Cardiac troponins and creatine kinase content of striated muscle in common laboratory animals

Animal models are important for the investigation of human heart pathology, novel treatments, and medical or surgical interventions for disease. Serum markers of myocardial damage may also be important tools within this field of research. In order to assess the cardiac specificity of widely utilised serum markers, we measured the cardiac troponins and creatine kinase (CK) isoenzymes in cardiac and skeletal muscle samples taken from dog, monkey, pig and rat. These samples were also analysed by immunoblotting for cardiac troponin I (cTnI) and cardiac troponin T (cTnT). The content of cTnI and cTnT in skeletal muscle was below 0.6% of that found in heart for all animal species studied. This low immunoreactivity in skeletal muscle was confirmed by immunoblot analysis. The content of CK was higher in skeletal muscle than in heart muscle for all species. The CK-MB/total CK ratio was lower in skeletal muscle than in cardiac muscle for all species. The differences in CK-MB content of skeletal muscle and heart muscle were much less pronounced than the tissue differences in the amounts of the cardiac troponins. The cardiac troponins are potentially useful serum markers of myocardial damage, with high specificity for myocardial muscle in these common laboratory animals. Creatine kinase-MB is much less cardiac-specific.     

Clinical and experimental results on cardiac troponin expression in Duchenne muscular dystrophy

BACKGROUND: Because of controversial earlier studies, the purpose of this study was to provide novel experimental and additional clinical data regarding the possible reexpression of cardiac troponin T (cTnT) in regenerating skeletal muscle in Duchenne muscular dystrophy (DMD). METHODS: Plasma from 14 patients (mean age, 7.5 years; range, 5.7-19.4 years) with DMD was investigated for creatine kinase (CK), the CK MB isoenzyme (CKMB), cTnT and cardiac troponin I (cTnI), and myoglobin. cTnT concentrations were measured by an ELISA (second-generation assay; Roche) using the ES 300 Analyzer. cTnI, myoglobin, and CKMB were measured by an ELISA using the ACCESS System (Beckman Diagnostics). Troponin isoform expression was studied by Western blot analysis in remnants of skeletal muscle biopsies of three patients with DMD and in an animal model of DMD (mdx mice; n = 6). RESULTS: There was no relation of cTnT and cTnI to clinical evidence for cardiac failure. cTnI concentrations remained below the upper reference limit in all patients. cTnT was increased (median, 0.11 microg/L; range, 0.06-0.16 microg/L) in 50% of patients. The only significant correlation was found for CK (median, 3938 U/L; range, 2763-5030 U/L) with age (median, 7.5 years; range, 6.8-10.9 years; r = -0.762; P = 0.042). Western blot analysis of human or mouse homogenized muscle specimens showed no evidence for cardiac TnT and cTnI expression, despite strong signals for skeletal muscle troponin isoforms. CONCLUSIONS: We found no evidence for cTnT reexpression in human early-stage DMD and in mdx mouse skeletal muscle biopsies. Discrepancies of cTnT and cTnI in plasma samples of DMD patients were found, but neither cTnT nor cTnI plasma concentrations were related with other clinical evidence for cardiac involvement.     

Evaluation and risk stratification of acute coronary syndromes using a low cut-off level of cardiac troponin T, combined with CK-MB mass determination

OBJECTIVES: To study the usefulness of combined cardiac Troponin T (cTnT) and CK-MB mass determinations in risk stratification of acute coronary syndromes. DESIGN AND METHODS: Blood samples for cTnT and CK-MB mass were collected at arrival and 4, 8, and 12-24 later in 301 consecutive patients with recent acute chest pain (ACP). Data were also collected for cardiac events. RESULTS: Combined cardiac mortality/nonfatal myocardial infarction over a period of 15 months was lowest in patients with <0.04 microg/l cTnT and -<5.0 microg/l CK-MB mass intermediate in those with elevated cTnT but normal CK-MB mass and highest when both markers were elevated, in absence of early reperfusion. CONCLUSION: The use of a low cut-off point of cTnT, combined wit CK-MB mass determination, offers a good strategy for risk stratification of ACP patients.     

Tissue specificity of cardiac troponin I, cardiac troponin T and creatine kinase-MB.

