．01）。结论：cTnI是反映心肌细胞损伤的灵敏性、特异性均较好的指标，cTnI定性检测可用于急性冠脉综合生早期鉴别诊断，其临床意义优于血清CK、CK－MB及AST。     

心肌梗死三合一快速诊断的临床应用

心肌梗死（AMI）的早期诊断中肌红蛋白（Mb）与肌酸激酶同工酶（CK—MB）出现得较早,亦可反映心肌损伤的程度,但缺乏特异性。肌钙蛋白I（cTnI）是一早期特异性指标,AMI患者胸痛发作4h内cTnI水平即超过正常,12h达到高峰,症状发作144h内均可检测到其水平增高,但有近20％的AMI患者cTnI呈阴性,所以临床全面、快速诊断AMI有赖于对Mb、CK—MB及cTnI这3项指标的联合检测。本文对Mb、CK—MB、cT—nl这3项的联合应用进行分析,报道如下。     

测定心肌型脂肪酸结合蛋白在早期诊断急性心肌梗死中的应用

目的：探讨测定心肌型脂肪酸结合蛋白（HFABP）在临床诊断早期急性心肌梗死的应用效果。方法：选择65例胸痛患者采用快速检测患者发病0～3h,3～6h和6h后血清H—FABP,并与常规静脉血心肌肌钙蛋白cTnI肌酸激酶同工酶（CK—MB）结果比较,分析3种心肌标志物在诊断不同发病时段AMI的敏感性和特异性。结果：在0～3h和3～6h时段诊断AMI的敏感性H—FABP（66．7％、92．3％）明显高于cTnI（33．3％、6125％）CK—MB（0％、61．5％）;特异性方面与CK—MB相当但明显优于cTnI。结论：H—FABP在AMI发生3h内较cTnI和cKMB更具有早期诊断实用价值。     

CTnI、MYO、CK—MB质量联合检测在急性心肌梗死诊断中的意义

目的探讨用化学发光法检测肌红蛋白（MYO）、肌酸激酶同工酶（CK—MB）质量、肌钙蛋白（CTnI）对急性心肌梗死（AMI）的诊断价值。方法以65例AMI临床确诊病例为研究组,65例不稳定型心绞痛（UAP）,65例其他心脏病患者和50例健康体检为对照组,于不同时间用化学发光法检测MYO、CK—MB、CTnI含量,比较诊断AMI的敏感性和特异性,并随访AMI组患者心脏病性猝死及心绞痛事件发生情况,确定联合检测和独立检测的最佳时间具有的不同诊断价值。结果AMI组（症状6～24h）CTnI、MYO、CK—MB均显著高于对照组,具有显著性差异（P〈0．01）。在症状发生后的2—6h采样分析,CTnI、MYO联合诊断AMI的敏感性和特异性分别是81．8％、87．8％;89．4％、50．6％,MYO有高的阴性预示值。在症状发生后的6—12h采样分析,CTnI、MYO、CK—MB联合诊断AMI的敏感性和特异性分别是95．4％、99．6％;98．9％、80．6％;90．6％、80．9％。有较高的敏感性和特异性。在症状发生后的12～24h采样分析,cTnI、CK—MB联合诊断AMI敏感性和特异性分别为100％、100％;96．9％、87．3％,可达到最佳敏感性和特异性。在症状发生后的24—72h采样分析,cTnI诊断AMI的敏感性和特异性分别是89．5％和100％。结论联合检测MYO、CK—MB、CTnI能够更准确的诊断AMI,不同时间段各项指标的敏感性和特异性差异较大,因此根据不同的选择可提高AMI的诊断率和制定最佳治疗方案。     

