Early Diagnostic Efficiency of Cardiac Troponin I and Troponin T for Acute Myocardial Infarction

Objective : To compare the early diagnostic efficiency of the cardiac troponin I (cTn-I) level with that of the cardiac troponin T (cTn-T) level, as well as the creatine kinase (CK), CK-MB, and myoglobin levels, for acute myocardial infarction (AMI) in patients without an initially diagnostic ECG presenting to the ED within 24 hours of the onset of their symptoms. Methods : A prospective, observational, cohort study was performed involving chest pain patients admitted to a large urban community hospital. Participants were consecutive consenting ED chest pain patients ≥30 years of age. Exclusions included duration of symptoms >24 hours, inability to complete data collection, receipt of CPR, and ST-segment elevation on the initial ECG. Measurements included levels of cTn-I, cTn-T, CK, CK-MB, and myoglobin at the time of presentation and 1, 2, 6, and 12–24 hours after presentation as well as presenting ECG and clinical follow-up. Confirmation of the diagnosis of AMI was based on World Health Organization criteria. Results : Of the 177 patients included in the study, 27 (15%) were diagnosed as having AMIs. The sensitivities of all 5 biochemical markers for AMI were poor at the time of ED presentation (3.7–33.3%) but rose significantly over the study period. The sensitivity of cTn-T was significantly better than that of cTn-I over the initial 2 hours, but both markers' sensitivities were low (<60%) during this time frame. The cTn-I was significantly more specific for AMI than was the cTn-T, but not significantly better than CK-MB or myoglobin. Likelihood ratio analysis showed that the biochemical markers with the highest positive likelihood ratios for AMI during the first 2 hours following ED presentation were myoglobin and CK-MB. From 6 through 24 hours, the positive likelihood ratios for cTn-I, CK-MB, and myoglobin were superior to those of CK and cTn-T. Conclusions : cTn-I, CK-MB, and myoglobin are significantly more specific for AMI than are CK and cTn-T. Myoglobin is the biochemical marker having the highest combination of sensitivity, specificity, and negative predictive value for AMI within 2 hours of ED presentation. Neither cTn-I nor cTn-T offers significant advantages over myoglobin and CK-MB in the early (≤2 hours) initial screening for AMI. The cardiac troponins are of benefit in identifying AMI ≤6 hours after presentation.     

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.     

Comparison of the diagnostic value of cardiac troponin I and T determinations for detecting early myocardial damage and the relationship with histological findings after isoprenaline-induced cardiac injury in rats

Cardiac troponins I (cTnI) and T (cTnT) have been shown to be highly sensitive and specific markers of myocardial cell injury. The purpose of this study was to investigate the diagnostic value of cTnI and cTnT with regard to creatine kinase (CK) and lactate dehydrogenase (LD) and to determine whether they can be used for early diagnosis of myocardial damage in rats, and to examine the relationship between cTnl and cTnT release with histological examinations, using isoprenaline-induced cardiac muscle damage as an experimental model in the rat. Eighteen Wistar rats per group were treated with a single dose of either isoprenaline (iso) or with normal saline as a control group. The anti-cTnI and cTnT monoclonal antibodies (mAbs) employed in the cTnI (Access) and cTnT (Elecsys) assays cross-react with cTnI and cTnT of the rat. A highly significant rise of cTnl or cTnT was found already 2 h after iso. The time-courses of cTnI and cTnT were monophasic in form. The highest cTnI (mean+/-S.D., 1.1+/-2.3 ng/ml) and cTnT (mean+/-S.D. 3.6+/-30 ng/ml) were found 4 h after iso. cTnI and cTnT significantly increased in iso-treated rats in comparison with controls whether the differences between 2-, 4- and 6-h levels and basal levels were considered or not. The areas under cTnl and cTnT curves (AUC) (0-6 h) and the maximal cTnI and cTnT (0-6 h) after iso were significantly different from the controls. For CK and LD, no elevation in comparison with controls could be detected (except a trend for LD whether or not the difference between 6-h levels and basal levels were considered (P=0.08) and for LD AUC (0-6 h) (P=0. 059)). Correlations between maximal cTnI and cTnT and AUC were 0.69 (P=0.0001) and 0.60 (P=0.0066), respectively. Histological examinations of iso-treated rats revealed acute focal or multifocal myofibrillar degeneration of the myocardial tissue in ten out of 14 rats and showed the earliest alterations 4 h after iso in one treated rat. Only four of the controls exhibited evidence of mild changes and slight mononuclear cell infiltration. cTnl and cTnT peak values to at least 0.35 and 1.3 ng/ml, respectively, were necessary to detect histological myocardial cell injury after iso. cTnI and cTnT were found to be early markers for diagnosing iso-induced myocardial damage in comparison with CK and LD. Elevations of cTnI and cTnT appeared to relate to the severity of histologic changes after myocardial injury. Although there was a difference in the absolute concentration of results between cTnI and cTnT assays, due to a lack of standardization and heterogeneity in the cross-reactivities of mAbs to various troponin I and T forms, cTnI and cTnT can be used as easily measurable target parameters for detection of cardiotoxic and/or cardiodegenerative effects in rats.     