The purpose of the paper is to review the tissue specificity of creatine kinase (CK)-MB, cardiac troponin I (cTnI), and cardiac troponin T (cTnT) in human and animal heart and skeletal muscle. Alterations are described which demonstrate that CK-MB is expressed in human skeletal muscle, and is not 100% specific for the heart. cTnI has been shown to be 100% specific for the heart. While cTnT isoforms are expressed in injured skeletal muscle, they are not detected by the diagnostic assays used in clinical practice. Therefore, cTnI or cTnT challenge CK-MB as the new standards for detection of myocardial injury.     

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

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

Cardiac troponin T content in heart and skeletal muscle and in blood samples from ApoE/LDL receptor double knockout mice

BACKGROUND: The isolated perfused mouse heart is a useful experimental model, and cardiac troponin T (cTnT) in coronary effluent may be a sensitive marker of myocardial damage. In recent years, the apolipoprotein E/low-density lipoprotein receptor double knockout (apoE/LDLr KO) mice have become valuable tools in atherosclerosis research. The aim of the study was to validate measurements of cTnT in heart, skeletal muscle, and serum of apoE/LDLr KO mice. METHODS: Wild-type C57BL/6J mice were fed with standard diet, and apoE/LDLr KO mice were fed an atherogenic diet. Blood was sampled from the jugular vein or the thoracic cavity. Heart and femoral skeletal muscle were sampled and homogenized. cTnT was measured with the third-generation cTnT assay (Troponin T STAT) on Elecsys 2010 immunoassay analyser (Roche Diagnostics). RESULTS: Median serum cTnT in samples from the thoracic cavity of C57BL/6J mice was about 20-90 times higher, and from ApoE/LDLr KO mice about 30 times higher than serum cTnT in samples from the external jugular vein. There was no difference in cTnT content (microg cTnT/g heart muscle) in hearts from C57BL/6J and apoE/LDLr KO mice. The median cTnT content in skeletal muscle was less than 0.1% of the cTnT content in heart muscle. CONCLUSION: There is no difference in cTnT content of heart muscle comparing C57BL/6J and ApoE/LDLr KO mice, which have larger hearts. Sampling from the thoracic cavity causes unacceptably high cTnT levels. Serum cTnT in samples from the jugular vein is only slightly elevated. Elevated baseline levels of cTnT in mice are not caused by troponin T from skeletal muscle.     

Cardiospecificity of the 3<Superscript>rd</Superscript> generation cardiac troponin T assay during and after a 216 km ultra-endurance marathon run in Death Valley

Background The reasons for the appearance of cardiacspecific troponin (cTnT) after strenuous exercise are unclear. The aim of the present study was to evaluate the cardiospecificity of the 3^rd generation cardiac cTnT assay during and after an ultra-endurance race of 216 km at extreme environmental conditions in Death Valley. Study design and methods We measured serially cTnT, creatine kinase (CK), activity and mass of the isoenzyme MB of CK (CK-MB_act and CK-MB_mass), and myoglobin in 10 well-trained athletes before, repeatedly during and after the race. Results Six of 10 participants finished the race within a preset time of 60 hours. Postrace values of biochemical markers CK, CK-MB_act, CKMB_mass, and myoglobin were significantly increased compared to baseline (p<0.05). CK-MB_act increased from (median (25^th/ 75^thpercentile) 12 (10/13) U/L to 72 (32/110) U/L, CK-MB_mass from 3.9 (2.9/5.6) U/L to 65 (18/80) U/L and CK increased from median 136 (98/ 228) U/L to 3,570 (985/6,884) U/L respectively. Pre-race myoglobin was 27 (22/31) μg/l compared to 530 (178/657) μg/l after the run. One runner developed significant exercise-induced rhabdomyolysis with spontaneous recovery. cTnT values remained below the 99^th percentile reference limit in all athletes including the runner who developed significant rhabdomyolysis (peak CK 27,951 U/L). Conclusions Strenuous endurance exercise, even under extreme environmental conditions, does not result in structural myocardial damage in well-trained ultra-endurance athletes. We found no crossreactivity between cTnT and CK, neither in exercise-induced skeletal muscle trauma nor after rhabdomyolysis underscoring the excellent analytical performance of 3^rd generation cTnT assay.     

