Evaluation of a New Assay for Cardiac Troponin I vs Creatine Kinase-MB for the Diagnosis of Acute Myocardial Infarction

Objective : To compare a new assay for cardiac troponin I (cTn-I) with an assay for creatine kinase-MB (CK-MB) for the diagnosis of acute myocardial infarction (AMI).
Methods : A prospective cross-sectional study of patients presenting with symptoms consistent with cardiac ischemia was performed at a university teaching hospital. Serum sampling for cTn-I and CK-MB was performed at 0, 1, 3, 8, and 16 hours after presentation. Normal values were defined as CK-MB ≤ 7 ng/mL and a relative index ≤ 2%, cTn-I ≤ 1.4 ng/mL. Final diagnosis was made using World Health Organization criteria, including standard enzyme sampling. Consecutive patients with AMI were compared with a randomly selected subset of patients without AMI to determine the sensitivity and specificity of the cTn-I and CK-MB assays for AMI, stratified by time from symptom onset. The ability of the biochemical cardiac markers obtained within 6 hours of symptom onset to predict later complications or need for interventions was assessed using odds ratios (ORs).
Results : Thirty-five patients who had AMI were compared with 136 patients who did not have AMI. The sensitivities and specificities of the cTn-I and CK-MB assays, stratified by time from symptom onset, were: Patients who had elevations in either CK-MB or cTn-I within 6 hours of symptom onset were at increased risk for cardiovascular complications and/or interventions (CK-MB, OR 5.8; cTn-I, OR 6.3).
Conclusion : cTn-I was as sensitive and specific for AMI as was CK-MB in ED patients who presented within 24 hours of symptom onset. However, cTn-I was more sensitive in patients who presented ≥ 24 hours after symptom onset. Elevations of either marker within 6 hours of symptom onset predict an increased risk of complications and/or need for interventions.     

The Prognostic Significance of Troponin I and Troponin T

Abstract. Objectives : To determine and compare the prognostic abilities of early, single-sample measurements of cardiac troponin I (cTn-I), cardiac troponin T (cTn-T), creatine kinase-MB (CK-MB) among ED patients with possible myocardial ischemia. Methods : Prospective collection of clinical and serologic data using an identity-unlinked technique from patients with possible myocardial ischemia at 2 urban EDs. Outcome data concerning the occurrence of adverse events (AEs) during the 14 days after enrollment were used to calculate and compare the relative risks (RRs) and predictive values (with 95% confidence intervals) of the 3 markers for predicting AEs. Results : Among the 401 study patients, 105 AEs occurred in 67 patients. cTn-I, cTn-T, and CK-MB were all significantly predictive of AEs, with RRs of 3.87 (2.39, 6.26), 3.03 (1.92, 4.79), and 6.45 (4.74, 8.77), respectively. For prediction of AEs, sensitivity for each of the 3 markers was low (cTn-I = 15.38, cTn-T = 24.62, CK-MB = 15.38), while specificity was high (cTn-I = 97.62, cTn-T = 93.15, CK-MB = 99.70). No significant difference in predictive ability was found between cTn-I and cTn-T. However, a positive CK-MB result was a stronger predictor of AEs than either cTn-I (p = 0.01) or cTn-T (p = 0.001). Conclusions : No significant difference in predictive abilities was found between cTn-I and cTn-T. However, routine testing for both CK-MB and either of the troponins may optimize early identification of high-risk patients so they may be targeted for a higher level of care and consideration of more aggressive therapies.     

Evaluation of a Bedside Whole-blood Rapid Troponin T Assay in the Emergency Department