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.     

Lipoprotein(a) levels in patients with unstable angina and their relationship with atherothrombosis and myocardial damage

The aim of the study was to compare lipoprotein(a) [Lp(a)] levels in patients with cTroponin-I (cTn-I)-positive or -negative unstable angina and to investigate their relationship with atherothrombosis. A total of 202 consecutive patients were enrolled in the study. Lp(a), fibrinogen, plasminogen, PAI-1 and t-PA levels were measured and C-reactive protein (CRP) assays were performed on admission for all patients, and venous blood samples were drawn 12 and 24 h later for cTn-I measurements. The patients were divided into cTn-I-negative (cTn-I < 1 ng/ml) and -positive (cTn-I > or = 1 ng/ml) unstable angina groups. Lp(a) levels of the cTn-I-positive patients were higher than those of the cTn-I-negative patients (52.9 +/- 6.0 and 15.7 +/- 2.5 mg/dl, p < 0.0001). There was a positive correlation between Lp(a) and cTn-I levels (r = 0.692; p = 0.0001). Increase in coagulation activity and impairment in fibrinolytic activity were significant in the cTn-I-positive patients. Elevated Lp(a) levels may have a role in the development of myocardial damage in patients with unstable angina.     

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.     

Evaluation of the analytical performance of the advanced method for cardiac troponin I for the AxSYM platform: comparison with the old method and the Access system.

BACKGROUND: The determination of cardiac troponins is routinely used for rule in/out, risk stratification, and follow-up of patients with acute coronary artery syndrome. We evaluated the analytical and clinical performance of the advanced immunoassay for troponin I (cTnI) carried out on an AxSYM platform (Abbott Diagnostic Division) and compared these characteristics to those of the previous version of this assay and to cTnI on the Access 2 immunoassay system (Beckman Coulter, Inc.). METHODS: We assayed plasma samples from healthy subjects (n=66) and cardiac patients (n=132) using AxSYM Plus system assays called the old (OLD AxSYM) and advanced TnI (ADV AxSYM) methods and using an Access system. RESULTS: An improvement in analytical sensitivity (detection limit) was observed for the advanced cTnI AxSYM compared to the previous method (0.014 vs. 0.31 microg/L), while the cTnI value for the 10% CV (i.e., functional sensitivity) was 0.41 microg/L for the ADV and 1.9 microg/L for the OLD method. The kinetics of cTnI release was similar, as evaluated in 25 patients with typical acute myocardial infarction (AMI). A close linear relationship was found between the two methods on the AxSYM system (OLD cTnI=7.436+6.858 ADV cTnI; R=0.968, n=214) and with the Access system (OLD AxSYM=7.154+7.9 Access, R=0.876, n=158; ADV AxSYM=0.23+1.209 Access, R=0.927, n=160). However, wide bias was found between the OLD and ADV AxSYM methods (mean difference 118.4 microg/L, p<0.0001), while more similar results were found between the ADV AxSYM and Access methods (mean difference 2.6 microg/L, corresponding to a mean percentage difference of 17%, p<0.0001). In 106 patients with symptomatic rheumatoid arthritis with high rheumatoid factor (RF) concentration, the mean cTnI measured by the ADV AxSYM method was 0.009+/-0.031 mug/L (range 0-0.23 microg/L) with a significant correlation (R=0.316, p=0.001) between cTnI and RF values. Furthermore, in 60 of these serum samples the cTnI concentration was also measured using the Access method; significant correlation with the values found by the ADV AxSYM method was observed (R=0.468, p=0.0002). CONCLUSIONS: The present study indicates that the AxSYM Troponin-I ADV immunoassay shows improved analytical sensitivity compared to the OLD AxSYM method, as well as very similar clinical results to those determined using the Access method.     