Analytical and diagnostic performance of troponin assays in patients suspicious for acute coronary syndromes

BACKGROUND: The controversy whether there is a clinically significant difference between troponin T (cTnT) and troponin I (cTnI) in regard to predictive value and cardiac specificity is still ongoing. METHODS: We evaluated enzyme-linked immunosorbent assay systems for cTnI and cTnT in patients with acute coronary syndromes and multiple control groups to define threshold values for risk stratification and compare their predictive value. RESULTS: In 312 patients with noncardiac chest pain, cTnI levels were below the detection limit of 0.2 microg/L and cTnT levels were 0.011 [0.010-0. 013] microg/L. In patients with end-stage renal failure (n = 26) and acute (n = 38) or chronic (n = 16) skeletal muscle damage, median concentrations were 0.20 [0.20-0.35], below the detection limit, and 0.20 [0.20-0.25] for cTnI, and 0.04 [0.01-0.10], 0.011 [0.005-0.025], and 0.032 [0.009-0.054] microg/L for cTnT. In patients with acute coronary syndromes (n = 1130), maximized prognostic value for 30-day outcome (death, infarction) was observed at a threshold level of 1.0 microg/L for cTnI (29.0% positive) and at 0.06 microg/L for cTnT (35. 0% positive). Significant differences in the area-under-the-curve values were observed between cTnI and cTnT (0.685 vs. 0.802; p = 0. 005). For both markers, the area-under-the-curve values did not increase with the second (within 24 h after enrollment) or third (48 h) blood draw. CTnI showed a less strong association with 30-day outcome than cTnT. When cTnI was put in a logistic multiple-regression model first, cTnT did add significant information. CONCLUSION: By using the defined threshold values and the employed test systems, single testing for cTnI and cTnT within 12 h after symptom onset was appropriate for risk stratification. Despite the lower cardiac specificity for cTnT, it appears to have a stronger association with the patients' outcome, whereas, as previously shown, the ability to identify patients who benefit from treatment with a GP IIb/IIIa receptor antagonist is similar.     

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.     

cTnT、CK-MB、FIB和DD联合检测在急性心肌梗死中的诊断价值

目的 通过对肌酸激酶同工酶(CK-MB)、肌钙蛋白T(cTnT)、纤维蛋白原(FIB)和D-二聚体(DD)联合检测为急性心肌梗死(AMI)患者的诊断和治疗提供依据.方法 临床及冠脉造影明确诊断的AMI患者67例为病例组,30例体检健康者为对照组,应用化学发光法、凝固法分别检测cTnT、CK-MB、FIB和DD等.结果 病例组CK-MB、cTnT、FIB、DD分别为(7.325±4.054)ng/mL、(12.201±8.235)ng/mL、(483.70±153.44)mg/dL、(725±363)μg/L;对照组CK-MB、cTnT、FIB、DD分别为(3.272±1.227)ng/mL、(0.045±0.042)ng/mL、(281.02±56.32)mg/dL、(426±151)μg/L;CK-MB、cTnT分别检测,CK-MB+cTnT联合检测,及4项指标联合检测的阳性率分别为58.2%、68.7%、77.6%、91.1%;病例组与对照组CK-MB、cTnT、FIB、DD含量比较差异有统计学意义(P<0.01).结论 CK-MB、cTnT、FIB、DD联合检测对AMI患者的早期诊断具有重要意义.     

Cardiac troponin T predicts long-term outcomes in hemodialysis patients

BACKGROUND: Increased plasma troponin T (cTnT), but not troponin I (cTnI), is frequently observed in end-stage renal failure patients. Although generally considered spurious, we previously reported an associated increased mortality at 12 months. METHODS: We studied long-term outcomes in 244 patients on chronic hemodialysis for up to 34 months, correlating the outcomes to plasma cTnT in routine predialysis samples. In addition, subsequent plasma samples at least 1 year later and within 6 months of data analysis were available in 97 patients and were used to identify patients with increasing plasma cTnT. The endpoints used were death and new or worsening coronary, cerebro-, and peripheral vascular disease and neuropathy. RESULTS: Transplantation occurred more frequently in patients with low initial cTnT: 31%, 13%, and 3% in the groups with cTnT < 0.010, 0.010-0.099, and > or = 0.100 microg/L, respectively. In the same groups, total deaths occurred in 6%, 43%, and 59% and cardiac deaths in 0%, 14%, and 24% of patients. In patients with follow-up samples, the group with increasing cTnT had a significantly increased death (relative risk, 2.0; P = 0.028). The increase was mainly in cardiac and sudden deaths. CONCLUSIONS: Higher plasma cTnT predicts long-term all-cause mortality in hemodialysis patients, even at concentrations < 0.100 microg/L, as does an increasing cTnT concentration over time.     

