Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a previous study on the diagnostic efficiency of troponin T measurements in patients with suspected acute myocardial infarction (AMI), the authors found a high variability of troponin T serum concentration changes on day 1 in patients with AMI who underwent thrombolytic treatment. Therefore, the aims of the present study were to investigate the intracellular compartmentation of troponin T and to analyze the effects of AMI reperfusion on the appearance kinetics of cardiac troponin T in serum. Cardiac troponin T was measured with a newly developed bideterminant sandwich assay using cardiospecific, affinity-purified polyclonal antibodies and peroxidase-labeled monoclonal antibody. An unbound cytosolic troponin T pool was found in ultracentrifuged homogenates of myocardial tissue of different species ranging from 0.013 to 0.036 mg/g wet weight. The soluble troponin T molecule had electrophoretic properties identical to troponin T compartmented in the myofibrils. The clinical study group comprised 57 patients with AMI undergoing thrombolytic treatment. Blood flow to the infarct zone and point of time of reperfusion were tested by immediate and late angiography. The appearance of troponin T in serum on day 1 after the onset of AMI depended strongly on reperfusion and on duration of ischemia before reperfusion. Thus, in patients with early reperfused AMI, a marked peak in troponin T serum concentrations was found at 14 hours after the onset of pain. This early troponin T peak was absent in patients with AMI reperfusion occurring greater than 5.5 hours after the onset of pain and in patients with nonreperfused AMI. By contrast, the kinetics of troponin T release after the first day after AMI were unaffected by reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intracellular compartmentation of cardiac troponin T and its release kinetics in patients with reperfused and nonreperfused myocardial infarction. 190 90

The marked differences in troponin T serum concentrations observed in patients with reperfused and non-reperfused myocardial infarction may be due to a perfusion dependent wash-out of an unbound fraction of cardiac troponin T. To test the release kinetics of troponin T experimentally, the isolated rat heart (Langendorff preparation) was damaged either by the calcium paradox or by no-flow ischemia. Following membrane damage by the calcium paradox troponin T (TNT) showed the same release kinetics in the coronary effluent as the cytosolic markers creatine kinase (CK) or lactate dehydrogenase (LDH). Peak levels of troponin T (282 +/- 58 micrograms/l), CK (6754 +/- 1642 U/l), and LDH (5817 +/- 1730 U/l) occurred 5 min after onset of reperfusion with calcium containing buffers and returned to 9.9%, 1.3%, and 1% of their respective peak levels within 55 min of reperfusion. During reperfusion after no-flow ischemia different release kinetics were found for cytosolic enzymes and troponin T. After 60 min of ischemia, troponin T levels in the coronary effluent increased over the entire reperfusion period of 55 min, almost doubling the 5 min value (191%). In contrast, cardiac enzymes rapidly declined to 18% (CK) and 23% (LDH) of their respective 5 min values at the end of reperfusion. Light microscopy after reperfusion with carbon black revealed a complete and homogeneous reperfusion of Langendorff hearts after no-flow ischemia. Immunoblot analysis confirmed the release of an undegraded 39 kDa troponin T molecule, both after global ischemia and the calcium paradox. These data indicate that prolonged ischemia induces a continuous liberation of cardiac troponin T, most probably from disintegrating myofibres, whereas membrane damage leads almost exclusively to leakage of a functionally unbound troponin T pool. These findings may explain the biphasic serum concentration changes of cardiac troponin T in patients with reperfused myocardial infarction.
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PMID:Intracellular compartmentation of troponin T: release kinetics after global ischemia and calcium paradox in the isolated perfused rat heart. 777 86

The aim of this study was to examine the effect of ischemic preconditioning on the releases of cardiac troponin T (TnT) during reperfusion in isolated rat hearts. Experiments were done on 22 rat hearts, which were perfused according to the method of Langendorff and were divided into the control group (n = 14) and the preconditioning group (n = 8). Double 5 min of ischemia each followed by 5 min reflow were applied as ischemic preconditioning. After 20 min of global ischemia, the releases of TnT, creatine kinase (CK), and lactate dehydrogenase (LD) in coronary effluent and the left ventricular developed pressure (LVP) were measured during 60 min of reperfusion. Ischemic preconditioning significantly suppressed the amounts of TnT released during reperfusion, as with those of CK and LD, and also improved contractile dysfunction (nine hearts in which ventricular fibrillation was sustained were excluded from the evaluation for hemodynamics), though the release kinetics of TnT was different from that of CK and LD. There were good inverse relationships between the LVP and the total amounts of TnT released during reperfusion period (sigma TnT) or TnT levels at 60 min of reperfusion. Cardiac TnT can be used as a useful biochemical marker for hemodynamics and myocardial damage after reperfusion.
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PMID:Effects of ischemic preconditioning on the release of cardiac troponin T in isolated rat hearts. 794 60