血清心肌肌钙蛋白-I、肌酸激酶同工酶对新生儿缺氧缺血性脑病心肌损伤的诊断价值

目的 探讨血清心肌肌钙蛋白I（CTn-I）、肌酸激酶（CK）、肌酸激酶同工酶（CK-MB）及CK-MB／CK对新生儿缺氧缺血性脑病（HIE）患儿心肌损伤的诊断价值。方法 对2001年8月至2003年12月78例HIE患儿与对照组同期入住新生儿病房26例无缺氧性脑痛的患儿于出生后18～24h取血，分别用快速固相免疫层析法、NAC-免疫抑制法、NAC法测定血清CTn-I、CK、CK-MB并计算CK-MB／CK值。结果 对照组、轻、中、重HIE四组患者间血清CTn-I、CK、CK-MB有显著性差异（P〈0．05）。其中3例重度HIE伴阵发性室性心动过速，CTn-I〉125ng／L；而CK-MB虽有升高，但无明显差异；CK-MB／CK值在各组中无明显差异。结论 重视对HIE患儿心脏功能的监测与治疗，对改善患儿的预后具有非常重要的意义，在评价HIE患儿心肌损伤时，CTn-I是比CK-MB及CK更敏感、更具有特异性的指标，所以CK-MB／CK不宜作为HIE患儿心肌损伤的生化指标。     

Performance evaluation of a new chemiluminescent cardiac troponin I assay

Cardiac troponin I is a marker for diagnosis of myocardial damage. Several immunoassays are currently available for determination of concentrations of troponin I in serum. We evaluated a chemiluminescent assay for troponin I using ACS:180 automated analyzer (Bayer Diagnostics). We compared our results with two other immunoassays using the OPUS Magnum (OPUS troponin I assay, Dade Behring) and AxSYM (microparticle enzyme immunoassay, Abbott) analyzers. The within-run and between-run CVs were less than 5% for all three levels of controls. The chemiluminescent assay for troponin I was linear up to a serum troponin I concentration of 50 ng/mL and the detection limit was 0.1 ng/mL of troponin. A good correlation between troponin I concentration measured by the chemiluminescent assay (y axis) and the microparticle enzyme immunoassay (MEIA) (x axis) was observed, although the concentrations of troponin I in individual specimens were approximately four times higher, when measured by the MEIA assay, than those measured by chemiluminescent assay. The correlation coefficient was 0.98 with the regression equation y = 0.22x + 1.125. We also observed a good correlation in troponin I concentrations obtained by the chemiluminescent assay (y axis) and OPUS troponin I assay (x axis). The correlation coefficient was 0.96 and the regression equation was y = 0.79x - 0.52. The correlation coefficient was 0.93 when we compared troponin I concentrations obtained by the OPUS assay (x axis) with the corresponding concentrations obtained by the MEIA assay (y axis). The corresponding regression equation was y = 0.25x + 3.5. We conclude that the chemiluminescent troponin I assay showed good analytical performance.     

