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.     

Lower cardiac troponin T and I results in heparin-plasma than in serum

BACKGROUND: The use of plasma rather than serum for determination of cardiac troponins can improve turnaround time and potentially avoid incomplete serum separation that may produce falsely increased results. We investigated the influence of incomplete serum separation and the effect of heparin-plasma on cardiac troponin concentrations. METHODS: Serum and heparin-plasma samples were drawn simultaneously from 100 patients (50 patients with acute coronary syndrome and 50 patients after open heart surgery) and measured on three different analytical systems, two for determination of cardiac troponin I (cTnI; Abbott AxSYM and Bayer ACS:Centaur) and one for cardiac troponin T (cTnT; Roche Elecsys cTnT STAT). Serum samples were reanalyzed after a second centrifugation to assess the influence of incomplete serum separation. RESULTS: Mean results (+/- 95% confidence interval) in heparin-plasma compared with serum were 101% +/- 2% (AxSYM cTnI), 94% +/- 3% (ACS:Centaur cTnI), and 99% +/- 3% (Elecsys cTnT). Differences >20% were seen in 11% of results on the ACS:Centaur, 9% of results on Elecsys cTnT, and 2% of results on the AxSYM. For the Elecsys cTnT assay, the magnitude of the difference between serum and plasma was independent of the absolute concentration and confined to individual samples, and was reversed by treatment with heparinase. A second centrifugation had no effect on serum results by any of the assays. CONCLUSION: The concentrations of troponins measured in heparin-plasma are markedly lower than in serum in some cases.     

Plasma or serum samples: measurements of cardiac troponin T and of other analytes compared.

Conflicting data in the literature concern possible differences in the immunochemical measurement of cardiac troponins, either in plasma or in serum. In order to address this specific point, 96 serum and heparin-plasma pairs were obtained for cardiac marker measurement [cardiac troponin T (cTnT); myoglobin (Myo) and creatine kinase-MB isoenzyme (CK-MB)]; 29 additional "common" analytes were measured in 77 such samples. The cardiac markers were measured by electrochemiluminescence (Elecsys 2010, Roche); the other analytes by established automated methods (Modular, Roche). Mean plasma/serum ratios for cTnT (0.95), creatine kinase-MB (1.01) and myoglobin (0.99) were comparable with those of the 29 common analytes (interval of means 0.83-1.05). The distribution of the plasma-serum differences also showed similarities between cardiac markers and other analytes. A few outlier plasma-serum differences (3-5%) were measured for both categories of analytes. Addition of heparin to serum (51 samples) caused decreased cTnT (mean ratio 0.92). In 3 of 51 such samples the cTnT decrease was more marked, but in a second sample from the same subjects (1 week later) such a prominent, heparin-induced loss of cTnT no longer appeared. In conclusion, plasma-serum differences in immuno-reactive cTnT compare with those observed for other analytes. In occasional heparin-plasma samples immunochemical measurement of cTnT may give exceptionally low values. However, in our sample group of 96 patients (cTnT lower or higher than the cut-off in, respectively, 24 and 72 patients), no misclassification occurred if plasma instead of serum cTnT values were considered.     

Myoglobin, creatine kinase MB, troponin T, and troponin I — rapid bedside assays in patients with acute chest pain

Three new rapid, qualitative bedside immunoassays were evaluated in the diagnosis of patients with acute chest pain. The subjects, 122 patients in group 1 (bedside tests for myoglobin, creatine kinase MB) and 233 patients in group 2 (bedside tests for troponin I and sensitive troponin T) were admitted to hospital with acute chest pain for less than 12 h. The bedside tests were performed on admission, and 2, 4, and 6 h later. The correlation between the two parts of the rapid creatine kinase MB/myoglobin test during the first 12 h after the onset of chest pain was moderate in all patients (κ=0.401, 95% confidence interval 0.321–0.483). The highest correlation was seen with the patients with definite and probable myocardial infarction. The correlations were smaller but significant also in other diagnostic groups (unstable angina pectoris, prolonged chest pain, and non-cardiac chest pain). The correlation between the rapid sensitive test for troponin T and rapid test for troponin I was significant in all groups (κ=0.776, 95% confidence interval 0.711–0.841). The myoglobin part of the rapid creatine kinase MB/myoglobin test may be too non-specific for clinical diagnostic purposes [in non-infarct patients the myoglobin part was significantly more often positive than creatine kinase MB or troponin tests (P<0.001)].     