慢性心衰患者血清肌钙蛋白T、心肌酶和IL-6浓度变化的临床意义

目的通过检测血清中肌钙蛋白T、肌酸磷酸激酶（CK）以及肌酸磷酸激酶同工酶MB（CK-MB）以及细胞因子IL-6在慢性心衰患者中浓度变化的临床意义及与心功能的关系。方法收集50例充血性心力衰竭病人,30例正常人血浆,进行定量检测cTnT、CK、CK-MB三项指标,用ELISA方法检测IL-6的浓度。结果充血性心力衰竭（CHF）患者血清肌钙蛋白T及心肌酶检测结果显著高于对照组（P〈0.001）;CHF患者血清中IL-6的浓度显著高于对照组（P〈0.01）。心功能Ⅳ级组各项指标检测结果显著高于Ⅲ级组（P〈0.01）。结论 cTnT、CK、CK-MB三项指标以及细胞因子IL-6的联合检测,对心功能损伤及其严重程度的判断具有重要意义,并且具有较高的灵敏度和较强的特异性。     

Comparison of plasma cardiac troponins T and I in chronically hemodialyzed patients in relation to cardiac status and age.

Cardiac troponins (cTnT and cTnI) are useful tools for risk stratification in patients with unstable angina. However, their value in patients with renal failure has been questioned. In this study, we determined cTnT and cTnI at 3-month intervals during 9 months in 97 chronic renal failure (CRF) patients treated with hemodialysis. cTnT was measured using a third generation immunoassay and cTnI by fluorimetric immunoassay with a detection limit similar to that of cTnT (0.01 microg/l). In the renal patients without coronary heart disease (CHD(-) group), cTnT was more frequently elevated above cut-off for acute myocardial infarction (AMI) (up to 21.6%) than cTnI (no patient). In the absence of CHD, cTnT levels were positively correlated to age, and more than half of the CHD(-) patients aged over 60 years had cTnT levels above the upper reference limit (URL) of 0.04 microg/l (0.059+/-0.042 microg/l). cTnI increased with age in parallel to cTnT but mean levels did not exceed the URL of 0.08 microg/l in the CHD(-) patients aged over 60 years (0.036+/-0.031 microg/l). In the patients with documented cardiac events (CHD(+)) we found higher troponin levels than in the CHD(-) patients of the corresponding age, but for cTnl the differences between CHD(+) and CHD(-) patients were significant in the patients aged < or =60 years only (0.049+/-0.054 vs. 0.019+/-0.018 microg/l, p<0.05). For cTnT, the differences between patients with and without coronary events also tended to be less important in the eldest patients. There was a significant correlation between cTnI and cTnT levels in the CHD(-) and in the CHD(+) groups. Changes in the plasma levels of cardiac troponins are common in hemodialysis patients in the absence of CHD, and advanced age appears to amplify these changes. The reason could be that most hemodialysis patients with advanced age have subclinical lesions and demonstrate release characteristics of troponins that compare to those in patients with symptomatic coronary events. Therefore, it will be important to analyze troponin elevations above the URL or above the cut-off concentration for AMI in asymptomatic renal patients in relation to prognosis.     