Objective : To evaluate the performance of a new bedside whole-blood rapid assay for cardiac troponin T (cTnT) in patients presenting to the ED with symptoms consistent with acute coronary ischemia. Methods : A prospective, observational trial was performed in 8 participating medical centers. Serial blood samples were obtained on presentation to the ED and 3 and 6 hours later. The cTnT whole-blood rapid assays were performed immediately at the site. Treating physicians and patients were blinded to the results of the rapid assays. Serum samples were analyzed at the core laboratory for serum cTnT, creatine kinase (CK)-MB, and myoglobin. The sensitivity of the rapid assay for detecting acute myocardial infarction (AMI) was compared with the sensitivities of serum cTnT, CK-MB, and myoglobin assays. Results : Of 721 patients, 102 were diagnosed as having AMI. The median elapsed time from symptom onset to ED arrival was 3 hours. The sensitivities of the rapid assay for detecting AMI were 19.6%, 59.0%, and 69.7% at 0, 3, and 6 hours, respectively. The sensitivities of the serum cTnT assay (p-values for comparison with the rapid assay for cTnT) were 25.0% (p = 0.18), 69.6% (p = 0.04), and 79.8% (p = 0.02) at 0, 3, and 6 hours, respectively. The CK-MB and myoglobin sensitivities were 21.9%, 64.5%, and 81.0%; and 43.8%, 77.4%, and 71.4%, respectively. There were 7 patients with AMI who had negative rapid assay readings and positive serum cTnT levels; 4 of these patients were enrolled at the same site. Twenty patients not diagnosed as having AMI had at least one positive rapid assay. Fourteen of these 20 patients had a diagnosis of clinically relevant cardiac disease. Conclusions : The sensitivity of this whole-blood rapid cTnT assay for detecting AMI is comparable to that of current serum assays and offers the advantage of providing rapid bedside results. Discrepancies between serum and whole-blood assays for cTnT noted in this study may indicate the need for further education for the test reader prior to patient use.     

Serum markers in the emergency department diagnosis of acute myocardial infarction

No currently used cardiac-specific serum marker meets all the criteria for an "ideal" marker of AMI. No test is both highly sensitive and highly specific for acute infarction within 6 hours following the onset of chest pain, the timeframe of interest to most emergency physicians in making diagnostic and therapeutic decisions. Patients presenting to the ED with chest pain or other symptoms suggestive of acute cardiac ischemia therefore cannot make a diagnosis of AMI excluded on the basis of a single cardiac marker value obtained within a few hours after symptom onset. The total CK level is far too insensitive and nonspecific a test to be used to diagnose AMI. It retains its value, however, as a screening test, and serum of patients with abnormal total CK values should undergo a CK-MBmass assay. Elevation in CK-MB is a vital component of ultimate diagnosis of AMI, but levels of this marker are normal in one fourth to one half of patients with AMI at the time of ED presentation. The test is highly specific, however, and an abnormal value (particularly when it exceeds 5% of the total CK value) at any time in a patient with chest pain is highly suggestive of an AMI. There have been several improvements of CK-MB assay timing and subform quantification that appear highly useful for emergency physicians. Rapid serial CK-MB assessment greatly increases the diagnostic value of the assay in a timeframe suitable for ED purposes but unfortunately still misses about 10% of patients ultimately diagnosed with acute MI. Assays of CK-MB subforms have very high sensitivity, and, although unreliable within 4 hours of symptom onset, have excellent diagnostic value at 6 or more hours after chest pain begins. Automated test assays recently have become available and could prove applicable to ED settings. The cardiac troponins are highly useful as markers of acute coronary syndromes, rather than specifically of AMI, and abnormal values at any time following chest pain onset are highly predictive of an adverse cardiac event. The ED applicability of the troponins is severely limited, however, because values remain normal in most patients with acute cardiac events as long as 6 hours following symptom onset. Myoglobin appeared promising as a marker of early cardiac ischemia but appears to be only marginally more sensitive than CK-MB assays early after symptom onset and less sensitive than CK-MB at 8 hours or more after chest pain starts. Rapid serial myoglobin assessment, however, appears highly useful as an early marker of AMI. The marker has a very narrow diagnostic window. The clinician is left with several tests that are highly effective in correctly identifying patients with AMI (or at high risk for AMI), but none that can dependably exclude patients with acute coronary syndromes soon after chest pain onset. A prudent strategy when assessing ED patients with chest pain and nondiagnostic ECGs is to order CK-MB and troponin values on presentation in the hope of making an early diagnosis of AMI or unstable coronary syndrome. Although it is recognized that normal values obtained within 6 hours of symptom onset do not exclude an acute coronary syndrome, patients at low clinical risk and having normal cardiac marker tests could be provisionally admitted to low-acuity hospital settings or ED observation. After 6 to 8 hours of symptom duration has elapsed, the cardiac-specific markers are highly effective in diagnosing AMI, and such values obtained can be used more appropriately to make final disposition decisions. At no time should results of serum marker tests outweigh ECG findings or clinical assessment of the patient's risk and stability.     

