An evaluation of the quantitative analysis of troponin T (a new marker of coronary disease) was carried out in the 150 patients of cardiovascular department of Hautepierre Hospital, Strasbourg Medical University, France from January to August 1998. The results have shown that the value of troponin T was much higher than this of creatinine Kinase (CK) and CK- MB in the diagnosis of acute myocardial infarction. The possitive predict value was 90% and the negative predicts value was less than 50%.
Coronary Disease ; Troponin T

No abstract available.
C-Reactive Protein* ; Emergencies* ; Emergency Service, Hospital* ; Troponin T* ; Troponin*

No abstract available.
C-Reactive Protein* ; Emergencies* ; Emergency Service, Hospital* ; Troponin T* ; Troponin*

BACKGROUND AND OBJECTIVES: Small myocardial infarction (MI) has been reported in 8 - 20% of patients undergoing percutaneous transluminal coronary angioplasty (PTCA). But neither appropriate threshold of cardiac enzyme nor useful biochemical marker for its detection has not yet been fully defined. We examined the cardiac enzyme to define more valuable biochemical marker for the detection of small MI after PTCA and to evaluate factors associated with small MI after PTCA. MATERIALS AND METHODS: This study population consisted of 209 consecutive patients who underwent PTCA. Cardiac enzyme levels were measured before and 8, 24 hours after PTCA for CK-MB, and before and 16 hours after PTCA for troponin T. We defined small MI when CK-MB levels were over 16U/L and/or troponin T levels were over 0.2 ng/ml. RESULTS: Incidence of small MI after PTCA was 28/209 (13.4%) and the most of those were non-Q MI (24/28, 86%). In the detection of small MI after PTCA, the sensitivity of troponin T was higher than CK-MB (92.9% vs 39.3%). Major complications (major dissection, acute coronary occlusion, and side branch occlusion) developed significantly more in patients with small MI than in patients without small MI (p=0.002). Three independent variables, which were significantly associated with small MI after PTCA, were age, total/subtotal occlusion, and acute coronary occlusion as complication (p=0.01, p=0.02, and p=0.04, respectively). CONCLUSIONS: Troponin T is more sensitive biochemical marker than CK-MB in the detection of small MI after PTCA. Major complications of angioplasty are frequently associated with small MI. Especially, age, total occlusion, and acute coronary occlusion as complication are independent factors significantly associated with small MI after PTCA.
Angioplasty ; Angioplasty, Balloon, Coronary* ; Biomarkers ; Coronary Occlusion ; Humans ; Incidence ; Myocardial Infarction ; Troponin T* ; Troponin*

BACKGROUND: The goal of this study is to assess the clinical utility of cardiac troponin T(cTnT) and creatine kinase MB(CK-MB) activity and to determine optimum decision thresholds by using receiver operating characteristic(ROC) curve for cTnT and CK-MB. METHOD: We evaluated serum cTnT(Elecsys 2010, Boeringer Manheim, Germany) and CK-MB activity(XRC, Johnson & Johnson Clinical Diagnostics, USA) in 15 cases(124 samples) of acute myocardial infarction(AMI) and 64 cases(98 samples) of non-AMI patients from April 1998 to October 1998. RESULTS: CK-MB activity [cut-off value 16 U/L, relative index(CK-MB 100/total CK) 4-25%)] and cTnT(cut-off value 0.1 ng/mL) were detected in serum within 3 hours after onset of chest pain and cTnT was persistent to longer times than CK-MB activity. Sensitivity of cTnT(69.6%) is not statistically different from CK-MB activity(72.9%) within 24 hours of chest pain but more sensitive after 24 hours of symptom. Specificity(87.9%) and negative predictive value(91.2%) of cTnT were superior to that of CK-MB activity within 24 hours of chest pain. ROC curve analysis demonstrated the following decision cutoff, sensitivity, specificity: cTnT 0.13 ng/mL, 76.7%, 100%; CK-MB activity 14 U/L, 84.7% and 71.0%. CONCLUSION: Measurement of cTnT was useful for late admitted AMI and together with CK-MB could improve the detection of myocardial infarction.
Chest Pain ; Creatine Kinase ; Humans ; Myocardial Infarction* ; ROC Curve ; Sensitivity and Specificity ; Troponin T* ; Troponin*