The influence of cardiopulmonary resuscitation without defibrillation on serum levels of cardiac enzymes: a time course study of out-of-hospital cardiac arrest survivors

BACKGROUND: The serum concentration of cardiac enzymes may be influenced by mechanical and electrical trauma due to cardiopulmonary resuscitation (CPR) attempts. This could complicate the determination of whether an acute myocardial infarction (AMI) had occurred. In this study, only patients without any of the known confounding factors affecting cardiac enzyme release were included, and the specific time course and patterns of serum cardiac enzyme levels after resuscitation were evaluated. The purpose is to help clinicians distinguish between spontaneous myocardial damage and that induced by CPR. METHODS AND RESULTS: This prospective, observational study was performed in the emergency department on eight patients surviving cardiac arrest. They were selected for not having heart disease, chest trauma or septic shock; and not receiving defibrillation. The median (range) duration of return of spontaneous circulation (ROSC) was 13 min (5-30 min). Cardiac enzyme measurements were taken immediately after ROSC and every 6h thereafter. Although cardiac troponin I (cTnI) level reached as high as 62.6 ng/ml at 24 h in one patient, five of the eight (62.5%) patients had their cTnI level fall below the normal reference range (i.e. 2 ng/ml) by 30 h. The time to maximum and peak concentration of cTnI was 16.50+/-10.99 h and 16.85+/-21.50 ng/ml, respectively. Both MB creatine kinase (CKMB) and total creatine kinase (CK) levels were above their normal reference ranges. In addition, the CKMB/CK ratio exceeded 5% in all patients at any time point during this study. CONCLUSION: In this study, the influence of resuscitative procedures - defibrillation excluded - on the release of cardiac enzymes were examined. During 30 h after ROSC cTnI level exhibited a bell-shaped configuration, which is distinct from that after AMI; whereas the enzymatic activities of CKMB and CK, as well as CKMB/CK ratio, were constantly higher than normal. This chronological pattern of cardiac enzyme levels may help physicians differentiate primary cardiac disease from other aetiologies in out-of-hospital cardiac arrests.     

Negative interference of bilirubin and hemoglobin in the MEIA troponin I assay but not in the MEIA CK-MB assay

Troponin I is a sensitive and specific marker for the diagnosis of myocardial infarction. Several commercially available immunoassays measure the concentration of troponin I in serum. The microparticle enzyme immunoassay (MEIA) for troponin I (Abbott Laboratories, Abbott Park, IL) is widely used in clinical laboratories, including our hospital laboratory. We studied the effect of bilirubin and hemolysis on the MEIA for troponin I and compared our assay with a newly available chemiluminescent assay (CLIA) for troponin I (Bayer Diagnostics, Tarrytown, NY). We also measured CK-MB concentration using the MEIA CK-MB assay. One serum pool was prepared by combining several specimens of one patient with elevated troponin I and with a diagnosis of myocardial infarction. Other serum pools were prepared by combining sera with similar troponin I values. All serum pools showed normal bilirubin concentrations and had no hemolysis. Then we supplemented aliquots of serum pools with various concentrations of bilirubin (5.0, 10.0, 15.0, and 20.0 mg/dL). After supplementation, troponin I concentrations were measured again using the MEIA and CLIA. We observed a statistically significant decrease in troponin I concentration in the presence of bilirubin with the MEIA. For example, in serum pool 1, the troponin I concentration was 16.3 (bilirubin: 0.8 mg/dL). In the presence of 5.0, 10.0, 15.0 and 20.0 mg/dL of added bilirubin, the cardiac troponin I concentrations were 13.9, 13.4, 13.3 and 13.0 ng/ml respectively. We observed similar negative interference of bilirubin in troponin I measurement by the MEIA in other pools. The troponin I value decreased slightly (not statistically significant) in one pool and did not change in two other pools in the presence of bilirubin when we measured troponin I concentration using the CLIA. Interestingly, bilirubin did not interfere with the MEIA CK-MB assay. Moderate hemolysis did not have any effect on the troponin I assay using either the MEIA or CLIA. However, gross hemolysis (hemoglobin > 40 mg/dL) interfered with both assays for troponin I.     

