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)

Activities of aspartate aminotransferase (AST) isoenzymes were determined in serial serum samples from 40 cases of acute myocardial infarction, and compared with activities of creatine kinase, CK-MB isoenzyme, lactate dehydrogenase, and alpha-hydroxybutyrate dehydrogenase for temporal changes. Cytosolic (soluble) AST (s-AST) and mitochondrial AST (m-AST) respectively increased 6.6 and 9.0 h after onset of chest pain. The median time at which serum m-AST activity peaked (15.8 U/L, range 6.4-53.5 U/L) was 47.8 h after the onset of infarction, 19.8 h later than the peak s-AST activity (171 U/L, range 53-517 U/L) and m-AST also disappeared from the serum more slowly than s-AST (p less than 0.001). Serum m-AST values were above normal for at least six days after the infarct. The ratio of m-AST to total AST in serum increased after myocardial infarction, being greatest (20%, range 11-32%) on the third day after onset. For individuals, peak activities of s-AST correlated well with total CK (r = 0.91) and CK-MB (r = 0.86) peak activities, indicating that s-AST also reflects the infarct size. However, m-AST correlated poorly with the enzymes commonly used in infarct diagnosis; it apparently provides different biological information.
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PMID:Activity of serum aspartate aminotransferase isoenzymes in patients with acute myocardial infarction. 380 98

The serum activities of aspartate aminotransferase, lactate dehydrogenase, creatine kinase and estimated creatine kinase isoenzyme MB (CK-B) were investigated in 12 patients before and after revascularization of ischaemic lower extremities. All patients suffered from sudden lower limb arterial occlusion and underwent embolectomy through a small arteriotomy in the groin. The median serum activity of all four enzymes was elevated before surgery and further increased during the first 24-48 h after revascularization. Median serum activity of aspartate aminotransferase, creatine kinase and lactate dehydrogenase were continuously elevated 7 days after the operation. A high relative CK-B activity coincided in one patient with the development of electrocardiographic evidence of acute myocardial infarction. It is concluded that any of these four enzymes should be used with caution in the diagnosis of acute myocardial infarction before, during or after operation in patients who have sustained prolonged ischaemia of the lower extremities.
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PMID:Evaluation of the usefulness of enzymatic diagnosis of myocardial infarction in patients with acute arterial occlusion of the lower extremities. 382 74

Serum (S) enzyme activity of aspartate aminotransferase (ASAT, E.C. 2.6.1.1.), heat stable lactate dehydrogenase (LD, E.C. 1.1.1.27.), creatine kinase (CK, E.C. 2.7.3.2.) and CK-B subunit and the respective standard electrocardiograms (ECG) were compared in 463 patients with suspected acute myocardial infarction (MI) in order to evaluate sensitivity and specificity. Serum ASAT was analysed daily for 3 days, S-heat stable LD every 12 h for 48-108 h, S-CK and S-CK-B every 6 h for 48 h and ECG once daily for 3 days. All four enzymes had a high sensitivity, varying from 99% for LD to 97% for CK-B. The highest specificity was observed for CK-B and CK (98%) as compared with heat stable LD (91%) and ASAT (74%). Standard ECG showed a high specificity (96%) and a low sensitivity (80%).
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PMID:The diagnostic value of different enzymes and standard ECG in acute myocardial infarction. 389 41

The maximum serum activity for aspartate aminotransferase (s-ASAT) during the first 3 days was recorded in 5,507 patients with suspected or definite acute myocardial infarction. The s-ASAT activity was corrected for the normal range from each center. The median s-ASAT activity was 4.9 arbitrary units in the placebo group versus 4.6 arbitrary units in the metoprolol group (p = 0.072). Univariate analyses indicated that the delay time between onset of symptoms and randomization and sympathetic activity at entry significantly influenced the effect of metoprolol. A similar decrease in serum enzyme activity after metoprolol treatment was observed independent of signs of infarct localization on the entry electrocardiogram.
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PMID:Metoprolol in acute myocardial infarction. Enzymatic estimation of infarct size. The MIAMI Trial Research Group. 390 91

