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

The effect of metoprolol in ECG experiments induced by a treadmill exercise test, was studied in 30 patients with stable angina pectoris. The study was a simple blind cross-over between metoprolol (150 mg/die) and placebo. The evaluation of ECG recordings (V5 lead) was carried out by a computer program. In order to assess the ST-segment depression, the ST 0.8 (Depression at 80 msec after R-peak) and AST (ST area) values were used. We observed an increased exercise tolerance after administration of metoprolol (P less than 0.001) and a significant reduction of ST segment depression for ST 0.8 (P less than 0.01) and AST (P less than 0.005) at the maximal commun work load attained by every patient in the metoprolol and placebo tests. When the evaluation of ECG measurements were performed at the maximal commun double product no significant modifications were observed.
G Ital Cardiol 1979
PMID:[Metoprolol effect on ECG exercise test in patients with stable angina pectoris. Computer analysis (author's transl)]. 26 57

Data were obtained and analyzed in 229 patients admitted to the coronary care unit from November 1988 through July 1989. The patients were classified into 2 groups: patients without or with only mild left ventricular failure (Killip class I or II) during their hospital stay (group I), and patients who were in Killip class I or II on admission but developed cardiogenic shock during hospitalization (group II). Discriminant function analysis was performed using the following variables: patients' age, history of previous myocardial infarction, diabetes mellitus, blood lactate, urea, creatinine, creatine kinase, aspartate aminotransferase, lactate dehydrogenase concentrations, and chest x-ray cardiothoracic ratio. Variables that were found to significantly discriminate the 2 groups of patients were age, previous infarction, x-ray cardiothoracic ratio, blood urea and lactate concentrations. The risk index was computed, and blood lactate was the variable with the greatest predictive power for shock development. The sensitivity, specificity and predictive value of the risk index, taking various cutoff points, were calculated. With a cutoff value of 1, sensitivity was 65%, specificity 91%, positive predictive value 36% and negative predictive value 97%. With a cutoff value of 2, sensitivity was 53%, specificity 99%, positive predictive value 82% and negative predictive value 96%.
Am J Cardiol 1991 Mar 15
PMID:Usefulness of blood lactate as a predictor of shock development in acute myocardial infarction. 200 Jul 87

The serum myoglobin (MG) was assayed by the radio-immunological method in 30 patients, all victims of a recent myocardial infarction (MI) and in 30 tests subjects suffering (21 cases) or not (9 cases) from heart diseases, but none from myocardial infarction (MI). The blood samples have been collected on hospital admission of the patient, then every four hours during the first 48 hours and finally, every 12 hours from the 48th to 72nd hour. The normal value is less than 85 micrograms/l. The creatine-kinase (CK), the aspartate aminotransferase (ASAT), the alanine aminotransferase (ALAT) and the lactate dehydrogenase (LDH) were also assayed each time. In MI, there is a significant increase in the serum MG level (731 +/- 323 micrograms/l against 174 +/- 198 micrograms/l in the test subjects; p less than 0.001). The sensitivity of this assay reaches 97%, its specificity 80%, its positive predictive value 83% and its negative predictive value 96%. Starting from the beginning of the characteristic pain of infarction, the MG level exceeds the normal values after 3.3 +/- 1.6 hours, reaches its maximum after 9.3 +/- 3.7 hours and comes back to normal after 38 +/- 8.1 hours. On the other hand, the MG level does not enable any conclusion regarding either the transmural/not transmural nature, or the site, or the acuteness of the MI.(ABSTRACT TRUNCATED AT 250 WORDS)
Ann Cardiol Angeiol (Paris) 1990 Mar
PMID:[Value of the assay of serum myoglobin in recent myocardial infarction]. 218 59