Different collection tubes in cardiac biomarkers detection

The role played by different collection tubes is one of the more frequently forgotten parameters, which influences the quality of laboratory results. We aimed to determine whether there is a significant difference in assay of myoglobin, cardiac troponin I, and CK‐MB depending on the presence of anticoagulant and gel separator in the collecting tubes. Blood samples were collected in 40 consecutive patients admitted for acute coronary syndrome. The samples were taken at the same moment in three different tubes (tubes without anticoagulant and with gel separator, heparin tubes with gel separator and heparin tubes without gelseparator;Venosafe, Terumo Europe, Leuven Belgium). Myoglobin, CK‐MB and cardiac troponin I were measured with a double side (sandwich) chemiluminescent immuenzymatic assay (Access Myoglobin, Access CK‐MB, Access AccuTnI). Cardiac troponin I was not influenced by the type of collection tube used. On the contrary, myoglobin and CK‐MB showed a statistical difference depending on the test tube. In particular, there was a significant difference between tubes without anticoagulant and with gel separator and tubes with heparin and without gel. J. Clin. Lab. Anal. 22:391–394, 2008. © 2008 Wiley‐Liss, Inc.     

Evaluation of cardiac troponin I and T levels as markers of myocardial damage in doxorubicin-induced cardiomyopathy rats,and their relationship with echocardiographic and histological findings

BACKGROUND: Cardiac troponins I (cTnI) and T (cTnT) have been shown to be highly sensitive and specific markers of myocardial cell injury. We investigated the diagnostic value of cTnI and cTnT for the diagnosis of myocardial damage in a rat model of doxorubicin (DOX)-induced cardiomyopathy, and we examined the relationship between serial cTnI and cTnT with the development of cardiac disorders monitored by echocardiography and histological examinations in this model. METHODS: Thirty-five Wistar rats were given 1.5 mg/kg DOX, i.v., weekly for up to 8 weeks for a total cumulative dose of 12 mg/kg BW. Ten rats received saline as a control group. cTnI was measured with Access(R) (ng/ml) and a research immunoassay (pg/ml), and compared with cTnT, CK-MB mass and CK. By using transthoracic echocardiography, anterior and posterior wall thickness, LV diameters and LV fractional shortening (FS) were measured in all rats before DOX or saline, and at weeks 6 and 9 after treatment in all surviving rats. Histology was performed in DOX-rats at 6 and 9 weeks after the last DOX dose and in all controls. RESULTS: Eighteen of the DOX rats died prematurely of general toxicity during the 9-week period. End-diastolic (ED) and end-systolic (ES) LV diameters/BW significantly increased, whereas LV FS was decreased after 9 weeks in the DOX group (p<0.001). These parameters remained unchanged in controls. Histological evaluation of hearts from all rats given DOX revealed significant slight degrees of perivascular and interstitial fibrosis. In 7 of the 18 rats, degeneration and myocyte vacuolisation were found. Only five of the controls exhibited evidence of very slight perivascular fibrosis. A significant rise in cTnT was found in DOX rats after cumulative doses of 7.5 and 12 mg/kg in comparison with baseline (p<0.05). cTnT found in rats after 12 mg/kg were significantly greater than that found after 7.5 mg/kg DOX. Maximal cTnI (pg/ml) and cTnT levels were significantly increased in DOX rats compared with controls (p=0.006, 0.007). cTnI (ng/ml), CK-MB mass and CK remained unchanged in DOX rats compared with controls. All markers remained stable in controls. Analysis of data revealed a significant correlation between maximal cTnT and ED and ES LV diameters/BW (r=0.81 and 0.65; p<0.0001). A significant relationship was observed between maximal cTnT and the extent of myocardial morphological changes, and between LV diameters/BW and histological findings. CONCLUSIONS: Among markers of ischemic injury after DOX in rats, cTnT showed the greatest ability to detect myocardial damage assessed by echocardiographic detection and histological changes. Although there was a discrepancy between the amount of cTnI and cTnT after DOX, probably due to heterogeneity in cross-reactivities of mAbs to various cTnI and cTnT forms, it is likely that cTnT in rats after DOX indicates cell damage determined by the magnitude of injury induced and that cTnT should be a useful marker for the prediction of experimentally induced cardiotoxicity and possibly for cardioprotective experiments.     

