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)

The activity of alpha-hydroxybutyrate dehydrogenase, creatine kinase, creatine kinase MB and aspartate aminotransferase was measured on serial plasma samples from patients with acute myocardial infarction. The study was part of a multicentre randomised trial of the effect of thrombolytic treatment in the acute phase of acute myocardial infarction. The applicability and comparability of enzyme tests for the estimation of myocardial injury were studied in 76 control patients and 74 patients treated with streptokinase. Treatment with streptokinase caused a considerable acceleration of enzyme release after acute myocardial infarction, both in patients with persistent coronary occlusion and in those with successful reperfusion. But this changed pattern of enzyme release did not affect the rate of enzyme elimination from plasma or the released proportions of different enzymes. Thus the assessment of infarct size by measurement of these enzyme activities can also be applied to patients treated with streptokinase. Moreover, the enzymes measured in the present study are all equally valid markers of myocardial injury.
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PMID:Enzyme tests in the evaluation of thrombolysis in acute myocardial infarction. 334 58

One of the secondary objectives of the MIAMI Trial which evaluated the role of the beta-1-selective blocker metoprolol in suspected acute myocardial infarction was to further assess whether early intervention with beta-blockade can limit infarct size. A total of 5,778 patients from 104 worldwide centres were randomized into the trial. Various enzymes such as aspartate aminotransferase (ASAT), creatine kinase (CK), CK MB, CK B, lactate dehydrogenase (LD) and LD isoenzyme I were analysed. All enzymes were used according to the clinical routine of the respective hospital, except ASAT which was analysed once daily for 3 days in the majority of cases and LD I which was analysed every 12 h for 72 h in a subsample. A consistent observation was the lower serum enzyme activity among patients receiving metoprolol and randomized early after onset of symptoms, whereas no difference between metoprolol and placebo was observed in patients treated later in the course. The results of the MIAMI Trial support previous observations that early institution of metoprolol therapy limits infarct size, as indicated by the maximum serum enzyme activity.
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PMID:Infarct size limitation after early intervention with metoprolol in the MIAMI Trial. 337 Jun 54

We compare the clinical features and hospital outcomes in 83 diabetic patients admitted with acute myocardial infarction and 380 nondiabetic patients with levels of glycosylated hemoglobin (HbA1c) low enough to exclude undiagnosed diabetes. The hospital mortality was 42.2% in diabetic and 24.7% in nondiabetic patients, an odds ratio of 2.22 (CI 1.37-3.60, P less than .002). The excess mortality was due to cardiogenic shock and left ventricular failure (pump failure). There was no difference in peak levels of aspartate transaminase between the groups. Among the diabetic patients, the admission levels of plasma glucose and peak levels of aspartate transaminase were higher among those who developed pump failure or died, but there was no relationship between outcome and gender, disease duration, or treatment. Prior blood glucose control, as judged by levels of HbA1c, was not related to hospital outcome (P greater than .5). In a further study, the 83 diabetic patients were compared with 249 age- and sex-matched diabetic subjects without myocardial infarction for treatment, disease duration, and control. There was an increased risk of admission with myocardial infarction of 2.35 (CI 1.41-3.92, P less than .005) within the first 5 yr of diagnosis of diabetes. Infarct patients had significantly lower levels of HbA1c than control subjects (P less than .005), but treatment did not differ between groups. Neither incidence nor case fatality of myocardial infarction in diabetic patients is positively associated with cumulative glycemic exposure.
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PMID:Determinants of hospital admission and case fatality in diabetic patients with myocardial infarction. 340 92