床边快速心肌肌钙蛋白I、肌红蛋白、肌酸激酶司功酶联合检测对急性心肌梗死早期诊断的价值

目的：探讨床边快速心肌肌钙蛋白I（cTnI）、肌红蛋白（Myo）和肌酸激酶同功酶（CK-MB）联合检测对急性心肌梗死（AMI）早期诊断的价值。方法：采用美国博适-Triage于式快速定量心肌梗死／心衰诊断仪，对急诊收治入院的46例急性胸痛病人，采静脉血动态测定cTnI、Myo和CK—MB含量，并结合临床症状、心电图动态变化综合分析。结果：对AMI诊断的敏感性：0-3h cTnI与CK—MB均为29．4％，低于Myo的47．1％，4-6hcTnI为80．0％，其余均为100．0％；对AMI诊断的特异性：cTnI、CK—MB各时间段均为100．0％，Myo0-3h为58．8％、4～6h为40．0％、12h以上为33．3％：三项联合检测0-3h的敏感性和特异性分别是35．3％和86．3％，4～6h为93．3％、80．0％、12h以上为100．0％、77．8％。结论：床边快速cTnI、Myo和CK—MB联合检测，有助于对AMI床边快速早期诊断和鉴别诊断，为AMI及时准确的治疗提供依据。     

滴金免疫法测定血清肌红蛋白在心肌梗塞诊断中的应用

用滴金免疫法对40例健康人、37例急性心肌梗塞（AMI）患者及86例非AMI患者的血清肌红蛋白（S－Mb）进行检测，并与四项心肌酶（CK、LDH、CK－MB、LDH1）和肌钙蛋白T（cTnT）作对比分析。结果显示：S－Mb对AMI的敏感性为97．3％，但特异性仅为76．5％。S－Mb对AMI的诊断价值与心肌酶测定相仿，且具有简便快速的优点，但不如cTnT，后者具有更高的特异性。     

血肌钙蛋白I更能预示透析患者的心血管死亡风险

心肌酶的检测，包括肌酸激酶（CK）、肌酸激酶心肌同功酶（CK-MB）、肌红蛋白（MB），对于诊断早期心肌坏死早有公论，但伴随肾功能的变化，这些酶往往有所上升而导致被重叠遮盖。近年引进了更加特异性的肌钙蛋白cTnT和cTnI检测，但是肾功能对它们的影响仍有疑问。本文对此作一初探，报告如下。     

测定肌钙蛋白I(cTnl)有助于轻度心肌缺血性损伤的诊断

作者在总CK活性没有超过正常上限两倍的轻度。心肌受损患者中,比较了血清心肌肌钙蛋白互（cTnI）和CK－MB对诊断的准确性。在该研究中,分析了48例有以下症状的轻度心肌缺血患者的血清总CK、CK－MB和cTnI：（1）提示意性心肌缺血的胸部不适。（2）总CK的峰值低于正常上限两倍。（3）ECG改变提示心肌缺血损害,或（4）双维超声。心动图改变表明一个新部位心壁运动异常。所选的48例病人中有28例（占58％）的总CK活性的最大值在正常范围以内。所有病人在入院后24～72h内进行了详细的临床检查。在入院和36h内每隔6～8h抽血,用特异性识别cTnI和CK－MB的单克隆抗体免疫学方法在StratusⅡ分析仪上检测cTnI和CK－MBS－CK－MB的上限参考值是50μg／L,检测下限是1.0μg／L,S－TnI的检测上限是0．8μg／L,下限是0．35μg／L。在症状发作6h内cTnI和CK－MB都不是心肌受损早期好的检测指标。CK－MB、cTnI峰浓度分别是16．4±11．8μg／L和13．2μg／L。在胸病发作后的7～36h,cTnI的最高生化标志物指数明显高于CK－MB,cTnI检测心肌受损的临床敏感性是100％,95％的可信区间是87．2％～100％,而CK－MB的敏感性仅为81．8％,其95％的可信区间是67.3％～91．8％。该研究表明对于总CK轻微上升的轻度心肌损伤病人的     

Correlation of antemortem serum creatine kinase, creatine kinase-MB, troponin I, and troponin T with cardiac pathology