急性心肌梗死早期患者3种血清测定及意义

目的探讨血清肌酸激酶同工酶-MB(CK-MB)、肌红蛋白(Myo)和人心肌肌钙蛋白I(CTnI)检测在急性心肌梗死(AMI)早期诊断中的意义。方法以40例健康体检者作对照,检测85例高度疑为AMI的患者在发病6 h内检测3个血清指标水平。比较其对AMI诊断的性能,以进行优化组合检测。结果 AMI患者在发病6 h内,CK-MB、Myo和CTnI的敏感性分别为82.35%、100.00%和92.64%;特异性分别为94.74%、89.47%和100.00%;单项比较:敏感度和阴性预期值以Myo最高,特异度、阳性预期值和可靠性则以CTnI最佳;并联组合比较:敏感度、特异度、阳性预期值和阴性预期值均以CTnI与Myo最理想;可靠性则以CTnI与CK-MB联合最好;串联组合比较:5项指标均以CTnI与Myo串联检测为最佳。结论血清CTnI在AMI早期诊断中具有良好的灵敏度、特异性和可靠性。CTnI和Myo联合检测可提高对AMI早期诊断的性能。     

Validation of NACB and IFCC guidelines for the use of cardiac markers for early diagnosis and risk assessment in patients with acute coronary syndromes

BACKGROUND: International guidelines have been established for the use of cardiac markers in the early diagnosis and risk assessment of patients with acute coronary syndromes. METHODS: A single center, prospective observational study was conducted in a tertiary care university hospital on 200 consecutive patients with suspected acute myocardial infarction (AMI). Blood was drawn on admission and after 2, 4, 8, 12 and 24 h for the measurement of CK-MB/CK activity, myoglobin, CK-MB mass and troponin I. A 6-week follow-up was undertaken for the combined end point of acute coronary syndrome and death. RESULTS: Myoglobin showed an early diagnostic sensitivity of 0.65 on admission, 0.90 after 2 h and 0.92 after 4 h compared with 0.46, 0.74 and 0.88 for CK-MB/CK activity. The combination of myoglobin and cTnI increased the diagnostic value compared with myoglobin alone on admission, 2 and 4 h later. In multivariate analysis, cTnI and CK-MB/CK mass, but not myoglobin and CK-MB/CK activity, were shown to be independent predictors on the 6-week follow-up. CONCLUSIONS: Repetitive myoglobin measurements within 4 h of admission, combined with at least one early troponin test, was shown to be the strategy of choice in early AMI diagnosis and prognosis assessment.     

Time-course of cardiac troponin I release from isolated perfused rat hearts during hypoxia/reoxygenation and ischemia/reperfusion.

The study was designed to determine the time-course of cardiac troponin I (cTn-I) release in isolated and Langendorff-perfused rat hearts during hypoxia and reoxygenation (H/Reox), and after various durations of total ischemia and subsequent reperfusion (I/R). For this purpose, in H/Reox, cTn-I was measured with the conventional Access immunoassay (ng/ml) and a new immunoassay which operates at pg/ml, and compared with creatine kinase (CK), lactate dehydrogenase (LD) and cardiac troponin T (cTn-T). In I/R, cTn-I was compared with CK and LD. The anti-Tn-I mAbs used in cTn-I assays cross-react with cTn-I of the rat. A clear difference between time-courses and concentration levels of cTn-I in I/R and H/Reox models was found. In I/R, maximum release of cTn-I, CK and LD similarly occurred within minutes following reperfusion; however cTn-I did not return to baseline values. cTn-I levels were not linked to the duration of ischemia. In I/R, we were only able to detect small cTn-I concentrations. In H/Reox experiments, cTn-I, CK and LD increased time-dependently. We found higher cTn-I maximal peak levels detected with the Access immunoassay than with the new assay (median, 0.346 ng/ml per min/g dry wt vs 132 pg/ml per min/g dry wt). cTn-T maximal concentrations were lower than maximal cTn-I levels (median, 0.117 ng/ml per min/g dry wt). Time-courses of cTn-I release were roughly similar with both assays in the H/Reox model (r = 0.90). These data indicate that the cTn-I time-course is related to experimental model (I/R or H/Reox), but also likely depends on the sensitivity of cTn-I assays in such experimental conditions.     