Hepatic enzymes, pulmonary function, serum amiodarone and desethylamiodarone (DEA) concentrations and erythrocyte superoxide dismutase (SOD) activity were monitored at regular intervals for 1 year in 30 patients receiving amiodarone. Subclinical hepatotoxicity developed in 5 patients. These patients had higher baseline alanine transaminase values (42.6 +/- 6.8 vs 22.9 +/- 1.8 U/liter) and had an increase in serum aspartate transaminase from 27 +/- 4.1 at baseline to 147 +/- 77.3 U/liter at 12 months. The other patients had little variation in aspartate transaminase. Six patients with normal baseline carbon monoxide diffusing capacity had subclinical pulmonary toxicity develop with a mean decrease in diffusing capacity to 0.7 +/- 0.05 of the baseline value, which correlated with decreasing erythrocyte SOD activity. Mean carbon monoxide diffusing capacity and SOD activity remained unchanged in the other patients. The mechanisms of hepatic and pulmonary injury remain unknown, but appear to be associated with exposure to higher total serum concentrations of amiodarone plus DEA. Patients who had hepatic and/or pulmonary abnormalities develop received higher doses of amiodarone (440 +/- 27 vs 340 +/- 18 mg/day), but also had a higher amiodarone:DEA ratio suggesting that dose-dependent kinetics contributed to the higher concentrations. Elevated baseline alanine transaminase may indicate increased risk for hepatotoxicity while a progressive decrease in erythrocyte SOD may be an early indication of pulmonary toxicity. The latter finding indicates a need to investigate the role of free radicals in the pathogenesis of amiodarone pulmonary toxicity.
Am J Cardiol 1990 May 15
PMID:Relation of amiodarone hepatic and pulmonary toxicity to serum drug concentrations and superoxide dismutase activity. 233 27

To evaluate whether the right ventricle releases significant amount of cardiac enzymes during myocardial infarction, a clinicopathologic study of 50 patients with 60 infarcts was performed. Myocardial infarct size was determined at autopsy and compared with the corresponding peak serum lactate dehydrogenase and aspartate aminotransferase. Anterior and posterior infarcts had similar anatomic size, peak enzyme values, and coefficients of correlation (r = 0.86-0.88 versus r = 0.82-0.84 for lactate dehydrogenase). However, by disregarding the right ventricular infarct component considering the left ventricular infarction only, the coefficient of correlation between infarct size and peak serum lactate dehydrogenase decreased from r = 0.84 to r = 0.59 (P = 0.09), in 14 posterior infarcts while no change was observed in 24 anterior infarcts (r = 0.88). This indicates, that a considerable amount of enzymes released during posterior infarction originated from the right ventricle which was not the case for anterior infarction.
Int J Cardiol 1989 Mar
PMID:Right ventricular infarction: larger enzyme release with posterior than with anterior involvement. 270 15

It is not known whether coronary vasospasm is associated with coronary thrombosis. In this study, plasma levels of fibrinopeptide A during anginal attacks in 24 patients with variant angina were examined. A hyperventilation test was used to induce angina. Hyperventilation induced angina and ST segment elevation (AST: 0.32 +/- 0.14 mV, p less than 0.01) in eight patients with variant angina. Fibrinopeptide A increased from 0.75 +/- 0.27 at control to 7.8 +/- 4.4 ng/ml (p less than 0.01) during anginal attacks in these eight patients. In addition, four patients had spontaneous attacks of angina; they also had elevated levels of fibrinopeptide A during attacks (from 2.0 +/- 1.2 at control to 21.9 +/- 18.0 ng/ml [p less than 0.01] during attacks). Hyperventilation did not induce either angina or ST segment elevation in 12 of the patients with variant angina. Fibrinopeptide A levels did not change with hyperventilation in these patients. To determine whether elevated plasma levels of fibrinopeptide A were associated with angina, the plasma levels of fibrinopeptide A were examined during exercise-induced angina in seven additional patients with stable effort angina. They all developed angina with treadmill exercise; however, plasma fibrinopeptide A did not change. Therefore, only the patients with variant angina demonstrated elevated levels of fibrinopeptide A during anginal attacks. These findings suggest that coronary vasospasm associated with myocardial ischemia may induce stasis of blood, resulting in fibrinogen-fibrin conversion in the coronary vessels.
J Am Coll Cardiol 1989 Sep
PMID:Increased fibrinopeptide A during anginal attacks in patients with variant angina. 276 8

