Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical significance of the serum enzymes creatine kinase (CK, EC 2.7.3.2), lactate dehydrogenase (LD, EC 1.1.1.27) and aspartate aminotransferase (EC 2.6.1.1), and the isoenzymes CK 1-3 and LD 1-5, in acute myocardial infarction (AMI) is reviewed. Particular attention is given to electrophoretic analysis of the isoenzymes (and the CK isoforms/subforms) following AMI and thrombolytic therapy. Other protein markers for the monitoring of AMI, including myoglobin and muscle contractile proteins, are also discussed and the potential for the detection of new marker proteins using high-resolution two-dimensional electrophoretic methods is demonstrated. Whilst emphasis is placed upon electrophoretic methods the value of complementary immunoassays is acknowledged in order to maintain a balanced perspective.
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PMID:Electrophoresis of serum isoenzymes and proteins following acute myocardial infarction. 193 92

Aspartate aminotransferase (AST, EC 2.6.1.1) exists in human tissues as two distinct isoenzymes, one located in the cytoplasm (c-AST), and the other in mitochondria (m-AST). Striated muscle, myocardium, and liver tissues are the main sources of AST. A growing body of information suggests that determination of AST isoenzymes in human serum is useful in evaluating damage to some of these organs. In hepatic disease, the test is used to assess liver necrosis and for determining prognosis. It may also assist in identifying patients with active alcoholic liver disease. In patients with acute myocardial infarction, measurement of AST isoenzymes provides diagnostic information that differs from that obtained by determination of total creatine kinase and lactate dehydrogenase enzymes, and their isoenzymes.
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PMID:Aspartate aminotransferase isoenzymes. 222 56

A new method is described for determining the prognosis of acute myocardial infarction (AMI) progress due to temporal increase in the isoenzyme, i.e. malic dehydrogenase (MDH), aspartate aminotransferase (ASAT), lactic dehydrogenase (LDH), and the increase in the creatine kinase (CK). It is shown that the time of enzymatic activity is an essential factor. If 25 hours of increase in enzymatic activity of MDH and CK are exceeded, AMI deteriorates dramatically.
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PMID:[Prognosis assessment of acute myocardial infarction on the basis of temporal changes of isoenzyme activities]. 233 Jul 42

The pattern of enzyme changes in elderly fallers admitted to an acute geriatric unit was investigated. Creatine kinase (CK), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) activities were measured daily for 3 days after admission in all patients in whom a fall preceded admission. Of 270 patients, 52 (19%) had fallen prior to admission, of whom five (10%) had an acute myocardial infarction (AMI). In fallers without an AMI in whom a history was available, CK and AST activities were significantly higher (p less than 0.05) in patients who had spent more than 1 hour on the floor than in those who had spent less than 1 hour. No other clinical factor affected enzyme activities. CK and AST activities were raised in 66% and 40%, respectively, of fallers without an AMI. Elevation of CK and AST activities in elderly fallers is likely to be a result of the fall itself rather than of an AMI.
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PMID:Cardiac enzyme changes in elderly fallers. 236 84

The diagnosis of acute myocardial infarction (AMI) in the elderly is difficult and often depends on the results of investigations. In a 3-month prospective study, 270 patients admitted to an acute geriatric unit were studied to determine the most effective diagnostic strategy for the diagnosis of AMI, and to assess the value of screening acute geriatric admissions for AMI. Patients were assessed clinically and investigated with serial electrocardiograms and measurements of serum creatine kinase (CK), aspartate aminotransferase (AST), and lactate dehydrogenase activities on three consecutive days after admission. Measurement of serum activity of CK and AST had a diagnostic sensitivity of 100% and specificity of 86.8% for AMI. This was the optimum combination of cardiac enzymes in the diagnosis of AMI. Although electrocardiograms on the first two days of admission had a low diagnostic sensitivity (33.3%) their usefulness was their high positive predictive value (100%) when characteristic of an AMI. AMI was considered in the differential diagnosis of 79 patients (29%). All 25 patients (9%) who had an AMI were in this group, and therefore screening all geriatric admissions for AMI is not clinically justified.
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PMID:The effective use of cardiac enzymes and electrocardiograms in the diagnosis of acute myocardial infarction in the elderly. 237 Nov 89

The delay between the onset of symptoms and the call for help is the longest single component of the time taken for patients with acute myocardial infarction to come under coronary care and receive thrombolytic therapy. In order to investigate factors influencing patient delay, visual analogue scores for pain, shortness of breath, and anxiety were obtained retrospectively from 250 patients with acute myocardial infarction, for the time of onset of symptoms, and for the time of the call for help. The predominant symptom was chest pain, followed by anxiety and breathlessness. Although all symptoms increased in severity after their onset, the initiation of a call was largely unexplained in terms of worsening symptoms. Patient delay had a skewed distribution with modal, median and mean values of up to 1 h, 1.5 h, and 11 h respectively. Patient delay was negatively correlated with the pain score at the time of calling, but most of the variance of patient delay could not be explained in terms of symptom scores. However, patient delay was independently and negatively related to maximum serum aspartate aminotransferase. During acute myocardial infarction, patients with higher cardiac enzyme levels experience more pain and delay less. This tendency for patients with more severe infarction and a greater risk of death to call for help sooner is an added reason for administering thrombolytic treatment at the first opportunity: those patients who call early have most to gain from prompt therapy.
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PMID:Association of patient delay with symptoms, cardiac enzymes, and outcome in acute myocardial infarction. 237 99