Cardiac markers protocols in a chest pain observation unit

The use of cardiac markers to identify high-risk patients in the observation unit is undeniable. As the literature reviewed here reveals, the history and ECG miss a significant portion of patients with acute cardiac ischemia. It appears that acute MI and some high-risk "unstable angina" observation unit patients can be identified within 6 hours of hospital presentation using a combination of cardiac markers. Testing these patients soon after symptom onset or on arrival in the ED for myoglobin, CK-MB subforms, or CK-MB delta appears to provide the best diagnostic usefulness. For testing later in the clinical course, CK-MB troponin I, or troponin T are of clear diagnostic and prognostic value. The markers currently used are unable to identify the significant subset of patients with "non-AMI" coronary syndromes, however. These patients require further testing with appropriate noninvasive or invasive diagnostic studies.     

Evaluation of a new automated system for the determination of ck-mb isoforms

We evaluated a new analyzer (Cardio REP) specifically designed for cardiac CK-MB isoenzyme and isoforms activity, with a performance time of 24 minutes. Ten AMI patients, with times elapsed between the onset of chest pain and admission to hospital ranging from 30 minutes to 4 hours, were monitored every 3–4 hours until the 16th hour of hospitalization. In each serum sample, in addition to total CK-MB and CK-MB isoforms measured by the Cardio REP analyzer, we also assayed total CK activity, CK-MB activity by immunoinhibition method, CK-MB mass concentration, CK-MB isoforms by REP method, troponin T, and myoglobin. The precision study demonstrated acceptable within assay and between assay CVs% for total CK-MB (8.1 and 10.4), MB₁ (9.1 and 14.2), and MB₂ (9.1 and 8.2) isoforms. The method was found to be linear up to 371 U/L for MB₂ isoform fraction and up to 516 U/L for total CK-MB. Results for CK-MB obtained with the Cardio REP correlated well with those for CK-MB activity obtained with the immunoinhibition method (r = 0.869) and those of CK-MB mass concentration (r = 0.923). The sensitivity of the Cardio REP CK isoforms method was found to be greater than that of the REP CK isoforms method. Time to first increased value of MB₂/MB₁ ratio and MB₂ isoform was earlier in comparison to that for CK-MB mass concentrations and similar to that for myoglobin, a marker that, however, lacks specificity. The diagnostic efficiency of CK-MB isoforms and the availability of a real-time, fully automated method for their measurement suggest the utilization of this biochemical marker in emergency for the early diagnosis of AMI.     

Elevation of creatine kinase in acute severe asthma is not of cardiac origin

OBJECTIVE: To study prospectively if, when plasma creatine kinase (CK) and plasma myoglobin are elevated, the origin of these abnormalities is cardiac or not, by measuring cardio-specific troponin T (cTT). METHOD: Fifteen patients with acute severe bronchial asthma (ASBA) were prospectively studied in the intensive care unit (ICU) with continuous electrocardiograph (ECG). Plasma CK, CK-MB, myoglobin and cTT were measured at 0, 4, 8, 12, 16 and 20 h in the ICU. RESULTS: Five out of 15 ASBA patients had elevated CK, four of them presenting with an increase in CK-MB. Plasma cTT was normal in every patient, including those with CK and/or myoglobin elevation. At admission to the ICU, myoglobin and CK were positively correlated (r = 0.760; p < 0.001). No patient was intubated. There was no difference in clinical signs or symptoms, medical history, laboratory values or ECG in patients with or without CK elevation. CONCLUSION: Patients admitted to an ICU for ASBA may present with an elevation of plasma CK, CK-MB and myoglobin not related to any heart injury. CK and CK-MB are not good markers of myocardial injury in ASBA patients due to the multitude of potential confounders. Therefore, troponin should be measured instead.     