BACKGROUND: Spurious increases in serum troponins, especially troponin T, have been reported in patients with and without acute myocardial syndromes. METHODS: We studied 78 autopsied patients without clinical myocardial infarction (MI) and correlated histologic cardiac findings with antemortem serum creatine kinase (CK), its MB isoenzyme (CK-MB), cardiac troponin I (cTnI), and cardiac troponin T (cTnT). RESULTS: There was no significant myocardial pathology in 15 patients. Cardiac pathologies were in five groups: scarring from previous MI or patchy ventricular fibrosis (n = 9), recent MI (n = 27), healing MI (n = 7), degenerative myocyte changes consistent with congestive heart failure (CHF; n = 12), and other cardiac pathologies (n = 8). The median concentrations in the five groups were not significantly different for either CK or CK-MB. Compared with the no-pathology group, only the MI group was significantly different for cTnI, and the MI and other pathology groups were significantly different for cTnT. For patients with MI, 22%, 19%, 48%, and 65% had increased CK, CK-MB, cTnI, and cTnT, respectively; for CHF and other cardiac pathologies combined, the percentages were 28%, 17%, 22%, and 50%. For patients with increased cTnI, 72% and 28% had MI and other myocardial pathologies, respectively; patients with increased cTnT had 64% and 36%, respectively. Patients without myocardial pathology had no increases in CK-MB, cTnI, or cTnT. CONCLUSIONS: All patients with increased serum CK-MB, cTnI, and cTnT had significant cardiac histologic changes. The second-generation cTnT assay appears to be a more sensitive indicator of MI and other myocardial pathologies than the cTnI assay used in this study.     

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.     

Utility of Troponin I in Patients with Cocaine-associated Chest Pain

Baseline electrocardiogram abnormalities and market elevations not associated with myocardial necrosis make accurate diagnosis of myocardial infarction (MI) difficult in patients with cocaine-associated chest pain. Troponin sampling may offer greater diagnostic utility in these patients. OBJECTIVE: To assess outcomes based on troponin positivity in patients with cocaine chest pain admitted for exclusion of MI. METHODS: Outcomes were examined in patients admitted for possible MI after cocaine use. All patients underwent a rapid rule-in protocol that included serial sampling of creatine kinase (CK), CK-MB, and cardiac troponin I (cTnI) over eight hours. Outcomes included CK-MB MI (CK-MB >or= 8 ng/mL with a relative index [(CK-MB x 100)/total CK] >or= 4, cardiac death, and significant coronary disease (>or=50%). RESULTS: Of the 246 admitted patients, 34 (14%) met CK-MB criteria for MI and 38 (16%) had cTnI elevations. Angiography was performed in 29 of 38 patients who were cTnI-positive, with significant disease present in 25 (86%). Three of the four patients without significant disease who had cTnI elevations met CK-MB criteria for MI, and the other had a peak CK-MB level of 13 ng/mL. Sensitivities, specificities, and positive and negative likelihood ratios for predicting cardiac death or significant disease were high for both CK-MB MI and cTnI and were not significantly different. CONCLUSIONS: Most patients with cTnI elevations meet CK-MB criteria for MI, as well as have a high incidence of underlying significant disease. Troponin appears to have an equivalent diagnostic accuracy compared with CK-MB for diagnosing necrosis in patients with cocaine-associated chest pain and suspected MI.     

Laboratory diagnosis of patients with acute chest pain.