Cardioprotection by remote ischemic preconditioning exhibits a signaling pattern different from local ischemic preconditioning

Remote ischemic preconditioning (RIPC) and local ischemic preconditioning (IPC) protect the myocardium from subsequent ischemia/reperfusion (I/R) injury. In this study, the protective effects of early RIPC, IPC, and the combination of both (RIPC-IPC) were characterized. Furthermore, the hypothesis was tested that protein kinase C (PKC) and mitogen-activated protein kinases (MAPKs), important mediators of IPC, are activated in RIPC. Infarct size, serum troponin T, and creatine kinase levels were assessed after 4 × 5-min noninvasive RIPC, local IPC, or a combination of both and 35 min of regional ischemia and 120 min of reperfusion. Protein kinase C ε and the MAPKs extracellular signal-regulated MAPK (ERK), c-jun N-terminal kinase (JNK), and p38 MAPK were analyzed by Western blot analysis and activity assays in the myocardium and skeletal muscle immediately after the preconditioning protocol. Remote ischemic preconditioning, IPC, and RIPC-IPC significantly reduced myocardial infarct size (RIPC-I/R: 54% ± 15%; IPC-I/R: 33% ± 15%; RIPC-IPC-I/R: 33% ± 15%; P < 0.05 vs. I/R [76% ± 14%]) and troponin T release (RIPC-I/R: 15.4 ± 6.4 ng/mL; IPC-I/R: 10.9 ± 7.0 ng/mL; RIPC-IPC-I/R: 9.8 ± 5.6 ng/mL; P < 0.05 vs. I/R [27.1 ± 12.0 ng/mL]) after myocardial I/R. Ischemic preconditioning led to an activation of PKCε and ERK 1/2, whereas RIPC did not lead to a translocation of PKCε to the mitochondria or phosphorylation of the MAPKs ERK 1/2, JNK 1/2, and p38 MAPK. Remote ischemic preconditioning did not induce translocation of PKCε to the mitochondria or phosphorylation of MAPKs in the preconditioned muscle tissue. Remote ischemic preconditioning, IPC, and RIPC-IPC exert early protection against myocardial I/R injury. Remote ischemic preconditioning and local IPC exhibit different activation dynamics of signal transducers in the myocardium. The studied PKC-MAPK pathway is likely not involved in the protective effects of RIPC.     