The sensitivity of cardiac markers stratified by symptom duration

We compared the sensitivity of three commonly used cardiac markers between two subpopulations, those who came to the Emergency Department (ED) late (6–24 h) after their symptoms began, and those who arrived earlier (<6 h), in a prospective comparative trial. Among all adult patients who presented to our ED with symptoms suggestive of acute myocardial infarction (MI), we drew serum for myoglobin, CK-MB, and troponin I upon arrival (time 0) and 2 h later. Outcomes, including acute MI, were determined. Sensitivities for all three markers between the subpopulations who arrived fewer than 6 h from symptom onset were compared to those who arrived later (6–24 h). We enrolled 346 eligible subjects, 36% of whom described cardiac symptoms as beginning 6 or more hours earlier; 14% suffered acute MIs. For time 0, the sensitivity of all three markers for acute MI was significantly higher among those subjects with symptoms of 6 or more hours’ duration as compared to those with less. For troponin I, the increase in sensitivity between these two subpopulations approached 300%. At the time of the 2-h sample, the differences in sensitivities were much less and were not statistically significant. We conclude that cardiac marker values obtained at time 0 among Emergency Department patients who arrive 6 or more hours after cardiac symptom onset provide significantly higher sensitivities as compared to those obtained in patients who arrive earlier. For troponin I, the increase in sensitivity approaches threefold.     

Serial Myoglobin Levels for Patients with Possible Myocardial Infarction

Objectives: To determine the sensitivity and specificity of a new myoglobin assay for acute myocardial infarction (AMI), considering both the total amount of serum myoglobin and its percentage change over 2 hours.
Methods: A prospective, observational test performance study for the recognition of AMI was done using serial myoglobin assays of 42 admitted chest pain patients at a large, urban teaching hospital ED. Myoglobin testing was performed at presentation (time 0) and at 1 and 2 hours after arrival. A myoglobin level >100 g/L (ng/mL) or a change >50% from baseline (increase or decrease) any time during the 2–hour period was considered positive. Patients and their physicians were blinded to the myoglobin results. The managing clinician's final diagnosis of the presenting event was used as the diagnostic criterion standard.
Results: The sensitivity of the myoglobin technique for detection of AMI in the first hours in the ED was 13/14 (93%; 95% CI: 66–100%). The 1 patient who had a false-negative test had evidence of AMI on the ECG and an initially abnormal creatine kinase-MB (CK-MB) assay. The specificity was 22/28 (79%; 59–92%). However, of the 6 patients who had "false-positive" myoglobin tests, all had serious illness: significant cardiac disease (n = 4), in-hospital death (n = 1), or deep venous thrombosis (n = 1).
Conclusion: Myoglobin level determinations are sensitive tests to detect AMI during the first 2 hours of a patient's stay in the ED and may complement current clinical tools.     

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.     

心型脂肪酸结合蛋白在急性心肌梗死早期诊断中的价值

目的探讨血清心型脂肪酸结合蛋白(H-FABP)在急性心肌梗死(AMI)早期诊断中的临床应用价值。方法随机选择110例临床疑似AMI胸痛患者,采用时间分辨免疫荧光测定法(TRIFA)检测患者入院即刻血清中H-FABP含量,并与心肌肌钙蛋白I(cTnI)、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、超敏C反应蛋白(hsCRP)和肌红蛋白(MYO)进行比较;对11例患者入院即刻和入院6 h后进行动态分析;以60例体检健康者作对照,绘制各心肌损伤标志物受试者工作特征(ROC)曲线并进行曲线下面积(AUC)比较,分析6种心肌损伤标志物诊断早期AMI的敏感度和特异度。结果 AMI患者入院即刻各心肌损伤标志物的AUC由大到小依次为H-FABP、hsCRP、cTnI、CK-MB、CK和MYO,最佳临界值诊断灵敏度分别为85.0%、78.7%、81.3%、73.8%、72.5%和61.3%,特异度分别为93.3%、95.0%、93.3%、100.0%、100.0%、98.3%。H-FABP的AUC与hsCRP、cTnI比较差异无统计学意义(P>0.05),与CK-MB、CK、MYO比较差异有统计学意义(P<0.05)。H-FABP诊断早期AMI的阳性率达85.0%。结论 H-FABP对于AMI早期诊断具有相对较早的检测窗口期和相对较好的特异度,在时效性、灵敏度和特异度等方面具有综合优势,可作为AMI早期诊断或排除诊断的血清标志物。多项心肌损伤指标联合检测可提高AMI实验室诊断的灵敏度、特异度及准确性。     

