Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of therapy with urokinase (UK) and with recombinant tissue plasminogen activator (rtPA) were compared in patients with acute myocardial infarction (AMI). To achieve homogenous therapeutic conditions the comparison was restricted to patients having their first AMI and to cases of clinically successful thrombolytic therapy (defined by non-invasive criteria, such as a 50% decrease in elevated ST-segment in the worst load of a 12 lead ECG within 300 min after onset of thrombolytic therapy, complete pain resolution during thrombolytic therapy, and later confirmed by angiography 10 days after AMI). Effects of UK and rtPA on continuous multilead ST-segment analysis and cardiac proteins (creatine kinase and its isoenzyme CK-MB, aspartate transaminase and hydroxybutyrate dehydrogenase) were analyzed during 24 hours following onset of therapy. Continuous ST analysis showed a faster resolution of the elevated ST-segments after thrombolytic therapy with rtPA than with UK(p < 0.01). Accelerated idioventricular rhythms (p < 0.05) occurred sooner following rtPA than UK treatment. The wash-out of creatine kinase was increased (p < 0.01) after rtPA. Although both drugs induced comparable, angiographically controlled reperfusion, the results suggest that the process of reperfusion was accelerated during thrombolysis with rtPA compared to UK. Thrombolytic therapy of AMI with rtPA may hence improve myocardial salvage.
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PMID:Accelerated ST-segment reduction after thrombolytic therapy with recombinant tissue plasminogen activator (rtPA) compared to urokinase. 863 24

In a randomised, double-blind placebo-controlled trial, the effects of the administration of oral L-carnitine (2 g/day) for 28 days were compared in the management of 51 (carnitine group) and 50 (placebo group) patients with suspected acute myocardial infarction. At study entry, the extent of cardiac disease, cardiac enzymes and lipid peroxides were comparable between the groups, although both groups showed an increase in cardiac enzymes and lipid peroxides. At the end of the 28-day treatment period, the mean infarct size assessed by cardiac enzymes showed a significant reduction in the carnitine group compared to placebo. Electrocardiographic assessment of infarct size revealed that the QRS-score was significantly less in the carnitine group compared to placebo (7.4 +/- 1.2 vs 10.7 +/- 2.0), while serum aspartate transaminase and lipid peroxides showed significant reduction in the carnitine group. Lactate dehydrogenase measured on the sixth or seventh day following infarction showed a smaller rise in the carnitine group compared to placebo. Angina pectoris (17.6 vs 36.0%), New York Heart Association class III and IV heart failure plus left ventricular enlargement (23.4 vs 36.0%) and total arrhythmias (13.7 vs 28.0%) were significantly less in the carnitine group compared to placebo. Total cardiac events including cardiac deaths and nonfatal infarction were 15.6% in the carnitine group vs 26.0% in the placebo group. It is possible that L-carnitine supplementation in patients with suspected acute myocardial infarction may be protective against cardiac necrosis and complications during the first 28 days.
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PMID:A randomised, double-blind, placebo-controlled trial of L-carnitine in suspected acute myocardial infarction. 874 85

Diagnosis of acute myocardial infarction is made with the aid of biomarkers such as structural myocardial proteins, myoglobin (MG) or specific enzymes, creatine phosphokinase isoenzyme MB (CK-MB) or non specific enzymes, lactic dehydrogenase (DHL) and aspartate aminotransferase (AST). We found good sensitivity (71%-50%), specificity (85%-100%) and predictive values (Pos. 77%-100%, Neg. 82%-72%) for Mg and CK-MB, supporting their clinical usefulness. In contrast DHL and AST were not clinically useful for early diagnosis.
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PMID:[The usefulness of determining myoglobin, creatine phosphokinase MB isoenzyme, lactate dehydrogenase and aspartate aminotransferase in the diagnosis of acute myocardial infarct]. 981 Mar 42

