Myocardial Injury and the Release of Troponins I and T in the Blood of Patients (original) (raw)
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Release kinetics of serum cardiac troponin i in ischemic myocardial injury
Clinical Biochemistry, 1996
Objectives: The study was undertaken to evaluate the release kinetics of cardiac troponin I (c'rn-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 (>t0.1 pg/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 (,o= 0.001), the overall sensitivity of cTn-I (93.9%) was higher than that of CK-MB activity (,c, = 0.00001). cTn-I was more sensitive at admission (,o = 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.
Circulation, 2000
Background —Cardiac troponin I and T (cTnI and cTnT) are specific biochemical serum markers for acute myocardial infarction (AMI). However, cTnI diagnostic assays are plagued by difficulties, resulting in ≥20-fold differences in measured values. These discrepancies may result from the release of the numerous cTnI modification products that are present in ischemic myocardium. The resolution of these discrepancies requires an investigation of the exact forms of cTnI present in the bloodstream of patients after myocardial injury. Methods and Results —A western blot–direct serum analysis protocol was developed that allowed us to detect intact cTnI and a spectrum of up to 11 modified products in the serum from patients with AMI. For the first time, we document both a cTnI degradation pattern and the existence of phosphorylated cTnI in serum. The number and extent of these modifications reflect patterns similar to the time profiles of the routine clinical serum markers of total creatine k...
Cardiac troponin I: the gold standard in acute myocardial infarction diagnosis
Bosnian journal of basic medical sciences / Udruženje basičnih mediciniskih znanosti = Association of Basic Medical Sciences, 2003
Cardiovascular diseases are leading cause of morbidity in the world. Measurement of the level of biochemical markers in the serum is one of World Health Organisation (WHO) criteria in diagnosing acute myocardial infarction (AMI). Non-specific clinical state of patients and insufficiently sensitive electrocardiographic (ECG) diagnostics, at patient's hospital admission time, point out the importance of biochemical markers in acute myocardial infarction diagnosis. Technology development and new diagnostic methods lead to the invention of highly sensitive and specific marker as myocardial damage evidence. Cardiac Troponin I (cTnI) is specific marker for myocardial damage1. Its elevation in the serum within myocardial ischemia symptomatology is important in diagnosis of myocardial infarction.
We examined the release of cardiac troponin T (cTnT) and I (cTnI) into the blood of patients after acute myocardial infarction (AMI). Three postAMI serum samples were applied in separate analytical runs onto a calibrated gel filtration column (Sephacryl S-200), and the proteins were separated by molecular weight. Using commercial cTnT and cTnI assays measured on collected fractions, we found that troponin was released into blood as a ternary complex of cTnT-I-C, a binary complex of cTnI-C, and free cTnT, with no free cTnI within the limits of the analytical methodologies. The serum samples were also examined after incubation with EDTA and heparin. EDTA broke up troponin complexes into individual subunits, whereas heparin had no effect on the assays tested. We added free cTnC subunits to 24 AMI serum samples and found no marked increase in the total cTnI concentrations, using an immunoassay that gave higher values for the cTnI-C complex than free cTnI. To characterize the cross-reactivity of cTnT and cTnI assays, purified troponin stan-
Diagnostic Efficiency and Prognostic Value of Troponin T Measurement in Acute Myocardial Infarction
2014
The diagnosis and prognosis of patients hospitalized with acute myocardial ischemia is quite variable. We examined the value of serum levels of cardiac Troponin T, serum CK-MB levels for detection of ischemic myocardial injury and risk stratification within 40 days in patients with acute myocardial ischemia with one specimen taken 2-8 hours of the onset of symptoms. Methods We studied 141 patients with a diagnosis of acute ischemic myocardial injury. The concentration of TnT and CK-MB is made on Coobas 6000 by a electrochemioluminescence and turbidometric methods. Results The median duration of the ischemic episodes qualifying the patients for the study was 4 hours. Chest pain was continuous in 51.8% and intermittent in 48.2%. Troponin T levels were elevated in 47 % of the patients whose ischemic symptoms had lasted more than seven hours (p= 0.06). 33% of the patients had the elevated troponin T level but CK-MB level was normal. Mortality within 40 days was significantly higher in t...