Release kinetics of serum cardiac troponin i in ischemic myocardial injury

Objectives: The study was undertaken to evaluate the release kinetics of cardiac troponin I (c-cTn-I) in ischemic myocardial injury.

Design and Methods: The reference range for cTn-I was established by determination of cTn-I in sera and plasma obtained from 622 healthy volunteers (Group 1). cTn-I was compared to: (a) Creatine kinase (CK) MB mass and myoglobin in 12 patients with severe skeletal muscle damage (Group 2); (b) CK-MB activity in 48 patients with myocardial infarction (MI) receiving intravenous thrombolysis (Group 3) (in this group, an additional 43 patients with MI were analyzed separately to characterize cTn-I patterns in thrombolyzed and nonthrombolyzed populations); and in 44 patients with unstable angina (Group 4).

Results: In Groups 1 and 2, no positive results (0.1 μg/L) were obtained. In Group 3, the time-courses of cTn-I were mostly monophasic in form. A pathologic increase occurred earlier in cTn-I than in CK-MB activity (p = 0.0002); the period with increased cTn-I was longer (p = 0.001), the overall sensitivity of cTn-I (93.9%) was higher than that of CK-MB activity (p = 0.00001). cTn-I was more sensitive at admission (p = 0.0004). In additional patients, the cTn-I peak occurred and cTn-I disappeared significantly later in nonthrombolyzed than in the thrombolyzed group. In Group 4, positive tests results were detected in 45% of patients for cTn-I, 16% for CK-MB activity, and 32% for CK-MB mass.

Conclusions: The cTn-I assay appears to be ideally suited for the detection of ischemic myocardial injury in complex clinical situations because of its high specificity; cTn-I indicates myocardial tissue damage in patients with unstable angina and is superior to CK-MB activity and mass in this respect.     

依达拉奉注射液对急性心肌梗死再灌注损伤的保护作用

目的探讨依达拉奉对急性心肌梗死(AMI)溶栓后再灌注损伤的影响。方法 72例AMI患者被随机分为治疗组(n=37)与对照组(n=35)。观察2组再灌注心律失常发生率,测定治疗后2 h、24 h磷酸肌酸激酶同工酶(CK-MB)、心肌肌钙蛋白I(cTnI)。结果 2组治疗后24 h CK-MB2、h、24 h cTnI均有显著性差异。结论在常规抗心肌缺血治疗基础上加用依达拉奉,可明显减轻再灌注损伤,改善AMI患者的生存率及预后。     