Differential diagnosis of patients who present with chest pain remains problematical. It has been shown that 11.8-7% of patients with acute myocardial infarction (AMI) are sent home from the emergency department (ED). Audit of our own ED has shown the incidence of missed prognostically significant myocardial damage to be 6.7%. Diagnostic criteria for AMI have classically been based on the triad of history, ECG and measurement of cardiac enzymes. The choice of 'cardiac enzymes' has been dictated by the evolution of laboratory techniques, commencing with measurement of aspartate transaminase and progressing to measurement of creatine kinase (CK) and its MB isoenzyme (CK-MB). Measurement of CK-MB has been shown by both clinical studies and rigorous statistical analysis to represent the best test for the diagnosis of AMI. The advent of real time immunoassay together with advances in therapeutic options for management of acute coronary syndromes (ACS) has resulted in a paradigm shift in the approach to laboratory testing. Immunoassay for CK-MB (CK-MB mass measurement) is diagnostically superior to CK-MB activity measurement and is the test of choice for 'classical' AMI. Development of immunoassays for the cardiac troponins, i.e. cardiac troponin T (cTnT) and cardiac troponin I (cTnI), has enhanced diagnostic specificity. These measurements are completely specific for cardiac damage, allow quantitation of the extent of infarction and are diagnostically superior to CK-MB measurement. Applications of this specificity have included the differential diagnosis of CK elevation in arduous physical training, detection of myocardial damage after DC cardioversion and prediction of ejection fraction. Of more interest is the utility of these markers in management of patients presenting without clear electrocardiographic changes. Diagnosis and management of patients presenting with ST segment elevation has been clarified by large clinical trials of thrombolytic agents. In such patients, thrombolysis is the treatment of choice. Patients presenting with ST segment elevation represents the minority of patients with probable ACS 9.6% of all patients presenting to our hospital. The majority require risk stratification into high- and low-risk groups. It is here that cardiac troponins have a major role. The measurement of cTnT has been shown in a large number of studies to enable risk stratification of patients with unstable angina. The combination of cTnT, admission ECG and stress ECG can be used for a comprehensive risk stratification of patients with unstable angina. The combination of cTnT, admission ECG and stress ECG can be used for a comprehensive risk stratification which can be completed by 24 h from admission, as well as allowing a safe discharge policy from the ED. Measurements of cardiac troponins can also be used to predict prognosis in patients with other diagnostic categories. Patients with cardiac failure can be risk stratified according to cTnT status. cTnT status on admission allows subdivision into high- and low-risk groups in patients presenting with ST segment elevation. Certainly, cTnT measurement can be incorporated into a clinical decision-making strategy to assign patients to investigation and management pathways. There is evidence that cTnT may be useful to guide therapeutic options. The major issue is one of cost. In the U.K. model of managed care with undemanding diagnostic standards, the role of cTnT will be to enhance clinical decision-making strategies, to provide accurate diagnosis and to reduce lengths of stay. This can be shown to have potential for major improvements in cost efficiency. Improvements in diagnostic accuracy can reduce inappropriate long-term drug therapy. In systems with a more aggressive laboratory investigation strategy, rationalization of test numbers will provide an immediate cost reduction while improving quality. Finally, use of point-of-care testing (POCT) means that biochemical testing can be pe
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PMID:Troponin T or troponin I or CK-MB (or none?). 985 34

For many years, serologic markers have been used to assist cardiologists in the diagnosis and management of patients with cardiovascular diseases. The use of laboratory markers has evolved and kept pace with the field of cardiology itself. The early markers involved testing for total enzyme activity such as aspartate aminotransferase, lactate dehydrogenase and creatine kinase. Shortly thereafter, the World Health Organization included serial enzyme markers as part of the triad for diagnosis of acute myocardial infarction (AMI). It was soon recognized that isoenzymes such as for CK-MB and LD-1 provided more specific organ specificity. The need for reporting rapid results led to the development of totally automated isoenzyme assays, which have evolved from immunoinhibition (INH) techniques to mass assays. The current emphasis for cardiac markers is use of protein markers such as cardiac troponin T (cTnT) and I (cTnI). These markers are more sensitive and specific than isoenzyme markers and enable risk stratification for non-AMI patients with unstable angina: patients with high troponin have a higher risk for AMI and cardiac death within the immediate future (4 to 6 weeks). Prospective management of cardiac patients requires more rapid testing and reporting of results. Point-of-care testing platforms on whole blood are now available for emergency testing at bedside.
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PMID:Cardiac markers: from enzymes to proteins, diagnosis to prognosis, laboratory to bedside. 1007 64