We studied the release kinetics of cardiac troponin T (TnT) from coronary effluent in a re-stenosis model of 13 isolated rat hearts. After a 20-min period of global ischemia, we reperfused the hearts for 60 min according to the method of Langendorff. A second period of global ischemia was then induced for 5 min (protocol A) or 20 min (protocol B), followed by a second 60-min period of reperfusion. Coronary flow was measured by a timed collection of the coronary effluent. Levels of TnT in the effluent were compared to those of creatine kinase (CK) and lactate dehydrogenase (LD). Levels of TnT increased after the second global ischemia, but no differences were found in the released levels of TnT between protocols A and B. However, the amounts of CK and LD released in protocol B were much greater than those released in protocol A. These studies indicate that the release kinetics of TnT are different from that of CK and LD during reperfusion. It appears that after the initial ischemic damage to TnT, subsequent ischemia causes damage to TnT regardless of the duration of the insult, whereas the damage to sarcolemma is dependent on the duration of the ischemia.
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PMID:Effects of repeated ischemia on release kinetics of troponin T, creatine kinase, and lactate dehydrogenase in coronary effluent from isolated rat hearts. 804 57

Previously, we reported that cardiac troponin T (TnT) can be detected and measured in coronary effluent from isolated rat hearts during hypoxia. The present study was designed to evaluate the release kinetics of TnT from post-ischemic rat hearts. Using the Langendorff technique, the hearts were reperfused for 4 h after 20 min or 60 min of global ischemia. Coronary flow was measured by timing the collection of the coronary perfusate that dripped from the hearts, and left ventricular pressure (LVP) was monitored continuously during the experiments. The amount of TnT released in 1 min was compared with the release of creatine kinase (CK) and lactate dehydrogenase (LD). The release kinetics of CK and LD showed a monophasic pattern and the levels at 4 h after reperfusion returned to baseline levels. By contrast, the release kinetics of TnT showed a small peak followed by a larger and more sustained peak. There were good negative correlations between developed pressure of LVP and both sigma TnT and the amount of TnT released within 1 min at 4 h after reperfusion. These results indicate that the release kinetics of TnT is different from that of CK and LD during reperfusion, and further that cardiac TnT is a useful indicator of myocardial cell damage and can be used to evaluate the degree of myocardial cell damage in both the early and late phase of acute myocardial infarction.
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PMID:Release kinetics and correlation with hemodynamic dysfunction of cardiac troponin T in coronary effluent from isolated rat hearts during reperfusion. 824 Feb 23

The development of methods for the detection of circulating CK-MB mass, cardiac troponin T (cTn-T) and troponin I (cTn-I) has increased the diagnostic potential in the identification of myocardial damage. Coronary angioplasty (PTCA) represents a widely accepted revascularization procedure and a clinical model of induced ischemia. Using these new biochemical markers, we evaluated the incidence and the clinico-procedural correlates of minor myocardial damage (MMD) in a series of patients treated with PTCA in our Department. In 57 consecutive patients (75% males; mean age 58 years; range 35-80) undergoing elective PTCA from March 1 to June 30, 1995, serum levels of CK-MB mass, cTn-T and cTn-I were measured at baseline and at 6, 12 and 24 hours after the procedure. Seventy-eight coronary stenoses were dilated (mean 1.4 lesion/patient), 17 of these were in infarct-related vessels; 8 were total occlusions and 2 were located in saphenous vein grafts. Twenty-two procedures were completed by coronary stenting (17 elective). cTn-T and cTn-I were considered abnormal when serum levels were > 0.2 ng/ml and > 0.6 ng/ml, respectively. CK-MB mass was also determined in all patients (abnormal > 5 ng/ml). No patients had clinical or electrocardiographic evidence of myocardial infarction after the procedure. Overall, 16 patients (28%) developed biochemical evidence of post-procedural MMD (defined as the presence of at least one abnormal sample of any among the three markers tested). Four (7%) had abnormal CK-MB mass (at least one sample), 9 (16%) abnormal cTn-T, and 15 (26%) abnormal cTn-I. When CK-MB mass was elevated, both cardiac troponins were also elevated. In patients positive for MMD and abnormal CK-MB mass, peak cTn-I was significantly higher than in patients with normal CK-MB (3.02 +/- 1.07 vs 1.02 +/- 0.11 ng/ml; p = 0.009). The difference was not evident when comparing the same groups of patients for cTn-T (0.26 +/- 0.04 vs 0.18 +/- 0.10 ng/ml; p = 0.16). Also, peak cTn-I but not peak cTn-T had a positive correlation with peak CK-MB mass (r = 0.89; p < 0.0001 and r = 0.23; p = 0.40). The elevation of either marker of MMD was not related to clinical, angiographic or procedural variables. A possible interpretation for MMD was found in 2/3 of cases: bail-out (2); late occlusion (1); minor side branch occlusion (3); distal embolization from saphenous vein grafts (2) or total occlusions (2). In our series, MMD after PTCA occurs in 28% of cases and is unrelated to clinical, angiographic and procedural variables. Both cTn-T and cTn-I increase the sensitivity of CK-MB mass in the detection of MMD after PTCA, cTn-I being the most sensitive marker. In about 1/3 of cases, the presence of MMD remains unexplained. The prognostic implications of MMD are as yet undefined.
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PMID:[Troponin T, Troponin I and CK-MB (mass) in the detection of periprocedural myocardial damage after coronary angioplasty]. 924 45