The enzyme activities of creatine kinase (CK), its isoenzyme MB (CK-MB) and of lactate dehydrogenase isoenzyme 1 (LD-1) have been used for years in diagnosing patients with chest pain in order to differentiate patients with acute myocardial infarction (AMI) from non-AMI patients. These methods are easy to perform as automated analyses, but they are not specific for cardiac muscle damage. During the early 90's the situation changed. First creatine kinase MB mass (CK-MB mass) replaced the measurement of CK-MB activity. Subsequently cardiac-specific proteins troponin T (cTnT) and troponin I (cTnI) appeared on the scene, displacing LD-1 analysis. However, troponin concentrations in blood increase only from four to six hours after onset of chest pain. Therefore a rapid marker such as myoglobin, fatty acid binding protein or glycogen phosphorylase BB could be used in early diagnosis of AMI. On the other hand, CK-MB isoforms alone may also be useful in rapid diagnosis of cardiac muscle damage. Myoglobin, CK-MB mass, cTnT and cTnI are nowadays widely used in diagnosing patients with acute chest pain. Myoglobin is not cardiac-specific and therefore requires supplementation with some other analyses such as troponins to support the myoglobin value. Troponins are very highly cardiac-specific. Only the sera of some patients with severe renal failure, which requires hemodialysis, have elevated cTnT and/or cTnI without there being any evidence of cardiac damage. On the other hand, the latest studies have shown that elevated troponin levels in sera of hemodialysis patients point to an increased risk of future cardiac events in a similar manner to the elevated troponin values in sera of patients with unstable angina pectoris. In addition, the bedside tests for cTnT and cTnI alone or together with myoglobin and CK-MB mass can be used instead of quantitative analyses in the diagnosis of patients with chest pain. These rapid tests are easy to perform and they do not require expensive instrumentation. For routine clinical laboratory practice we suggest that in diagnosis of patients with chest pain, myoglobin and CK-MB mass measurements should be performed whenever they are requested (24 h/day) and cTnT or cTnI on admission to the hospital and then 4-6 and 12 hours later.     

Diagnosis and risk stratification of patients with anginal pain and non-diagnostic electrocardiograms

Patients with acute chest pain suggestive of myocardial ischaemia, and normal or non-diagnostic electrocardiograms, form a difficult subgroup for diagnosis and early risk stratification. We prospectively evaluated the role of troponin T (cTnT), troponin I (cTnI), CKMB mass and myoglobin, in the diagnosis and risk stratification of 214 patients with acute chest pain of < or = 24 h and non-diagnostic or normal ECGs admitted directly to the Cardiac Unit of the Royal Victoria Hospital Belfast from the Mobile Coronary Care Unit or the Accident/Emergency Department. This was a single-centre prospective study, and follow-up (3 months) was complete for all patients. Blood was assessed for quantitative cTnT, cTnI, CKMB mass and myoglobin, and qualitative cTnT on admission and at 12 h. Diagnosis of index event and incidence of new cardiac events (death, non-fatal myocardial infarction, revascularization, or readmission for unstable angina) over 3 months were assessed. Based on standard criteria, myocardial infarction occurred in 37/214 (17%), and unstable angina in 72/214 (34%). At 12 h from admission, cardiac troponins had higher sensitivity for the diagnosis of acute coronary syndromes (myocardial infarction and unstable angina) than conventional markers (cTnI 48%, cTnT 38%, CKMB mass 30% or myoglobin 27%). At 3 months, a new cardiac event had occurred in 42/214 (20%). Significantly higher event rates occurred when any of the biochemical markers was elevated, but the statistical significance was highest for patients with elevated cTnI (p < 0.0001). Whilst gender, history of ischaemic heart disease (IHD), stress test response, cTnT, cTnI, CKMB mass and myoglobin were univariate predictors, cTnI at 12 h and stress test response were the only two independent significant predictors for a subsequent cardiac event at 3 months. Raised cTnI at 12 h after admission had the highest sensitivity for the diagnosis of acute coronary syndromes, and was independently associated with a 2-3 times increased risk of future cardiac events within 3 months among patients with acute chest pain suggestive of myocardial ischaemia but with normal or non-diagnostic ECGs.     

肌钙蛋白I和T测定对急性心肌梗塞的诊断意义

目的探讨肌钙蛋白I（cTnI）和肌钙蛋白T（cTnT）测定对急性心肌梗塞（AMI）的诊断价值。方法对52例AMI患者采用免疫层析法进行检测cTnI和cTnT,以对照区和检测区均有显色带者为阳性,并作灵敏度和特异性的比较。结果以胸痛0～3h、4～6h两个时段观察其灵敏度,cTnI为56.7%和96.1%;cT-nT为50.0%和92.3%。特异性cTnI为100%和96.2%;cTnT为100%和91.6%。cTnI灵敏度高于cTnT,特异性cTnI与cTnT之间无显著性差异。结论对AMI急性胸痛患者可同时进行cTnI和cTnT检测,有利于AMI的诊断和治疗。     