The aim of this investigation was to study central haemodynamics in initially uncomplicated acute myocardial infarction (AMI) with respect to natural history, relation to enzyme estimated infarct size, mortality and effects of metoprolol. A total of 212 patients with AMI but without clinical signs of serious heart failure or hypotension and with a mean delay from onset of pain to study entry of about 7 hours were studied. They were randomised to placebo or metoprolol (15 mg i.v. + 50 mg orally q.i.d.) treatment. Central pressures and cardiac output were evaluated by repeated measurements over 24 hours by means of pulmonary artery catheters. The pharmacokinetics of metoprolol were studied in further 20 patients with AMI. The natural history, as reflected by the placebo group, was observed to be a gradual significant fall in systemic artery pressures, pulmonary capillary wedge pressure (PCWP; 13.6-10.5 mmHg) and stroke volume, while heart rate increased, leaving cardiac output unchanged. The decrease in PCWP was confined to the group with baseline pressure above the median of 13 mmHg and was of equal magnitude in the group given concomitant medication to that of those who required no such therapy. Significant but weak correlations between the peak serum aspartate aminotransferase level and the baseline PCWP (r = 0.28) and stroke volume (r = 0.22) were found. Non-survivors had a significant baseline depression of cardiac output and stroke volume, while PCWP was increased. However, the overlap with survivors was large. The dosage of metoprolol used resulted in mean plasma levels of about 200 nmol/l, which should induce a rapid and sustained degree of beta-blockade. The patients randomised to placebo or metoprolol were assessed according to initial heart rate. The haemodynamic changes induced by metoprolol were similar but were more pronounced in patients with high heart rate compared to those with low rate. In patients with heart rate greater than 65 beats/min, the metoprolol treated group, in comparison to the placebo group, was characterised by a decrease of 10-20% in systolic artery pressure and heart rate, suggesting a decreased myocardial oxygen consumption. Cardiac index (2.9-2.2 l/min/m2) and stroke volume index (36-32 ml/beat/m2) decreased to a minimum after 30 minutes and gradually rose thereafter. The PCWP increased from 13.7 to 15.4 mmHg, 30 minutes after the injection of metoprolol. This increase was confined to the group with baseline low pressure and the difference compared to the placebo group disappeared after 8 hours.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Central haemodynamics in acute myocardial infarction. Natural history, relation to enzyme release and effects of metoprolol. 353 97

A rapid selective method for measuring the activity of lactate dehydrogenase isoenzyme LD-1 in serum by using 1,6-hexanediol as an inhibitor of the M-subunit was developed. Hexanediol was added to serum at a final concentration of 0.7 mol/l. After incubation at 30 degrees C for 15 min, the activity was measured with an automatic analyser. The inter-assay coefficient of variation was 6.9% for the lactate dehydrogenase isoenzyme LD-1 measurement. The results obtained from the sera of 100 patients analysed by the proposed selective method and by the conventional electrophoretic method, respectively, showed an excellent correlation. This selective method was used to determine the lactate dehydrogenase isoenzyme LD-1 activity of sera from patients with acute myocardial infarction, and the results were correlated well with those obtained by the immunological, Roch Isomune method. Addition of 1,6-hexanediol did not affect the measurement of activities of other enzymes such as alkaline phosphatase, gamma-glutamyltransferase, aspartate aminotransferase and alanine aminotransferase.
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PMID:Selective determination of lactate dehydrogenase isoenzyme 1 in serum after inhibition by 1,6-hexanediol. 369 31

In 67 patients with a clinical history of suspected acute myocardial infarction (MI) who developed T-wave inversions in standard ECG and had normal serum aspartate aminotransferase activity (possible MI) the clinical outcome was compared with that in patients fulfilling criteria for subendocardial infarction. Patients with possible MI had a lower mortality (p = 0.02) and also a lower reinfarction rate (p = 0.14) during the first 2 years as compared with those with subendocardial MI. Although patients with subendocardial MI had more problems with chest pain in the acute phase, angina pectoris occurred more frequently in patients with possible MI during a longer follow-up period. Congestive heart failure occurred more frequently in patients with subendocardial MI during initial hospitalization, whereas treatment for heart failure appeared similar in the two groups during a longer follow-up time. We conclude that the clinical course in patients with possible MI, here defined as chest pain and appearance of T-wave inversions without elevation of serum enzyme activity, seems to differ from that in patients with subendocardial MI, particularly regarding long-term survival and incidence of angina pectoris.
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PMID:Appearance of T-wave inversions without raised serum enzyme activity in suspected acute myocardial infarction: clinical outcome in relation to subendocardial infarction. 370 48