In animal experiments, dobutamine infusion was found to impair the oxygen supply-demand balance in hypoperfused areas of hibernating myocardium which may induce myocardial damage. The aim of our study was to assess whether dobutamine echocardiography can induce myocardial damage detected by an increase in the cardiac troponin T level in blood. Twenty seven patients with coronary artery disease and severe stenosis of at least one major coronary artery (> or = 90% of luminal diameter narrowing) supplying dysfunctional myocardial segments underwent dobutamine echocardiography. Dobutamine was infused in 3 min dose increments of 5, 10, 20, 30, and 40 microg per kg body weight per minute with the addition of atropine up to 1 mg if ischemia or an 85% predicted maximal heart rate were not achieved. In 15 patients the protocol with prolonged application of 40 microg per kg per minute of dobutamine for 6 min and for the next 5 min with the addition of atropine was used. To exclude minor myocardial damage, an increase in the cardiac troponin T blood level was assessed qualitatively by the TROP T sensitive Rapid Test 20 h after dobutamine echocardiography. In 20 patients the dysfunctional segments were found to be viable with inducible ischemia exhibiting either continuous worsening in systolic thickening or "biphasic" response characterised by the improvement of their systolic thickening with a small dose and by a worsening of the thickening with a high dose of dobutamine. No patient exhibited positive TROP T sensitive Rapid Test result. In patients with coronary artery disease and severe stenosis of a major coronary artery supplying dysfunctional but viable myocardial segments, dobutamine echocardiography does not induce myocardial damage detectable by an increase in cardiac troponin T level.
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PMID:Can dobutamine echocardiography induce myocardial damage in patients with dysfunctional but viable myocardium supplied by a severely stenotic coronary artery? 931 12

A reliable serum assay that can discriminate between cardiac and skeletal muscle injury is not available for diagnostic use in laboratory animals. We tested and supported the hypotheses that serum cardiac troponin T (cTnT) was widely applicable in laboratory animals as a biomarker of cardiac injury arising from various causes; that it increased in proportion to severity of cardiac injury; and that it was more cardiospecific than creatine kinase (CK) or lactate dehydrogenase (LD) isozyme activities. In canine and rat models of myocardial infarction, cTnT concentration increased 1,000- to 10,000-fold and was highly correlated with infarct size within 3 h of injury. Serum CK and LD isozymes were substantially less effective biomarkers and, in contrast to cTnT, were ineffective markers in the presence of moderate skeletal muscle injury, with resulting serum CK activity > 5,000 U/L. Using these animal models, and mouse and ferret models, we also showed cTnT to be an effective biomarker in doxorubicin cardiotoxicosis, traumatic injury, ischemia, and cardiac puncture. Reference range serum concentrations for all species were at the detection limit of the assay, except those for mice, in which they were slightly increased, possibly because mice were used to generate assay monoclonal antibodies. We conclude that cTnT is a powerful biomarker in laboratory animals for the sensitive and specific detection of cardiac injury arising from various causes.
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PMID:Cardiac troponin T is a sensitive, specific biomarker of cardiac injury in laboratory animals. 935 91

In patients with end-stage renal disease (ESRD), the serum concentration of cardiac troponin T (cTnT) may be increased without cardiac ischemia. One reason for this unexplained increase could be the extracardiac expression of cTnT. However, truncal skeletal muscle biopsies of five patients with ESRD showed no evidence of the expression of either cTnT mRNA (reverse transcription-PCR) or protein (immunoblot, immunofluorescence). We also measured the serum concentration of cTnT in 97 patients with ESRD. The serum cTnT concentration determined in both first and second generation cTnT assays was significantly lower P <0.01 in patients with a low cardiac risk than in patients with positive indicators of coronary artery disease. The correlation between cTnT and indicators of coronary artery disease is consistent with the hypothesis that cTnT in the serum of patients with ESRD originates from the heart.
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PMID:Cardiac troponin T in patients with end-stage renal disease: absence of expression in truncal skeletal muscle. 1070 39

The main purpose of laboratory tests in patients with acute coronary syndromes is the exclusion of an acute myocardial infarction and the detection of myocardial micronecrosis. Patients with minor myocardial cell damage can best be identified by measurement of cardiac troponin T and possibly also cardiac troponin I levels. Other serum markers of acute ischemia lack specificity and are, therefore, currently of little clinical significance.
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PMID:[Value of laboratory parameters in risk assessment of patients with coronary heart disease and chronic myocardial ischemia]. 982 68


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