For a rapid diagnosis of acute myocardial infarction, a sensitive troponin assay is needed in the near-patient testing setting

An early diagnosis of myocardial infarction in the emergency setting would be advantageous for both patients and the physicians treating these patients. Guidelines currently recommend serial samples that are drawn at presentation and 6-9 h later to be measured for cardiac troponin to aid in this diagnosis. However, much effort has been directed to decrease the time to make a diagnosis in this setting, and there has been renewed interest in shortening the time between serial measurements as well as the turnaround time for reporting the results. By eliminating the blood sample transit time to the central laboratory, point-of-care testing or near-patient testing can reduce the turnaround time for reporting the results, however this is possibly at the cost of decreased diagnostic performance. In this article, we discuss the recent results from the RATPAC study, which evaluated whether the combination of myoglobin, the MB isoenzyme of creatine kinase (CKMB) and a sensitive troponin assay would be superior to troponin alone.     

Cardiac markers: point of care testing.

Point-of-care (POC) or "near-patient" testing allows diagnostic assays to be performed in locations such as the emergency department or intensive care unit where treatment decisions are made and care is delivered based on the results of these assays. Presently, there exist POC immunoassays for several cardiac markers including creatine kinase MB (CK-MB), myoglobin, troponin I, and troponin T that yield qualitative and quantitative results comparable to traditional central lab assays. In the evaluation of emergency room patients with chest pain, POC cardiac markers may improve triage and clinical outcomes. Existing POC assays combining myoglobin and CK-MB have high sensitivity and specificity for diagnosing acute myocardial infarction and may provide the earliest identification of myocardial injury. POC Troponin T assays are the most studied POC cardiac marker assays. Along with POC troponin I assays, these tests provide more sensitive identification of myocardial injury and valuable prognostic information. Prior studies of POC cardiac marker assays have not addressed whether POC testing affects patient outcome or process of care. In situations in which caregivers base triage, treatment and monitoring decisions on time-sensitive diagnostic results, POC tests linked with improved triage and treatment strategies may improve resource utilization and clinical outcomes.     

Etude de la myoglobinemie et de son evolution au cours de l'infarctus du myocardeStudy on myoglobinemia and its development during myocardial infarction

Thirty six patients suffering from myocardial infarction were investigated by assay of their serum myoglobin, total creatine kinase and creatine kinase isoenzyme MB activities. Determination of serum myoglobin presents, with regard to creatine kinase MB, two major advantages: a very early increase after the onset of the pain (about three hours later) and a very quick clearance, allowing the diagnosis of a second episode of necrosis after about one day.     

Myoglobin,creatine kinase MB isoforms and creatine kinase MB mass in early diagnosis of myocardial infarction in patients with acute chest pain

OBJECTIVES: Measurements of myoglobin and creatine kinase (CK)-MB isoforms have been suggested to be sensitive tests for the early diagnosis of myocardial infarction (MI). We have investigated the utility of myoglobin, creatine kinase (CK)-MB isoforms and creatine kinase MB mass (CK-MBm) in early diagnosis of MI using cardiac troponin T (cTnT) positivity as a reference. DESIGN AND METHODS: The study population comprised 440 patients who had had chest pain for less than 12 h. Patients were divided into cTnT negative (cTnT-) or cTnT positive (cTnT+) patients (concentration of cTnT >0.1 microg/L at two different time points during 72 h). RESULTS: At the time of admission to the emergency department receiver operating characteristics (ROC) curves of CK-MB isoforms and CK-MBm were not better than that of myoglobin. Six hours after admission CK-MB isoforms and CK-MBm provided statistically significantly larger areas under the curve (AUC) than myoglobin (p < 0.01). When ROC curves were related to the onset of chest pain (< 3 h, 3-6 h, and > 6 h) there were no significant differences between the cardiac markers studied. CONCLUSIONS: According to the present findings, CK-MB isoforms or myoglobin offer no advantage over CK-MBm as early markers of myocardial infarction.     