Atherosclerosis, 2012
Background: High-sensitive Troponin I (hsTnI) facilitates the early diagnosis of myocardial infarction (MI). However, since hsTnI has not been well characterized in non-ischemic cardiac conditions, the predictive value of hsTnI for MI remains unclear. Methods: hsTnI (ADVIA Centaur, Siemens) on admission was analyzed in 929 patients with acute cardiac condition and invasive ascertainment of coronary status by catheterization. Results: Hs-TnI upon presentation was higher in patients with STEMI (median 1.27 ng/mL, IQR 0.13-14.5 ng/mL) as compared to patients with Non-STEMI (0.66 ng/mL, IQR 0.10-4.0 ng/mL, p < 0.001) whereas it did not differ from STEMI in Tako-Tsubo cardiomyopathy (2.57 ng/mL, IQR 0.17-8.4 ng/mL) and myocarditis (9.76 ng/mL, IQR 2.0-27.0 ng/mL). In patients with resuscitation of non-ischemic cause (0.31 ng/mL, IQR 0.06-1.3 ng/mL), acute heart failure (0.088 ng/mL, IQR 0.035-0.30 ng/mL) and hypertensive emergency (0.066 ng/mL, IQR 0.032-0.34 ng/mL), hs-TnI was elevated above the recommended threshold of 0.04 ng/mL. At this cutpoint of 0.04 ng/mL, hsTnI indicated acute MI (STEMI or Non-STEMI) with a sensitivity of 88% and a specificity of 45% (ROC-AUC 0.748). When patients with STEMI were excluded, hsTnI indicated Non-STEMI with a sensitivity of 87% and a specificity of 45% (ROC-AUC 0.725). When sequential measurements were taken into account in a restricted cohort, a maximum hsTnI of ≥0.40 ng/mL provided a sensitivity of 89% and a specificity of 85% (ROC-AUC 0.909) for Non-STEMI. Conclusions: HsTnI is a sensitive, albeit unspecific marker of MI. In patients with mildly elevated hsTnI and without evidence for STEMI, we suggest serial assessment of hsTnI and a 10-fold higher cutpoint of 0.40 ng/mL before Non-STEMI is assumed.
Clinical Biochemistry, 2013
Objectives: ST-elevation and non-ST-elevation myocardial infarction (STEMI, NSTEMI) are considered two distinct pathophysiologic entities. We evaluated cardiac troponin I (cTnI) release in STEMI and NSTEMI using a "contemporary" (CV > 10 to 20% at the 99th percentile concentration) cTnI assay for patients undergoing early percutaneous coronary intervention (PCI). Design and methods: 856 patients with suspected acute coronary syndrome consecutively admitted to the Emergency Department of the Maggiore Hospital of Novara (225 STEMI and 135 NSTEMI) were selected according to: 1) early (≤4 h from admission) and successful PCI; and 2) cTnI measurements at ED presentation and within 24 h. The influence of the MI type on cTnI concentrations at baseline and after PCI as well as the velocity of cTnI [cTnI V = absolute increase (after log conversion of cTnI measurements) / delay between the two measurements] was studied by multiple regression analysis, adjusting for patient parameters. Results: A statistically significant interaction between MI type and time from symptoms was reported on cTnI concentrations (p b 0.0001): STEMI and NSTEMI differed for cTnI releases at admission and after revascularization. Higher cTnI V in STEMI was detectable in patients admitted within 6 h from symptoms. Baseline cTnI concentrations were lower in patients with a history of coronary artery disease (CAD) and increased with aging (p b 0.0001). In the elderly (>75 years), the cTnI V was significantly increased. Conclusion: STEMI and NSTEMI patients have different patterns and dynamics of cTnI release influenced by the interaction with time from symptoms, by aging and history of CAD.
Diagnostics on acute myocardial infarction: Cardiac troponin Biomarkers
Biosensors and Bioelectronics, 2015
Acute myocardial infarction or myocardial infarction (MI) is a major health problem, due to diminished flow of blood to the heart, leads to higher rates of mortality and morbidity. Data from World Health Organization (WHO) accounted 30% of global death annually and expected more than 23 million die annually by 2030. This fatal effects trigger the need of appropriate biomarkers for early diagnosis, thus countermeasure can be taken. At the moment, the most specific markers for cardiac injury are cardiac troponin I (cTnI) and cardiac troponin T (cTnT) which have been considered as 'gold standard'. Due to higher specificity, determination of the level of cardiac troponins became a predominant indicator for MI. Several ways of diagnostics have been formulated, which include enzyme-linked immunosorbent assay, chemiluminescent, fluoro-immunoassays, electrical detections, surface plasmon resonance, and colorimetric protein assay. This review represents and elucidates the strategies, methods and detection levels involved in these diagnostics on cardiac superior biomarkers. The advancement, sensitivity, and limitations of each method are also discussed. In addition, it concludes with a discussion on the point-of care (POC) assay for a fast, accurate and ability of handling small sample measurement of cardiac biomarker.