PURPOSE: This study was designed to evaluate diagnostic accuracy of serial electrocardiograms(ECG), myocardial band of creatinine phosphokinase(CK)(CK-MB/CK ratio) and two dimensional echocardiography(ECHO) for myocardial injury in patients with blunt chest trauma. METHODS: We prospectively investigated 54 patients(male : 38, female : 16, mean age : 41) with severe blunt chest trauma. Presence of myocardial injury was determined by increase(>0.1ug/L) of peak serum troponin T(TnT) concentration from serial mesurements. RESULTS: Among 54 patients with blunt chest trauma, 23 patients(43%) had increased peak TnT level which suggested of myocardial injury. Among 23 patients with increased TnT, abnormal ECG findings were found in 18(78%) and echocardiographic abnormalities were observed in 17(74%). Cardiovascular events in 9(39%) of 23 patients with increase Tnt. There was no cardiovascular events in patients with normal TnT. CONCLUSION: Significant proprotion of patients with blunt chest trauma had elevated TnT value which suggested of myocardial injury. We recommend echocardiagraphy and serial tracing of ECG to verify the clinical significance of elevated TnT in patients with blunt chest trauma.
Creatinine ; Diagnosis* ; Echocardiography ; Electrocardiography ; Female ; Humans ; Prospective Studies ; Thorax* ; Trinitrotoluene ; Troponin ; Troponin T

PURPOSE: The aim of this study was to evaluate the clinical efficiency of cardiac troponin T(cTnT) in detecting myocardial damage in neonatal asphyxia and to compare the diagnostic value of cTnT with creatine kinase MB(CK-MB). METHODS: Sixty-three neonates were enrolled in this study, consisting of 27 asphyxiated infants(asphyxiated group; 1-min or 5-min Apgar score< or=6) and 36 healthy infants(control group). The two groups were divided to 4 subgroups as follows; group I(17 preform asphyxiated neonates), group II (10 full-term asphyxiated neonates), group III(16 preterm healthy neonates), group IV(20 full-term healthy neonates). Serum cTnT was measured within 24 hours, at 24-47 hours, and 48-72 hours after birth, respectively. Serum CK-MB was measured within 24 hours after birth. RESULTS: 1) cTnT within 24 hours in asphyxiated group was significantly higher than in the control group(P<0.05). 2) cTnT in group II was not significantly higher than in group I (P>0.05), whereas CK-MB in group II it was higher than in group I (P<0.001). Between group III and IV, cTnT and CK-MB showed significant differences(P<0.05). 3) cTnT did not change with gestational age or birthweight. CK-MB was correlated to birthweight and gestational age. 4) Twelve asphyxiated infants had at least one abnormal cTnT(>0.2 microgram/L). Ten of them(83%) had a tricuspid insufficiency of moderate or severe degree. CONCLUSION: cTnT is a more heart-specific serodiagnostic marker than other markers in asphyxiated neonates with suspected myocardial damage.
Asphyxia* ; Creatine Kinase ; Gestational Age ; Humans ; Infant ; Infant, Newborn ; Parturition ; Troponin T* ; Troponin*

BACKGROUND AND OBJECTIVES: Human Troponin T & I (TnT, TnI) has several isoforms which have different functional property. This study was designed to describe the isoform expression of TnT & TnI in failing and hypertrophic human heart and during normal development. MATERIALS AND METHOD: Myocardium was attained from hypertrophic hearts (n=10) of TOF patients who underwent myomectomy, from failing hearts (n=10) of transplant recipients, from normal hearts (n=5) of patients in brain death and from aborted fetal hearts (n=5). After the extraction of RNA, RT-PCR was performed for TnT & TnI isoforms and GAPDH to evaluate the isoform expression qualitatively and quantitatively. RESULTS: In terms of TnI, slow skeletal TnI was expressed more than cardiac TnI in fetal hearts[ratio of Troponin over GAPDH (R)=1.3:0.5] but cardiac TnI was dominant in adult hearts (r=0.3:1.1) (p 0.05). Failing hearts showed similar pattern with adult hearts (r=0.3:1.2) and hypertrophic hearts showed the intermediate pattern (r=0.9:1.3). In terms of TnT, T1 and T3 were expressed in fetal hearts (r=0.04, 0.8) but only T3 was expressed in adult hearts (r=1.1). Failing hearts and hypertrophic hearts showed similar pattern with adult hearts and no differences in the amount of expression (r=1.4, 1.3). CONCLUSION: There is isoform switch from fetal to adult form during development and it might be responsible for the differences of myocardial functional property between fetal and adult heart. Failing and hypertrophic hearts showed no differences with normal hearts, which means the isoform switch of TnT & I might have no significant role in functional disturbances in these conditions.
Adult ; Brain Death ; Fetal Heart ; Heart* ; Humans* ; Myocardium ; Protein Isoforms ; RNA ; Transplantation ; Trinitrotoluene ; Troponin T* ; Troponin*