心肌标志物检测在早期诊断急性心肌梗死中的价值

目的探讨胶体金免疫层析法检测血清肌钙蛋白Ⅰ、肌酸激酶同工酶（CK-MB）、肌红蛋白在急性心肌梗死（AMI）患者早期不同时间段的诊断价值。方法收集该院2011年1月至2012年12月收治的89例AMI病例,根据发病时间分为两组,2～〈6h组42例,6～12h组为47例,非心肌梗死对照组70例。采用血清肌钙蛋白Ⅰ、CK-MB、肌红蛋白三合一诊断试剂对选取的病例进行测定。结果AMI患者肌钙蛋白Ⅰ、CK-MB、肌红蛋白的阳性率均高于对照组（P〈0．05）,在2～〈6h时间段内三者的敏感度分别为35．7％、64．3％、52．4％,均低于6～12h时间段的48．9％、85．1％、76．6％,结果差异有统计学意义（P〈0．05）。CK-MB用于诊断的敏感度在两个时间段内分别为：64．3％、85．1％,较肌钙蛋白I（35．7％、48．9％）、肌红蛋白（52．4％、76．6％）高,差异有统计学意义（P〈0．05）,而肌红蛋白敏感度较肌钙蛋白Ⅰ高（P〈0．05）。将三者联合测定时,阳性率高于单独测定时的阳性率,2～6h组阳性率为69．0％,6～12h组阳性率为89．4％。结论在AMI早期,肌钙蛋白Ⅰ、CK-MB、肌红蛋白单独测定阳性率较低,不能满足临床需要,而采用胶体金法心肌三合一诊断试剂盒,对肌钙蛋白Ⅰ、CKMB、肌红蛋白进行联合测定能提高AM1的早期诊断阳性率,以便为临床提供可靠的实验信息,及时采取有效的治疗措施,从而降低患者的病死率。     

心肌标志物作用的系统分析

目的：获取心肌生化标记物的最佳应用证据。方法：查循、浏览对心肌肌酸激酶同工酶MB（CK－MB）、肌红蛋白、心肌肌钙蛋白T（cTnT）和心肌肌钙蛋白I（cTnI）用于诊断心肌梗塞（MI）和对急性冠状动脉综合症分级的系统评价和Meta－分析的文献资料。结果：在症状发生后的12－48小时采样分析CK－MB质量对于诊断MI的临床灵敏度和牧场划性分别是98．8％和89．6％。肌红蛋白有高的阴性预示值,在症状发生后的2－6小时采样分析有高的临床灵敏度。在症状发生后的12采样cTnI,诊断MI的临床灵敏度和特异性分别是98．2％和68．8％,其临床特异性降低与检测到微小心肌受损有关。结论：cTnT和cTnI比CK－MB对诊断心肌梗死和预测急性冠状动脉综合症危险性更有价值。     

乳酸评价急性胸痛的临床研究

目的　检验乳酸诊断急性心肌梗死(AMI)及判断危重心脏病患者预后的假说。方法　急性胸痛或其它典型AMI症状的患者检测静脉血乳酸。高于2.0mmol/L作为急性心脏疾病的预测值。同时检测心肌磷酸激酶(CK)和同工酶(CK-MB),记录ECG。结果　全部114例患者,65例乳酸高于2.0mmol/L。25例(22%)确诊为急性心肌梗死(AMI),其乳酸为2.7±0.7mmol/L。而Non～AMI乳酸为2.2±0.8mmol/L(P＜0.05)。乳酸诊断AMI的敏感性为96%(95%CI为89%～100%),特异性为55%(95%CI为45%～64%),乳酸阴性预计值为96%(95%CI为89%～100%)。胸痛患者乳酸升高的平均时间为发病3h以内。死亡或要求ICU治疗48h以上的患者其乳酸也明显升高,与不要求ICU治疗者比较其乳酸分别是5.0±4.3mmol/L比1.9±0.6mmol/L(P＜0.01)。结论　乳酸对AMI具有较高的阴性预计值,高乳酸血症与急性心脏病患者病死率及要求住院有明显的相关性。     

肌钙蛋白Ⅰ与CK-MB联合检测对急性心肌梗死的诊断价值

目的探讨肌钙蛋白I(cTnI)与CK-MB联合检测对急性心肌梗死(AM I)的临床诊断价值。方法采用罗氏电发光2010自动生化分析仪和日立7180生化分析仪,测定62例AM I患者、50例健康体检者血清的cTnI、肌酸激酶(CK)和CK-MB,并对结果进行统计学分析。结果AM I组血清cTnI、CK和CK-MB高于正常对照组(P<0.01)。cTnI与CK-MB联合检测阳性率为96.7%,高于前三者,且动态检测对早期AM I敏感性更高、阳性持续时间更长。结论肌钙蛋白I与CK-MB联合检测能提高早期急性心肌梗死的检出率,具有更宽的诊断时间窗。