The antibody configurations of cardiac troponin I assays may determine their clinical performance

BACKGROUND: Previous studies have shown superior clinical performance of the cardiac troponin I (cTnI) assay from Beckman-Coulter Diagnostics. This assay had a unique combination of monoclonal antibodies with 2 monoclonal antibodies directed against epitopes near the NH(2) terminus of the heart-specific region of troponin I. The approach has been adopted by the new cTnI assay from Abbott Diagnostics. The aim of our study was to investigate whether this approach affects the clinical performance of cTnI assays. METHODS: Cardiac troponin concentrations were measured in a random sample of patients with unstable coronary artery disease included in the GUSTO IV trial (n = 696) by the AccuTnI (Beckman-Coulter Diagnostics), Architect cTnI (Abbott Diagnostics), Immulite 2500 cTnI (Diagnostics Products Corporation), and Elecsys 2010 cTnT (Roche Diagnostics) assays and related to the 1-year mortality. The primary cutoff concentrations were based on the 99th percentile upper reference limits and an imprecision (CV) < or =10%. RESULTS: The sensitivities of the AccuTnI and Architect cTnI assays in identifying patients who died within 1 year were equal and were significantly higher (P <0.05) than those of the Immulite 2500 cTnI and the Elecsys cTnT assays. The concordance between the AccuTnI and Architect cTnI assays was 97%, but concordances between the Architect cTnI and the Elecsys cTnT assays were 89%-92% with more at-risk patients (P <0.01 to P <0.001) identified by the Architect cTnI assay. CONCLUSIONS: The Architect cTnI assay has clinical performance similar to that of the AccuTnI, probably as a result of the inclusion of a monoclonal antibody against troponin I epitope 41-49 in the assay.     

For a rapid diagnosis of acute myocardial infarction,a sensitive troponin assay is needed in the near-patient testing setting

Evaluation of: Collinson P, Goodacre S, Gaze D et al. Very early diagnosis of chest pain by point-of-care testing: comparison of the diagnostic efficiency of a panel of cardiac biomarkers compared with troponin measurement alone in the RATPAC trial. Heart 98(4), 312–318 (2012).

An early diagnosis of myocardial infarction in the emergency setting would be advantageous for both patients and the physicians treating these patients. Guidelines currently recommend serial samples that are drawn at presentation and 6–9 h later to be measured for cardiac troponin to aid in this diagnosis. However, much effort has been directed to decrease the time to make a diagnosis in this setting, and there has been renewed interest in shortening the time between serial measurements as well as the turnaround time for reporting the results. By eliminating the blood sample transit time to the central laboratory, point-of-care testing or near-patient testing can reduce the turnaround time for reporting the results, however this is possibly at the cost of decreased diagnostic performance. In this article, we discuss the recent results from the RATPAC study, which evaluated whether the combination of myoglobin, the MB isoenzyme of creatine kinase (CKMB) and a sensitive troponin assay would be superior to troponin alone.     

Monoclonal antibody–based immunoassays for serum myoglobin quantification in acute myocardial infarction

We have developed a monoclonal antibody–based enzyme immunoassay and a solid-phase radioimmunoassay for human myoglobin. Both assays are based on competition for the monoclonal antibody between the free myoglobin present in the standards or serum samples and the myoglobin coated to the wells of microtiter plates. Consequently, the absorbance at 630 nm and the radioactivity are inversely related to the concentrations of free myoglobin. The sensitivity of both assays was 10 μg/L with linearity up to 1,000 μg/L. There was no interference with other serum proteins, as judged from analysis of specimens with high concentrations of lactate dehydrogenase, creatine kinase, or hemoglobin. The average serum myoglobin concentration in 30 normal individuals was 67 μg/L. Five patients with cardiac arrhythmias had normal values (average, 63 μg/L) while four patients with myocardial infarction had abnormally high concentrations of myoglobin (300–1,000+ μg/L). In a typical case of myocardial infarction, serum myoglobin rose 21 hr earlier and peaked 12 hr earlier than creatine kinase and its cardiac isoenzyme. These rapid imrnunoassays appear to be useful for the early detection of increased serum myoglobin indicative of myocardial infarction.     

Myoglobin and creatine kinase isoenzyme MB mass assays: intermethod behaviour of patient sera and commercially available control materials

The low biological variation of myoglobin and creatine kinase isoenzyme MB mass (CK-MBm) requires accurate measurements. In the standardization process, in order to effectively measure and correct intermethod variability, the intermethod behaviour of control materials must be the same of patient sera, i.e. they must be commutable. In this work we checked the commutability of some commercially available control materials in pairs of methods for myoglobin and CK-MBm measurements; we assessed the impact of commutable and non-commutable control materials when used for equalizing patient sera results by two different methods and discussed the problems related to external quality assessment schemes. Myoglobin and CK-MBm were measured in sets of 49 and 56 patient sera and in 13 commercially available control materials with two automatic analytical systems. The non-commutability rate was 8.3% for myoglobin and 23.1% for CK-MBm. Recalculation of serum samples results with a control material as calibrator lowered or increased the bias originally present according to whether the material itself was commutable or not. We conclude that also for myoglobin and CK-MBm assays it is necessary to check the commutability of materials to be used in external quality assessment schemes, or to normalize patient results by different methods.     