Cardiac troponins and left ventricular hypertrophy in hemodialysis patients

BACKGROUND: Cardiovascular diseases are the leading cause of death in hemodialysis patients. Left ventricular (LV) hypertrophy is an important predictor of cardiovascular morbidity and mortality in these patients. Cardiac troponins (cTnT and cTnI) are indicators of myocardial cell damage. AIM: The aim of this study was to determine prevalence of LV hypertrophy, prevalence of elevated serum cTnT and cTnI in hemodialysis patients, and identify the correlation between cardiac troponins and LV hypertrophy. METHODS: The study included 115 hemodialysis patients (71 men and 44 women), mean age 53.30 +/- 12.17 years, mean time on dialysis 4.51 +/- 4.01 years and average Kt/Vsp 1.17 +/- 0.23. Mean serum cTnT was 0.14 +/- 0.23 ng/ml, mean serum troponin I 0.20 +/- 0.48 ng/ml. Mean LV posterior wall thickness in diastole (LVPWd) was 11.44 +/- 2.09 mm, mean LV interventricular septal wall thickness in diastole (IVSd) 11.21 +/- 2.12 mm, mean LV end diastolic volume index (iLVEDV) 100.80 +/- 34.62 mL/m2 and mean LV mass index (LVMi) 143.85 +/- 41.21 g/m2. RESULTS: We found statistically significant positive correlations (p <0.05) between serum troponin T concentration, IVSd, LVPWd and iLVEDV. A highly significant positive correlation (p < 0.01) was found between serum troponin T and LVMi. One-year follow-up showed that patients with cardiac troponin T > 0.10 ng/ml and cardiac troponin I > 0.15 ng/ml had significantly lower (p < 0.01) survival rate than patients with troponin T < or = 0.10 ng/ml and troponin I < or = 0.15 ng/ml. CONCLUSION: A significant positive correlation exists between serum troponin T concentration and echocardiographic indicators of LV hypertrophy in hemodialysis patients. Patients with higher serum levels of cardiac troponins have lower survival rates during one year follow up.     

Serum and plasma as alternative sample types in analysis of cardiac markers in the clinical routine

There is an increasing demand for the results of cardiac markers (troponin I or T, creatine kinase MB mass and myoglobin) to be made available promptly after sample-taking. In order to shorten the turnaround time, the possibility of using EDTA- or heparin-plasma instead of serum was investigated. The study population comprised 391 patients with acute chest pain. Four different instruments and systems routinely used in Finland giving quantitative results were studied for the assays of creatine kinase isoenzyme MB mass, myoglobin, and troponin I or troponin T. In addition to serum samples, heparin-plasma seems to be useful for all three assays using the Access and Immulite systems, while EDTA-plasma seems to be useful for all three assays with the Access and Elecsys systems. For the AxSYM assays, serum samples seem to be the best alternative. In conclusion, it is possible to use a single EDTA- or heparin-plasma sample for Access, Elecsys and Immulite analysers, and thereby to shorten the turnaround time. In this way the quantitative analyses from plasma can be performed 30 min after taking the sample.     

Serum and plasma as alternative sample types in analysis of cardiac markers in the clinical routine

There is an increasing demand for the results of cardiac markers (troponin I or T, creatine kinase MB mass and myoglobin) to be made available promptly after sample-taking. In order to shorten the turnaround time, the possibility of using EDTA- or heparin-plasma instead of serum was investigated. The study population comprised 391 patients with acute chest pain. Four different instruments and systems routinely used in Finland giving quantitative results were studied for the assays of creatine kinase isoenzyme MB mass, myoglobin, and troponin I or troponin T. In addition to serum samples, heparin-plasma seems to be useful for all three assays using the Access and Immulite systems, while EDTA-plasma seems to be useful for all three assays with the Access and Elecsys systems. For the AxSYM assays, serum samples seem to be the best alternative. In conclusion, it is possible to use a single EDTA- or heparin-plasma sample for Access, Elecsys and Immulite analysers, and thereby to shorten the turnaround time. In this way the quantitative analyses from plasma can be performed 30 min after taking the sample.     