Sixty patients with a first acute myocardial infarction and no current treatment with cardioactive drugs were included in a prospective study of the relationship between serum potassium concentration and the early occurrence of ventricular tachycardia and premature ventricular contractions (PVCs). Serum potassium level (range 2.5 to 5 mmol/liter) was estimated 3.8 +/- 2.5 hr (mean +/- SD) after the onset of the infarction, and Holter monitoring was performed during the subsequent 12 hr. In multivariate analysis, serum potassium level was negatively and age positively related to ventricular tachycardia. Among the subclasses of PVCs (frequent unifocal, multifocal, couplets, bigeminy), serum potassium concentration was negatively related to the frequent unifocal subclass; hypertension was related to couplets and to the presence of any of the subclasses, and serum aspartate aminotransferase concentration was related to multifocal PVCs. Heart failure leading to death was related to all subclasses of PVC. Serum potassium concentration is an independent inverse predictor of the occurrence of ventricular tachycardia and frequent unifocal PVCs early in acute myocardial infarction.
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PMID:Serum potassium concentration as a risk factor of ventricular arrhythmias early in acute myocardial infarction. 397 35

The concentrations of pyridoxal 5'-phosphate, and the holoenzyme activities and apoenzyme contents of alanine aminotransferase and aspartate aminotransferase in plasma were determined simultaneously in healthy individuals, patients with renal insufficiency with and without chronic haemodialysis and in patients with acute myocardial infarction. Plasma pyridoxal 5'-phosphate is significantly diminished in uraemic patients and in post-myocardial infarct sera, healthy females have lower pyridoxal 5'-phosphate levels (26.2 +/- 9.0 nmol/l) than healthy males (41.0 +/- 15.1 nmol/l). The stimulation in vitro of the activities of aspartate aminotransferase and alanine aminotransferase by addition of pyridoxal 5'-phosphate (0.1 mmol/l) was found to be independent of the endogenous coenzyme level. In sera of uraemic patients without chronic haemodialysis an inverse statistic correlation between pyridoxal 5'-phosphate-induced stimulation of aspartate aminotransferase activity and the concentrations of urea (r = -0.696) and creatinine (r = -0.715) was found. The respective correlations are much weaker for alanine aminotransferase. The apoenzyme fraction was highest in post-myocardial infarct sera. Follow up of these patients did not reveal any relationship between the fluctuations of pyridoxal 5'-phosphate levels and apoenzyme contents of both alanine aminotransferase and aspartate aminotransferase. The results permit the conclusion that the degree of in vitro stimulation of aminotransferases by pyridoxal 5'-phosphate can not be predicted from the endogenous coenzyme level.
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PMID:Plasma pyridoxal 5'-phosphate concentrations in relation to apo-aminotransferase levels in normal, uraemic, and post-myocardial infarct sera. 406 14

Sixty-four patients over the age of 40 years, undergoing elective surgery of at least one hour's duration, were randomized to treatment with either a thromboembolic deterrent ( TED ) stocking (Kendall Co.) or subcutaneous low-dose heparin 5 000 IU every 12 hours. Serum levels of alanine aminotransferase (S-ALAT), aspartate aminotransferase (S-ASAT), gamma-glutamyl transpeptidase (S-gamma-GT) and alkaline phosphatase (S-ALP) were measured. S-ALAT increased significantly on the 5th and 10th postoperative day, from 27 +/- 2 (x +/- SE) to 40 +/- 4 (p less than 0.01) and 55 +/- 7 U/l (p less than 0.001), respectively, in the heparin group and was significantly higher in the heparin than in the TED group both on the 5th (p less than 0.01) and 10th (p less than 0.05) postoperative day. S-ASAT and S-gamma-GT increased significantly during heparin treatment, but did not differ significantly from the values of the TED group. No change in S-ALP was registered in either group. It is concluded that prophylactic treatment with low-dose heparin induces a significant increase in S-aminotransferase levels, especially in S-ALAT. The phenomenon has profound differential diagnostic implications in conditions such as pulmonary embolism and acute myocardial infarction.
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PMID:Heparin-induced increase in serum levels of aminotranferases. A controlled clinical trial. 637 73