血清心脏型脂肪酸结合蛋白联合糖原磷酸化酶脑型检测在小儿脓毒症心肌损伤诊断中的临床价值

目的研究小儿脓毒症心肌损伤诊断中血清心脏型脂肪酸结合蛋白(FABP3)联合糖原磷酸化酶脑型(GPBB)检测的应用价值。方法采用回顾性分析方法,研究对象为2019年1月至2020年1月葫芦岛市中心医院收治的87例脓毒症患儿,根据是否出现心肌损伤划分为2组,心肌损伤患儿列入A组,共38例,未出现心肌损伤患儿列入B组,共49例;同时,选取同一时期入院就诊的44例的非脓毒症感染性疾病患儿作为研究对象,列入C组。3组患儿均选取用全自动血气分析仪测定肌红蛋白、肌钙蛋白Ⅰ,并选取酶联免疫吸附实验法测定GPBB、FABP3及肌酸激酶同工酶,比较3组患儿肌红蛋白、肌钙蛋白Ⅰ、GPBB、FABP3及肌酸激酶同工酶水平,并分析心肌损伤指标肌红蛋白、肌钙蛋白Ⅰ、肌酸激酶同工酶与血清FABP3、GPBB相关性。结果A组[(396.85±13.07)ng/mL、(3.08±0.06)ng/mL、(22.78±1.02)ng/mL、(34.45±2.41)ng/mL、(44.08±6.53)U/L]、B组[(68.26±12.45)ng/mL、(0.12±0.04)ng/mL、(9.17±1.08)ng/mL、(13.64±2.52)ng/mL、(20.85±7.01)U/L]患儿肌红蛋白、肌钙蛋白Ⅰ、GPBB、FABP3及肌酸激酶同工酶水平明显高于C组[(17.16±10.09)ng/mL、(0.04±0.03)ng/mL、(2.58±1.02)ng/mL、(4.34±3.02)ng/mL、(9.17±6.73)U/L],差异有统计学意义(P<0.05);A组患儿肌红蛋白、肌钙蛋白Ⅰ、GPBB、FABP3及肌酸激酶同工酶水平明显高于B组,差异有统计学意义(P<0.05)。脓毒症患儿血清FABP3、GPBB与肌红蛋白、肌钙蛋白Ⅰ、肌酸激酶同工酶均呈正相关(r=0.602、0.521;r=0.466、0.494;r=0.528、0.489,P<0.05)。结论小儿脓毒症心肌损伤诊断中血清FABP3联合GPBB检测的应用效果显著,可用于评估脓毒症患儿心肌损伤严重程度。     

Acute effect of haemodialysis on serum markers of myocardial damage

Cardiac markers are more likely to be elevated in dialysis patients than in patients with renal failure not on dialysis. In this study, 31 patients (20 males, 11 females) undergoing chronic haemodialysis were enrolled. The effect of haemodialysis on cardiac troponin T (cTnT), I (cTnI), creatine kinase MB (CKMB) mass, CKMB activity and myoglobin assays was assessed by comparing pre- and post-haemodialysis determinations. After correcting for haemoconcentration, significant differences were observed (mean +/- SEM, pre- vs post-dialysis) for myoglobin (178.9 +/- 19.3 vs 225.0 +/- 28.4 ng/ml; p=0.006) for cTnT (0.111 +/- 0.028 vs 0.148 +/- 0.037 ng/ml; p=0.004), for CKMB mass (2.75 +/- 0.37 vs 2.59 +/- 0.37 ng/ml; p=0.000) and CKMB activity (14.8 +/- 0.9 vs 13.1 +/- 0.9 U/l; p=0.000) assays. Our study questions the reliability of cardiac markers in dialysis patients and suggests that the clinical threshold value and diagnostic efficiency of each assay needs to be validated. Although these differences exceeded clinical threshold values in only a few patients, serum markers of myocardial damage in dialysis patients should be interpreted with caution.     

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.     

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.     