BACKGROUND: The point-of-care (POC) troponin T assay has been used in various clinical settings. Recently, a POC troponin T assay with an extended measurable range (40 ng/L-2,000 ng/L) was introduced. We aimed to evaluate the analytical performance of the Roche Cardiac POC Troponin T assay (POC TnT, Roche Diagnostics, Switzerland) using the cobas h 232 POC system. METHODS: The repeatability and within-laboratory imprecision of the POC TnT assay were evaluated using the Roche Cardiac POC Troponin T level 2 control. Repeatability was also assessed using patient samples. Linearity of the POC TnT assay was evaluated using patient samples containing five different concentrations of troponin T. Performance of the Elecsys Troponin T high sensitivity assay (hs-TnT) was compared with that of the POC TnT assay using 40 patient samples. RESULTS: The repeatability (%CV), and within-laboratory imprecision (%CV) using the level 2 control solution (mean troponin T, 441.6 ng/L) were 8.5% and 8.6%, respectively. The repeatability of patient samples containing 88.7 ng/L and 454.6 ng/L TnT was 7.5% and 7.2%, respectively. The POC TnT assay was confirmed to produce linear data between 54.0 ng/L and 1,347.7 ng/L. Relative to the hs-TnT assay, the Passing-Bablok linear regression equation (correlation coefficient) was y=0.8933x+6.24 (r=0.988). At a troponin T concentration of 40 ng/L, the estimated bias of the POC TnT assay was 1.972 ng/L (4.93%). CONCLUSIONS: Our data suggest that the Roche Cardiac POC Troponin T assay is reliable in cases where POC troponin T testing is required.
Bias (Epidemiology) ; Humans ; Linear Models ; Point-of-Care Systems* ; Trinitrotoluene ; Troponin T* ; Troponin*

OBJECTIVE: To evaluate the accuracy of cardiac troponin (cTn) levels in the diagnosis of acute myocardial infarction (AMI) in patients with chronic kidney disease (CKD) and explore a potential strategy for improving the diagnostic accuracy. METHODS: We retrospectively analyzed the data from patients with high-risk chest pain admitted in Zhujiang Hospital from January, 2018 to December, 2020, including 126 patients with and 272 patients without CKD, and 122 patients diagnosed to have AMI and 276 patients without AMI. The baseline clinical data of the patients and blood test results within 12 h after admission were collected. RESULTS: In patients without AMI, cTnT level was significantly higher in those with co-morbid CKD than in those without CKD (P < 0.001), and showed a moderate negative correlation with eGFR (r_s=- 0.501, P < 0.001), while cTnI level did not differ significantly between the two groups (P=0.72). In patients with CKD, the optimal cutoff level was 0.177 μg/L for cTnT and 0.415 ng/mL for cTnI for diagnosis of AMI, for which cTnI had a higher specificity than cTnT. The diagnostic model combining both cTnT and cTnI levels [P=e^Y/(1+ e^Y), Y=6.928 (cTnT)-0.5 (cTnI)-1.491] had a higher AUC value than cTn level alone. CONCLUSION In CKD patients, the cutoff level of cTn is increased for diagnosing AMI, and cTnI has a higher diagnostic specificity than cTnT. The combination of cTnT and cTnI levels may further improve diagnostic efficacy for AMI.
Humans ; Retrospective Studies ; Myocardial Infarction/diagnosis* ; Comorbidity ; Troponin T ; Troponin I ; Renal Insufficiency, Chronic/diagnosis* ; Biomarkers