心肌损伤标志物在非Q波型急性心肌梗死早期诊断中的应用

目的探讨心肌损伤标志物在非Q波型急性心肌梗死（AMI）早期诊断中的应用,减少非Q波型AMI误诊的机会。方法通过单克隆金标志双抗免疫渗滤快速分析法,动态观测心肌标志物在非Q波型AMI时的敏感性、特异性、漏诊率及诊断符合率。结果心肌肌钙蛋白I（cTnI）、肌红蛋白（Myo）、肌酸激酶-同工酶质量（CK-MB mass）对非Q波型AMI的相对敏感性为38．3％～85．1％,诊断符合率为62．1％～82．8％,均随时间增加逐渐增高;相对特异性为75．0％～100％,漏诊率为14．9％～61．7％,均随时间增加降低;心肌肌钙蛋白T（cTnT）、cTnI在不同时间均优于CK-MB mass,Myo相对敏感性在6h后迅速从85．1％下降至44．7％、12．8％,漏诊率在6h只有14．9％。结论cTnT、cTnI、Myo、CK-MBmass对非Q波型AMI的早期、快速诊断具有一定价值,其临床应用将减少非Q波型AMI误诊的机会。     

Comparative study of cardiac troponin I and T measurements in a routine extra-cardiological clinical setting.

This study compared troponin I (cTnI) to troponin T (cTnT) in a population admitted to General Medicine Divisions in whom acute myocardial infarction (AMI) was suspected; 98 consecutive patients were included. Diagnoses were made without knowledge of troponin results: 51 patients had AMI, and 47 (including 8 with unstable angina) had no AMI. Patients were considered to be troponin positive if the marker concentration was >99th percentile value of the reference population. Both troponins were associated with an almost absolute sensitivity for AMI (100% for cTnI and 98.0% for cTnT), while the specificity was marginally higher for cTnI (78.7% vs. 68.1%). Increased cTnI and/or cTnT were observed in 15 patients out of 39 without acute coronary syndromes. Simultaneous positivity was seen in 8 patients with severe disorders and complications. Discordances were more frequent in favor of increased cTnT (n = 5) than the opposite (n = 2), even if this difference did not achieve statistical significance. cTnI and cTnT detected AMI with comparable efficiency. Cases without coronary syndrome positively concordant for troponins confirmed the ability of these biomarkers to detect myocardial injury undetectable by conventional diagnostic approaches.     

心脏型脂肪酸结合蛋白对急性心肌梗死早期诊断的临床价值研究

目的探讨心脏型脂肪酸结合蛋白（H—FABP）在急性心肌梗死（AMI）早期诊断中的临床应用价值。方法将来本院的AMI疑似患者156例,按就诊时发病时间分为2组,分别在发病后0～3、3～6h内同时检测H—FABP、肌钙蛋白T（cTnT）、肌酸激酶同工酶（CK—MB）。计算各项指标的灵敏度、特异性、准确度,并进行比较分析。结果H-FABP在发病0～3h内诊断的灵敏度为70．7％,特异性为97．0％,准确度为82．4％,显著高于cTnT和CK—MB,差异有统计学意义（P〈0．05）。在发病3～6h内诊断的灵敏度为100．0％,显著高于cTnT,差异有统计学意义（P％0．05）,特异性为92．6％,准确度为97．6％。结论H—FABP是AMI早期诊断最敏感的指标,具有非常重要的临床应用价值。     

血清肌钙蛋白Ⅰ对急性心肌梗死早期诊断的临床价值

目的观察急性心肌梗死(AMI)患者入院前后血清肌钙蛋白I(cTnI),心肌肌酸激酶同工酶MB(CK-MB)测定值的变化。探讨cTnI对早期诊断AMI的价值。方法对50例AMI患者和50例健康人血清进行cTnI和CK—MB的检测。结果 AMI后3h内cTnI阳性检出率94．0％,明显高于CK-MB24．0％,AM15d后cTnI阳性84．0％,而CK-MB仅为6．0％。结论血清cTnI能早期确切诊断AMI,具有较宽的诊断窗,是急性心肌梗死早期诊断较敏感和特异的血清标志物。