The course of plasma catalytic activities of total creatine kinase, creatine kinase isoenzyme MB, total, cytoplasmatic and mitochondrial aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, alpha-hydroxybutyrate dehydrogenase, glutamate dehydrogenase and concentrations of myoglobin, urea, acidic alpha 1-glycoprotein and creatinine were followed in 33 patients suffering from acute myocardial infarction. All patients were randomized in a double-blind, prospective study. One group (18 patients) was infused with streptokinase 1.5 X 10(6) units/90 minutes; the control group received routine continuous i.v. heparin treatment (1000 units/h). Ten hours after completion of the study protocol, treatment of both groups of patients was continued with heparin, 1000 units/h and Aspisol, 1 g/day2). Streptokinase treatment induced earlier wash-out and therefore earlier peak levels of several enzymes: total creatine kinase (11 hours), creatine kinase isoenzyme MB (6 hours), total and cytoplasmatic aspartate aminotransferase (6 hours) and lactate dehydrogenase (9 hours). Total creatine kinase peak catalytic activity and myoglobin peak concentration were higher in the group receiving thrombolytic therapy. A significantly different course of catalytic activity between both treatment groups was found for total creatine kinase and creatine kinase isoenzyme MB, total and cytosolic aspartate aminotransferase, lactate dehydrogenase and alpha-hydroxybutyrate dehydrogenase. The course of mitochondrial aspartate aminotransferase catalytic activity was different only 12 hours after the beginning of treatment. The shift of several catalytic activities to an earlier peak level in plasma may indicate reperfusion of ischaemic myocardium due to thrombolytic therapy.
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PMID:Systemic short-term fibrinolysis with high-dose streptokinase in acute myocardial infarction: time course of biochemical parameters. 639 65

In a group of 37 patients with definite acute myocardial infarction (AMI) allocated to treatment with either alprenolol (n = 20) or placebo (n = 17) serial determinations of concentrations in serum of myoglobin (S-Mb), creatine kinase (S-CK), aspartate aminotransferase (S-ASAT) and lactate dehydrogenase (S-LDH) were performed. The median peak levels of S-Mb, S-CK and S-LDH were significantly (P less than 0.05) lower among patients treated with alprenolol. The median of the estimated infarct size based on S-CK curves was also significantly (P less than 0.01) lower in the alprenolol group. There was no significant difference between the estimated infarct size based on S-Mb values in the two groups. It is concluded that the present study provides indirect evidence for the assumption that early beta-blockade in AMI can reduce infarct size.
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PMID:The effect of alprenolol on serum myoglobin levels in acute myocardial infarction. 653 53

To investigate the possibility of limiting infarct size by decreasing afterload 32 normotensive patients with uncomplicated acute myocardial infarction (AMI) were put on prazosin and compared with 32 control patients. Blood pressure fell significantly lower in the prazosin group without increase of heart rate. The mean daily and peak levels of serum aspartate transaminase and lactic dehydrogenase and the calculated from the 12 lead ECG mean daily sum of ST segment elevation, number of leads with ST greater than or equal to 0.1 mV, mean ST elevation, number of new Q waves greater than or equal to 0.03 s and the loss of height of R waves were significantly less in the prazosin group. ST segment re-elevation occurring on 2nd-3rd day in the control group was absent or minimal in the prazosin group. The enzyme levels and the change of the ECG variables correlated fairly well with the change of blood pressure. These findings indicate that, at least in the selectively good risk cases of our material, reduction of afterload without increase of heart rate induced by prazosin may favorably influence the balance of myocardial oxygen supply and demand early in AMI and prevent death of jeopardized ischaemic tissue, thus limiting the final extent of the infarct.
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PMID:Limitation of infarct size by decrease of afterload with prazosin. 660 21


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