Cardiac troponin and beta-type myosin heavy chain concentrations in patients with polymyositis or dermatomyositis

Cardiac troponin T (cTnT), cardiac troponin I (cTnI), myosin heavy chains (MHC), myoglobin, creatine kinase (CK), and creatine kinase isoenzyme MB (CKMB), were measured in blood samples from 39 polymyositis (PM) or dermatomyositis (DM) patients without clinical evidence for cardiac involvement to evaluate their clinical usefulness in this patient population. MHC, myoglobin, and CKMB were frequently elevated and correlated with each other and with disease severity. Undetectable cTnI in all but one patient indicated that MHC was released from skeletal muscle, thereby providing the first laboratory evidence of frequent slow-twitch muscle fibre-necrosis in patients with PM or DM. CKMB was elevated in 51%, cTnT in 41%, and cTnI in only 2.5% of patients. cTnI did not correlate with other markers or with disease severity scores. The close correlations found between cTnT and skeletal muscle damage markers and the relationship between cTnT with disease severity without clinical evidence for myocardial damage suggest a release of cTnT from skeletal muscle. The relationship of cTnT with disease severity indicates a possible role of the marker for risk stratification. However, the prognostic values of cardiac troponins and other muscle damage markers in PM/DM patients remain to be compared in prospective outcome trials.     

Plasma 99th percentile reference limits for cardiac troponin and creatine kinase MB mass for use with European Society of Cardiology/American College of Cardiology consensus recommendations

BACKGROUND: The European Society of Cardiology/American College of Cardiology (ESC/ACC) consensus document for definition of myocardial infarction (MI) is predicated on increased cardiac troponin or creatine kinase (CK) MB mass above the 99th percentile reference limit. The purpose of this study was to determine the plasma (heparin) 99th percentile reference limits for the leading in vitro diagnostic cardiac troponin and CKMB mass assays. METHODS: Blood (heparin plasma) was obtained from healthy adults (n = 696; age range, 18-84 years) stratified by gender and ethnicity. Cardiac troponin I (cTnI) and T (cTnT) and CKMB mass concentrations were measured by eight assays. Reference limits were determined by nonparametric statistical analysis. RESULTS: Two cTnI assays demonstrated at least a 1.2- to 2.5-fold higher 99th percentile for males vs females, with the mean concentrations significantly higher for males (P <0.05). Two cTnI assays also demonstrated a 1.1- to 2.8-fold higher 99th percentile for blacks vs Caucasians, with the mean concentrations significantly higher for blacks (P = 0.05). There was a 13-fold variance between the lowest measured 99th percentile (0.06 microg/L) and the highest (0.8 microg/L). All CKMB assays demonstrated a 1.2- to 2.6-fold higher 99th percentile for males vs females, with mean concentrations significantly higher for males (P <0.0001). Four CKMB assays also showed significantly higher (1.2- to 2.7-fold) mean concentrations for blacks (P <0.02) vs Caucasians. CONCLUSIONS: The heparin-plasma 99th percentile reference limits for cardiac troponin and CKMB mass provide an evidence base in support of the ESC, ACC, and American Heart Association guidelines for detection of myocardial injury. Selective gender and ethnic differences were demonstrated. These data allow clinicians, trialists, and epidemiologists a common point for operational use.     

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。     

Asystole and increased serum myoglobin levels associated with ‘packing blackout’ in a competitive breath‐hold diver

Many competitive breath‐hold divers use ‘glossopharyngeal insufflation’, also called ‘lung packing’, to overfill their lungs above normal total lung capacity. This increases intrathoracic pressure, decreases venous return, compromises cardiac pumping, and reduces arterial blood pressure, possibly resulting in a syncope breath‐hold divers call ‘packing blackout’. We report a case with a breath‐hold diver who inadvertently experienced a packing blackout. During the incident, an electrocardiogram (ECG) and blood pressure were recorded, and blood samples for determinations of biomarkers of cardiac muscle perturbation (creatine kinase‐MB isoenzyme (CK‐MB), cardiac troponin‐T (TnT), and myoglobin) were collected. The ECG revealed short periods of asystole during the period of ‘packing blackout’, simultaneous with pronounced reductions in systolic, diastolic, and pulse pressures. Serum myoglobin concentration was elevated 40 and 150 min after the incident, whereas there were no changes in CK‐MB or TnT. The ultimate cause of syncope in this diver probably was a decrease in cerebral perfusion following glossopharyngeal insufflation. The asystolic periods recorded in this diver could possibly indicate that susceptible individuals may be put at risk of a serious cardiac incident if the lungs are excessively overinflated by glossopharyngeal insufflation. This concern is further substantiated by the observed increase in serum myoglobin concentration after the event.