The vitamin B6 status of 84 patients with acute myocardial infarction was compared with that of 84 control subjects. Pyridoxal and pyridoxal 5'-phosphate (PLP) in plasma and erythrocytes, as well as the basal and total potential activity of the PLP-dependent enzyme aspartate aminotransferase in erythrocytes, were measured for a comprehensive assessment of vitamin B6 status. The mean levels of all vitamin B6 indexes (except pyridoxal) were lower in the patients than in the control subjects. The differences were statistically significant, except for erythrocyte PLP and total potential enzyme activity. The adjusted relative odds of a myocardial infarction for subjects in the lowest quartile of plasma PLP was about 5 times higher when compared with those in the highest quartile (relative odds = 5.2, 95% confidence interval = 1.4 to 18.9). Similar findings were found with the other vitamin B6 indexes. No significant association between infarct size, as estimated by creatine kinase level, and the vitamin B6 indexes was observed.
Am J Cardiol 1989 Mar 01
PMID:Low vitamin B6 status in patients with acute myocardial infarction. 291 56

Because clinical and laboratory criteria cannot accurately establish the presence or absence of acute myocardial infarction (AMI) at the time of initial presentation, this diagnosis is not confirmed in the majority of patients admitted to coronary care units. To study the effectiveness of serial changes in enzyme activity in specimens taken at presentation and 8 hours later in establishing the likelihood of AMI, the results in 1,214 patients with acute cardiac symptoms of less than 24 hours' duration were retrospectively evaluated. In 1,007 patients with initially normal creatine kinase (CK), an increase in CK (positive delta-CK) occurred in 98% of patients with AMI and 16% of patients without AMI. In 196 patients with elevated total CK, a low ratio of CK to aspartate aminotransferase was found in 98% of patients with AMI and 33% of patients without AMI. These 2 enzyme ratios had a sensitivity greater than 90% in patients with typical and atypical histories. The overall predictive value of serial enzyme measurements for AMI was 53%, compared with 18% in patients selected for admission. These results suggest that serial enzyme measurements could be used in the initial evaluation of patients with suspected AMI, and have the potential to reduce the number of patients admitted to coronary care units who do not have AMI.
Am J Cardiol 1989 Mar 15
PMID:Rapid serial enzyme measurements in evaluation of patients with suspected myocardial infarction. 280 47

The mechanism by which early intervention with beta-blockers reduces mortality in acute myocardial infarction is unclear. Therefore the effects of intravenous, followed by oral, metoprolol on indices of infarct size were studied in a double-blind fashion with a median delay of 6.75 hours from onset of symptoms. In 129 patients peak enzyme release and QRS score on the electrocardiogram were assessed, while myocardial perfusion score on thallium-201 scintigraphy was studied in 45 patients. There was a close correlation between all the indices of infarct size. While the correlation coefficients did not appear to be influenced by metoprolol treatment, the slope of the regression was affected. Peak aspartate aminotransferase and lactic dehydrogenase were lower by 11 and 7%, respectively, in the metoprolol-treated group, but no reduction was noted in QRS score or in thallium-201 perfusion defect size in the actively treated group. Thus, it seems likely that early intervention with metoprolol in acute myocardial infarction reduces mortality, not by limiting infarct size, but by some other mechanism.
Int J Cardiol 1988 Sep
PMID:Does acute-phase beta-blockade reduce mortality in acute myocardial infarction by limiting infarct size? 304 3

The mechanism by which pentylenetetrazole provokes convulsions in animals has been investigated by measuring its influence in vitro on the activities of several enzymes of glutamate metabolism in rat brain homogenates. Pentylenetetrazole does not affect the specific activities of glutamine synthetase, glutaminase, or glutamate decarboxylase; it inhibits those of glutamate dehydrogenase and aspartate aminotransferase, and stimulates that of gamma-aminobutyric acid (GABA) aminotransferase. The overall consequence of the action of pentylenetetrazole on the activities of these enzymes should be an increase in the concentration of glutamate and a decrease in that of GABA. This modulation of glutamate and GABA metabolism by pentylenetetrazole could contribute to the triggering of convulsions.
 ...
PMID:Pentylenetetrazole inhibits glutamate dehydrogenase and aspartate aminotransferase, and stimulates GABA aminotransferase in homogenates from rat cerebral cortex. 321 59


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