Cardiac troponin T circulates in the free, intact form in patients with kidney failure

BACKGROUND: The clinical significance of the increased concentrations of cardiac troponins observed in patients with end stage renal disease (ESRD) in the absence of an acute coronary syndrome (ACS) is controversial. One proposed explanation is that immunoreactive fragments of cardiac troponin T (cTnT) accumulate in ESRD. We used gel-filtration chromatography (GFC) to ascertain whether fragments of cTnT, which could cross-react in the commercial diagnostic immunoassay (Roche Diagnostics), were the cause of the increased cTnT in the serum of patients with ESRD. METHODS: We subjected sera from ESRD patients (n = 21) receiving dialysis and having increased cTnT concentrations to size-separation GFC. We detected cTnT in the chromatography fractions by use of the same antibodies used in the commercial assay for serum cTnT. RESULTS: In all patients, cTnT immunoreactivity eluted as a major, homogeneous peak in an identical position between the peaks of serum prolactin [relative molecular mass (Mr) 23,000] and albumin (Mr 67,000): the elution pattern of cTnT in samples obtained from ACS patients was identical to that of the ESRD patients. There was no evidence that low-molecular-mass (Mr < 23,000) cTnT fragments were the cause of the increased cTnT in the patients studied. CONCLUSIONS: The form of cTnT observed in the serum of patients with kidney failure and immunoreactive in the diagnostic assay is predominantly the free intact form, as in patients with ACS. Our data are consistent with the view that circulating cTnT in renal failure reflects cardiac pathology.     

血清心肌肌钙蛋白T在病毒性心肌炎诊断及预后影响研究

目的：探讨血清心肌肌钙蛋白T（cTnT）在病毒性心肌炎（VM）诊断及预后判断中的应用.方法：回顾性分析自2000～2004年采用酶联免疫测定法对126例不同病程的VM患者及60例正常者（正常组）检测血清cTnT及肌酸激酶-MB同工酶（CK-MB）.长期随访观察cTnT：采用超声心动图测定,观察心脏大小及心室功能变化.结果：VM患者cTnT的阳性率显著高于CK-MB.随着病程的延长,cTnT的阳性率降低;对照组全部阴性.随着入院时血清cTnT水平的由低至高,左室舒张末内径增大而射血分数降低.结论：cTnT是心肌细胞急性损伤的指标优于CK-MB.cTnT水平高低与患者心脏大小以及远期心室功能发展有关,对拟诊VM患者检测cTnT为VM的治疗转归和预后提供重要线索.     

Effect of hemodialysis on traditional and innovative cardiac markers

The diagnostic approach to acute coronary syndrome (ACS) is challenging in patients with impaired renal function since most serum biomarkers are commonly increased in this clinical setting. Cardiac troponin T (cTnT), creatine kinase isoenzyme MB (CK MB), myoglobin, and ischemia modified albumin (IMA), were assayed in 45 patients prehemodialysis (pre-HD) and posthemodialysis (post-HD), and results were adjusted for hemoconcentration. The pre-HD values of serum IMA and cTnT were above the respective diagnostic thresholds (IMA<85 K units/L; cTnT <0.03 ng/mL) in six (13%) and 27 (60%) patients undergoing chronic HD, respectively. A significant (105.0 vs. 79.0 K units/L, P<0.0001) and variable (+38%; 95% confidence interval [CI], 12-65%) increase of serum IMA was observed post-HD, whereas the other biomarkers significantly decreased (cTnT: 0.029 vs. 0.044 ng/mL, P=0.016; CK-MB: 2.33 vs. 2.50 microg/L, P<0.0001; myoglobin: 128.1 vs. 148.7 microg/L, P<0.0001). Biomarkers of myocardial injury, especially cTnT and IMA, might be used in HD patients, provided that an appropriate diagnostic interpretation is guarantee, according to individual baseine value, metabolism, and time of sampling. Moreover, IMA might be reliably applied to stratify the long-term risk of these patients, but not for diagnosing an ACS during or immediately post-HD.     

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

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

Diagnostic utility of new immunoassays for the cardiac markers cTnI, myoglobin and CK-MB mass

OBJECTIVES: We investigated the diagnostic value of a new system, the Innotrac Aio! immunoassays for troponin, myoglobin and CK-MB, in 270 samples from patients with ACS, after bypass surgery (CABG) or with stable heart failure in comparison to the respective Roche assays. RESULTS: The values of the cardiac markers assessed by the respective assays correlated (cTnT/cTnI Rho = 0.94, myoglobin Rho = 0.87, CK-MB Rho = 0.84). If values were dichotomised, we found a high concordance of test positive and negative classified patients by troponins with the respective assays. CONCLUSION: There is strong evidence that the Innotrac Aio! system for cTnI measurement can be used reliably.     

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.