In a study of 1033 consecutive patients with acute myocardial infarction, serum potassium concentrations were determined on admission to hospital and studied with respect to the subsequent occurrence of atrial fibrillation and flutter and of ventricular tachycardia and fibrillation. The study cohort fulfilled the inclusion criteria for the Norwegian timolol trial in which they later took part. In multivariate analysis, with serum potassium concentrations as a continuous variable, age, the presence of ventricular tachycardia and fibrillation, and maximum level of aspartate aminotransferase greater than four times the upper limit of normal were significantly associated with the occurrence of atrial fibrillation and flutter, while serum potassium concentration was not. Serum potassium concentrations and time from onset of the infarction to hospital admission were significantly negatively associated with the occurrence of ventricular tachycardia and fibrillation; while age, cardiomegaly, transient hypotension, pathological Q-waves in the electrocardiogram, atrial fibrillation and flutter, and ventricular premature beats were positively related to these arrhythmias. Thus, there is an independent inverse relationship between serum potassium concentrations and ventricular arrhythmias in acute myocardial infarction.
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PMID:Serum potassium concentrations are inversely related to ventricular, but not to atrial, arrhythmias in acute myocardial infarction. 370 55

Estimation of enzyme release in plasma requires knowledge of the fractional catabolic rate constant (FCR) for the elimination enzyme activity from plasma. However, the total plasma content of such enzymes usually consists of several isoenzymes with different values of FCR. Thus, the use of a single overall value for FCR may cause error. This problem was studied by determination of the plasma isoenzyme activities of creatine kinase, lactate dehydrogenase, aspartate aminotransferase and alpha-hydroxybutyrate dehydrogenase in patients after cardiac surgery and after acute myocardial infarction. Values of FCR and the cumulative release of activity in plasma are estimated for separate isoenzymes and for total enzyme activity. Results are compared with the enzyme content of myocardium, skeletal muscle and blood cells. It is concluded that isoenzyme separation is not required for the quantitative use of such data. The implications for the validation of enzymatic estimation of cardiac injury are discussed. The results indicate that local inactivation of enzymes after cardiac injury must be limited.
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PMID:Enzymatic assessment of myocardial injury after infarction or cardiac surgery. Is isoenzyme analysis required? 371 82

The relation of central haemodynamic changes to subsequent mortality and peak enzyme activity was investigated in 190 patients with acute myocardial infarction. The mean delay time from onset of symptoms to the haemodynamic study was 7.2 hours. Major exclusion criteria were heart rate less than 65 beats min-1, systolic blood pressure less than 105 mmHg and lung rales to a distance of greater than 10 cm above the lung bases. Nine patients (4.7%) died within 15 days and 16 patients (8.4%) within 90 days after the infarction. Compared to survivors, non-survivors were characterized by baseline depression of cardiac index, stroke volume index and left ventricular stroke work index, while pulmonary capillary wedge pressure and peripheral resistance were increased. However, a wide overlap between survivors and non-survivors makes the predictive value low in the individual patient. Peak serum aspartate aminotransferase (S-ASAT) activity was weakly related to baseline pulmonary capillary wedge pressure (r = 0.28; P less than 0.001) and stroke volume index (r = -0.22; P less than 0.01). The correlation to pulmonary capillary wedge pressure was only found in anterior (r = 0.34) infarcts. Peak serum lactate dehydrogenase (LD1) was not correlated with baseline haemodynamics.
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PMID:Central haemodynamics in acute myocardial infarction in relation to mortality and peak enzyme activity. 373 97

Serum kinetics of total creatine kinase (CK), CK-MB isoenzyme, aspartate aminotransferase (AST), lactate dehydrogenase (LD) and alpha-hydroxybutyrate dehydrogenase (HBD) activities were studied in twenty patients with acute myocardial infarction randomly assigned to receive either intracoronary urokinase (group A) or conventional (control) therapy (group B). The temporal characteristics of enzyme changes described were the time lag from onset of chest pain until maximum catalytic concentration value, the rate at which enzymes are released into blood, the peak value of the serum enzyme curves and (d) the fractional disappearance rate (Kd) for each enzyme considered. Thrombolytic treatment induced earlier peak times in group A: for CK, 10.8 vs 27.0 h, for CK-MB, 10.4 vs 23.1, for AST, 13.9 vs 31.3, for LD, 24.4 vs 49.1, and for HBD, 20.5 vs 48.5 (for all enzymes, p less than 0.001). The maximal rate of release for the enzymes was at least twofold greater in group A. Enzyme peak activities and Kd were not significantly different between the groups. The most significant discrimination between the two groups was obtained with AST peak time (Hartz overlap index (Oi) = 0.11) and CK-MB peak time (Oi = 0.12).
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PMID:Serum enzymes in acute myocardial infarction after intracoronary thrombolysis. 376 94


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