Although serum total sialic acid has been shown to be a cardiovascular risk factor, with elevated levels associated with increased cardiovascular mortality and also with cerebrovascular disease, the reason for the elevation in serum sialic acid content remains obscure. It has been shown that an increased output of serum proteins by the liver due to some type of acute phase reaction may be one of the possible sources of an increased serum sialic acid concentration in patients with myocardial infarction. An increase in the activity of sialidase, which cleaves the terminal sialic acid residues from oligosaccharides, glycoproteins and gangliosides, may also play an important role in the elevation of serum total sialic acid in myocardial infarction. Elevated serum total sialic acid in the blood might result either from the shedding or secreting of sialic acid from the cell membrane surface, or releasing of cellular sialic acid from the cell into the bloodstream due to cell damage after myocardial infarction. The purpose of the present study is to investigate serum total and lipid-bound sialic acid and the enzymes serum lactate dehydrogenase, creatine kinase and aspartate aminotransferase in patients with acute myocardial infarction, at 24 h post-infarction (day 1), 48 h post-infarction (day 2) and 72 h post-infarction (day 3). A possible role of cell damage in the elevation of serum total and lipid-bound sialic acid levels in these patients was also evaluated. In this study, 40 patients with myocardial infarction ranging in age from 42 to 68 years, and 26 healthy volunteers ranging in age from 45 to 71 years were included. Serum total sialic acid determination was carried out by the thiobarbituric acid method of Warren and lipid-bound sialic acfd by the method of Katopodis. Our data shows that a) there is a gradual increase in the levels of serum total sialic acid and lipid-bound sialic acid during the first three days after the acute myocardial infarction and b) the elevation in serum total sialic acid levels correlates with the elevation in lactate dehydrogenase activity only on day 1 following infarction. Therefore, either the shedding or secreting of sialic acid from the cell or cell membrane surface may be partly responsible for an increased serum sialic acid concentration especially on day 1 following myocardial infarction.
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PMID:Serum total and lipid-bound sialic acid levels following acute myocardial infarction. 1120 89

Acute myocardial infarction (AMI) is often a fatal disorder in humans seen throughout the world. It was earlier diagnosed with some serum enzymes like aspartate transaminase, creatine phosphokinase and its isoenzyme CPK-MB and lactate dehydrogenase which were shown to be increased in AMI. However, in the last few years importance has been given to measuring serum troponins released from the injured myocardium to confirm an AMI. Troponin estimation involves immunological technique, which is expensive with other associated problems like shelf life of reagents, number of samples to be analysed and availability of the kit itself, used for estimation. Under these circumstances the present work involves the measurement of total salt soluble proteins which are proteins associated with troponins also released from myocardium of a patient with AMI. This new test overrules all the disadvantages of the troponin test but seems equally viable and useful for diagnosis of AMI.
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PMID:New, simple and cheap alternative to troponin test for diagnosis of acute myocardial infarction. 1262 17

The myotoxic activity of the venom of Crotalus durissus terrificus is demonstrable by increased serum levels of the enzymes creatine kinase (CK), lactate dehydrogenase (LD), and aspartate aminotransferase. Serial measurements of CK, LD and their isoenzymes in bite victims showed a pattern similar to that observed in acute myocardial infarction, although the clinical course and electro- and echocardiographic data did not suggest cardiac involvement. These data have raised the hypothesis that crotalid venom preferentially causes damage to type I and/or type IIa fibers, which contain quantities of CK-MB and LD1 similar to those found in cardiac fibers. In order to detect a possible concomitant silent cardiac involvement, seven children with severe crotalid envenoming were studied. Serum troponin I, determined more than once in each patient, were found to be normal. These data demonstrate the absence of cardiac involvement in these patients envenomed by C. durissus terrificus and confirmed the skeletal muscle origin of the elevated CK-MB.
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PMID:Absence of myocardial involvement in children victims of Crotalus durissus terrificus envenoming. 1475 4

For many years, cardiac markers have been used to assist cardiologists in the diagnosis and management of patients with cardiovascular disease. At first, enzyme activities of aspartate aminotransferase, lactate dehydrogenase and creatine kinase have been used in diagnosing patients with chest pain in order to differentiate those with acute myocardial infarction. In the field of cardiac markers, emphasis is currently put on the use of protein markers such as myoglobin, and cardiac troponin T or I. Troponins are very highly cardiac specific and their concentration in blood increase only from four to six hours after the onset of chest pain. Today we obligatorily use two markers, the first being the early one (myoglobin, isoform of creatine kinase), which is very sensitive and shows up in the circulation one to two hours after myocardial damage. Confirmation of myocardial damage can be obtained by definite markers (troponin I or T), which are highly specific of myocardial damage.
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PMID:[Biochemical markers in acute coronary syndrome]. 1520 94

In this report, we describe a simple and fast method for creating a murine myocardial infarction model and providing a useful and convenient tool for the research in ischemic heart disease. We established acute myocardial infarction in the Kunming-strain mouse within 2 minutes by ligating the left anterior descending coronary artery. The model was evaluated by observing the changes in histology and in the serum levels of aspartate aminotransferase and lactate dehydrogenase. Obvious myocardial necrosis was found in the 24-hr experimental (ligation) group. The average size of the infarction was 44.3% +/- 2.9% of the left ventricle. Serum levels of aspartate aminotransferase and lactate dehydrogenase reached their peak in the 24-hr experimental group and were normal in the 72-hr experimental group. We set forth a simple and quick method for producing acute myocardial infarction experimentally in the mouse. The model can be reproduced in a stable manner, under experimental conditions that are easy to duplicate.
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PMID:A simple and fast experimental model of myocardial infarction in the mouse. 1704 83


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