Effects of contemporary troponin assay sensitivity on the utility of the early markers myoglobin and CKMB isoforms in evaluating patients with possible acute myocardial infarction

BACKGROUND: The 2003 American Heart Association (AHA) definition for myocardial infarction (MI) requires an "adequate set" (i.e. at least 6 h between measurements) of biomarkers and specifically troponin for the diagnosis of MI. The aim of the present study was to assess the performance of myoglobin, the CKMB isoforms, and cardiac troponin I (cTnI) in specimens earlier than the requisite 6 h after presentation, in a population originally characterized using World Health Organization (WHO) criteria. METHODS: In 1996, 228 acute coronary syndrome patients with an "adequate sample set" had their specimens assayed for CKMB isoforms and myoglobin. In 2003, the same specimens were analyzed with the AccuTnI troponin I assay and myoglobin (Beckman Coulter Access immunoassay). RESULTS: The clinical sensitivities for both myoglobin and the CKMB isoforms were >90% when the population was classified by WHO criteria. However the sensitivities were <70% when the ESC/ACC MI definition was used. Analyzing cTnI at earlier time points as long as there was at least 3 h between specimens or at least 1 specimen 6 h from pain onset did not misclassify subjects based on adverse outcomes in the year following their presentation. CONCLUSION: Contemporary assays for cTnI with increased analytical sensitivity reduce the utility of myoglobin and CKMB isoforms to rule-out an AMI.     

成人水痘患者心肌肌钙蛋白I水平监测及临床意义

目的探讨心肌肌钙蛋白1（cTnI）水平变化对评估成人水痘患者心肌损伤的临床意义。方法应用全自动微粒子化学发光免疫分析系统2（Beckman Coulter Access Immunoassay System 2）对成人水痘患者和健康者血清cTnI水平进行测定。结果血清eTnI均值成人水痘组为（0．029±0．021）ng／L,心电图异常组为（0．032±0．012）ng／L,正常组为（0．027±0．012）ng／L。3组两两间比较差异无统计学意义（P〉0．05）。结论96例成人水痘患者未发现cTnI明显异常,成人水痘患者心肌损伤的发生率可能较低。     

Myocardial necrosis in ICU patients with acute non-cardiac disease: a prospective study

Objective: To ascertain if, after an episode of hypotension, unnoticed myocardial necrosis could occur in critical care patients with acute non-cardiac illness and to search for signs of cardiac necrosis. ¶Design: A prospective observational study.¶Setting: General intensive care unit (ICU) at a tertiary level hospital.¶Patients: Thirty-one patients in two groups. Group 1 included 19 patients with severe sepsis/septic shock (ACCP/SCCM Consensus Conference). Group 2 included 12 patients with hypovolemic shock.¶Interventions: Biochemical markers of myocardial necrosis (cardiac troponin I (cTnI), creatine kinase (CK), creatine kinase MB mass (CKMB) and myoglobin) were measured at 12 h (T1), 24 h (T2) and 48 h (T3) after enrollment.¶A standard 12-lead ECG was recorded upon enrollment (T0) and at T2. Anomalous Q-waves or ST segment depression or elevation was considered diagnostic for acute myocardial infarction (AMI). A hypotensive episode (arterial systolic pressure < 90 mmHg at heart rate > 100 bpm) was considered moderate if it lasted 30–60 min or severe if longer than 60 min.¶Measurements and results: At T0 none of the patients had AMI on ECG. At T2 a non-Q AMI developed in five patients. Increased levels of troponin I, myoglobin, CK and CKMB were found in 74.2 %, 96.8 %, 74.2 % and 67.7 % of the patients, respectively. Cardiac troponin I increased in 11 out of 19 septic patients and in all hypovolemic patients. There was a significant difference between the groups (p < 0.05). All biochemical markers increased in relationship to the degree of hypotension with cTnI again showing a significant difference. The longer the hypotensive episode was, the greater was the increase (moderate hypotension: median 1.16; quartiles 0.55–3.44 ng/ml, severe hypotension: median 8.53; quartiles 1.1–20.7 ng/ml; p < 0.05). Abnormal levels of cTnI were more frequent in non-survivors than in survivors (p < 0.05).¶Conclusions: Hypotension may cause cardiac damage in critically ill patients with acute non-cardiac diseases as shown by abnormal levels of cTnI. It is likely that a high number of these myocardial necroses may go unnoticed on the ECG.