A new method is described for estimation of the prognosis of acute myocardial infarction progress due to temporary decrease in the isoenzymes, i.e. malic dehydrogenase (MDH), aspartate aminotransferase (ASAT), lactic dehydrogenase (LDH), and the decrease in the creatine kinase (CK). It is shown that the time of enzymatic activity is an essential factor. If 120 hours of decrease in enzymatic activity of MDH, LDH, and CK are exceeded, the prognosis of the myocardial infarction deteriorates dramatically.
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PMID:[Assessment of prognosis in acute myocardial infarct after reaching the maximum enzyme activity]. 237 31

Stroke distance was measured by means of doppler ultrasound in 100 consecutive patients with acute myocardial infarction. Mean stroke distance on days 1-5 after infarction was 72% of the predicted normal value for age and rose to 77% of normal by days 6-10. Stroke distance was lower after anterior (65%) than inferior infarction (75%), and was negatively correlated with peak serum aspartate aminotransferase (r = 0.47, p less than 0.001). Of 16 patients whose stroke distance on days 1-5 was below 50% of normal for age, 4 died, all within the first week. Of 84 patients whose stroke distance was 50% of normal or higher, only 1 died (at 13 days). The simple bedside measurement of stroke distance offers a practical method of monitoring left ventricular function in acute myocardial infarction: the measurement may have prognostic value.
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PMID:Stroke distance in acute myocardial infarction: a simple measurement of left ventricular function. 256 67

Recent investigations have shown that cardiac isoenzymes change with mechanical overload and possibly with myocardial ischaemia. This complicates the interpretation of serum enzyme changes in acute myocardial infarction. We have therefore investigated the rate of release of isoenzymes from necrosing myocardium and the effect of ischaemia per se. Discrete myocardial infarction was produced in 35 male Wistar rats by ligation of left coronary artery. Six (n = 7), 12 (n = 6), 24 (n = 9), 72 (n = 7) h and 3 weeks (n = 6) after surgery, total and isoenzyme activities of creatine kinase (CK), lactate dehydrogenase (LD) and aspartate aminotransferase (AST) were measured in the infarcted myocardium. Untreated rats (n = 12) were used as the control (time 0). Sham operation was performed in 36 rats. During the early period (0 to 12 or 24 h) of infarction, each (iso)enzyme disappeared monoexponentially from the myocardium (mean r = 0.88) with different disappearance rates. Cytosolic isoenzyme fractions decreased more rapidly than mitochondrial fractions. CK MB and the LD-H subunit decreased faster than CK MM and the LD-M subunit. Such differences in the disappearance rate may be related to subcellular localisation of each isoenzyme. In the late period (72 h and 3 weeks), CK BB and the LD-M subunit showed significant reaccumulation in the infarcted myocardium. Although inflammatory cells can be responsible for the reaccumulation of LD-M subunit, the origin of CK BB is unknown.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disappearance and appearance of isoenzymes of creatine kinase, lactate dehydrogenase and aspartate aminotransferase in the myocardium undergoing infarction. 259 Sep 8

Plasma levels of glutamate, alanine, free fatty acids (FFA), citrate, glucose, insulin, lactate, creatine kinase and aspartate aminotransferase were determined frequently during the first 2-48 h after onset of chest pain in 10 patients who developed acute myocardial infarction (AMI) and in 8 who did not (non-AMI). An initial decrease in plasma glutamate and increase in alanine was found in AMI compared to non-AMI patients. The AMI group showed early, moderate rises of plasma FFA and citrate concentrations, positively related to the initial ST-segment elevation and to the enzymatic estimated infarct size. The AMI patients were continuously hyperglycaemic, but their relative insulin response i.e. plasma glucose/insulin ratio was identical to that of non-AMI patients. Lactate values did not differ between the two groups. Via participation in the malate-aspartate shuttle and by shunting pyruvate to alanine instead of lactate, glutamate is of importance for maintaining myocardial glucose utilization. Our finding of initial low plasma glutamate concentrations after onset of myocardial infarction suggests insufficient glutamate supply to the ischaemic myocardium. On basis of this and animal experiments, an external supply of glutamate might be a 'metabolic' treatment of AMI, alternative or additional to glucose-insulin-potassium infusion in order to promote myocardial glucose oxidation.
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PMID:Altered plasma concentrations of glutamate, alanine and citrate in the early phase of acute myocardial infarction in man. 287 95


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