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 use of serum myoglobin determinations in the diagnosis and quantitation of acute myocardial infarction was studied in 53 patients. Serial blood samples collected for the first 72 h after pain were analysed for serum myoglobin using a radioimmunoassay procedure. Samples were also assayed for serum creatine kinase (CK) and its myocardial isoenzyme CK-MB, aspartate aminotransferase (AST) and alpha-hydroxybutyrate dehydrogenase (alpha HBDH). Analysis of first and second samples obtained at mean times of 7.6 and 10.7 h respectively after pain produced the following detection rate: serum myoglobin 85% and 98%; serum CK 71% and 85%; serum AST 58% and 81%; serum CK-MB 29% and 60%; serum alpha HBDH 23% and 33% respectively. Total CK-MB and myoglobin release from damaged myocardium were calculated using the method of Norris et al. [16]. A significant correlation was obtained between infarct size calculated from CK-MB and myoglobin in the whole group (n = 29, r = 0.71, p < 0.001). The correlation was even more significant for smaller infarcts with CK-MB release < 220 U/l (n = 13, r = 0.92, p < 0.001).
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PMID:The role of serum myoglobin in the detection and measurement of myocardial infarction. 740 5

Out of 368 patients admitted to hospital for chest pain and suspected acute myocardial infarction, 267 were discharged within 24 hours on the basis of the clinical picture, electrocardiogram, and serum activities of aspartate transaminase, alpha-hydroxybutyrate dehydrogenase, and creatine phosphokinase. The patients were followed up for 28 days, during which 17 were readmitted, two of them twice and one three times. Two of the patients were readmitted with non-fatal acute myocardial infarction, and two died. The patients had been primarily divided into two groups: those admitted with presumably non-coronary chest pain (77 patients) formed group 1 and those with obvious coronary chest pain (190 patients) group 2. Both deaths occurred in patients in group 2 but the incidences of events during the follow-up period were otherwise similar in the two groups, and some patients in both groups may have had small acute myocardial infarctions when first admitted. The decision to keep in hospital or discharge a patient with chest pain of recent onset can be made within 24 hours of admission. To discharge the patient acute myocardial infarction need not necessarily be excluded and conventional tests are enough to enable a decision to be made.
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PMID:How long should patients with suspected myocardial infarction be under observation in hospital? 742 22

Zinc concentrations in serum from 99 patients with acute myocardial infarction were correlated with the incidence of further complications and with activities in serum of the "cardiac" enzymes aspartate aminotransferase and lactate dehydrogenase. A significantly subnormal zinc concentration was observed for the patients, the lowest values being observed on the second and third days after infarct, particularly in patients with serious complications. Moreover, a linear correlation was observed between zinc values and enzyme activities until the fourth day after infarct. We conclude that measurement of zinc in the serum may have diagnostic value for acute myocardial infarction, although its prognostic value is still speculative.
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PMID:Zinc concentrations in serum as related to myocardial infarction. 742 47

The change of mitochondria aspartate aminotransferase (m-AST)/soluble-AST (s-AST) ratio was examined in 22 cases of acute myocardial infarction (AMI). The m-AST/s-AST was 40.8 +/- 18.9% at admission to a hospital (2.9 +/- 1.6h). The m-AST/s-AST decreased to normal value rapidly after peak and then increased again gradually. The decrease ratio of m-AST/s-AST per minute at early stage of 8 cases, who were succeeded to reperfusion, was 0.28 +/- 0.20%, and that was significantly higher than of conventionally treated 7 cases and non-reperfused 7 cases (0.11 +/- 0.07%). These results indicated that (1) m-AST/s-AST may be an excellent indicator for AMI in early stage. (2) The decrease ratio of m-AST/s-AST would predict whether reperfusion is successful or not at an earlier stage of AMI.
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PMID:[Early diagnosis and detection of successful reperfusion by mitochondrial-AST/soluble-AST ratio after acute myocardial infarction]. 788 69

The diagnostic value of serum myoglobin as compared to MB iso-enzyme of creatine phosphokinase and aspartate aminotransferase was investigated in 25 patients admitted on suspicion of acute myocardial infarction with a duration of symptoms less than 6 hours. In group 1 (acute myocardial infarction group), the first blood sample, obtained at a mean time of 3.27 hours after onset of infarction, invariably showed increased myoglobin (mean 2.6-fold normal) whereas MB iso-enzyme of creatine phosphokinase and aspartate aminotransferase were often normal. Peak myoglobin values occurred earlier than peak serum MB iso-enzyme of creatine phosphokinase values. The highest peak values of serum myoglobin were found in patients with extensive myocardial infarction. In group 2 (non-acute myocardial infarction or control group) serial determinations of serum myoglobin, serum MB iso-enzyme of creatine phosphokinase and aspartate aminotransferase were within normal limits. Hence the importance lies with the early detection of serum myoglobin in acute myocardial infarction.
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PMID:The roles of myoglobin, MB iso-enzyme of creatine phosphokinase and aspartate aminotransferase in serum in the acute phase of myocardial infarction. 793 Jun 58

A complex of enzymatic tests, characterizing the liver function and cellular cytolysis in patients with acute myocardial infarction of various severities (without complications and with various types of complications and outcomes) was used in examinations over the first week of the disease. Significant changes in five of the seven tested enzymes were found: aspartate aminotransferase, glutamate dehydrogenase, sorbitol dehydrogenase, cholinesterase, alanine aminotransferase, the degree and incidence of changes in their activities being the lowest in the patients with acute myocardial infarction without complications, higher in those with this condition with isolated complications, still higher in those with combined complications and a favorable outcome, and the highest in those with combined complications and a lethal outcome. Secondary hepatopathy in patients with acute myocardial infarction augments as the complications develop, particularly in arrhythmia, disordered conductivity, and combined complications. Measurements of glutamate dehydrogenase and sorbitol dehydrogenase are recommended starting from the first day of the disease, of cholinesterase from the third day of the disease for a dynamic monitoring of the liver status in order to timely detect and correct hepatopathy and assess the status of patients with complicated acute myocardial infarction.
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PMID:[Enzyme diagnosis of liver dysfunction in acute myocardial infarct and its complications]. 800 Jul 90

A monoclonal enzyme immunoassay for measuring human ventricular myosin light chain isotype 1 (HVMLC1) in serum has been developed. To evaluate the method in patients with suspected myocardial injury, we studied 51 patients (16 acute myocardial infarction (AMI), 19 unstable angina pectoris (UAP), 9 stable angina pectoris, 3 nonischemic heart disease, 4 hip surgery patients), and 190 controls (blood donors). Serial blood-samples were drawn from patients; a single blood-sample from controls. The diagnostic value of the HVMLC1 assay was compared with total creatine kinase (CK), CKMB activity, CKMB mass concentration, lactate dehydrogenase isoenzyme 1 (LD1), troponin T (TnT) and mitochondrial-aspartate aminotransferase (m-ASAT). The detection limit of HVMLC1 was 0.4 microgram/l (linear range 0-20 micrograms/l). Sera from 190 reference persons did not contain detectable levels of HVMLC1 (< 0.4 microgram/l; 99% percentile). The coefficients of variation were 13% (1.0 microgram/l) and 3.1% (17.7 micrograms/l). Cross-reactivity with myosin from skeletal muscle was seen. Times to peak value were: CK 19.3 +/- 2.0, LD1 43.4 +/- 3.2, HVMLC1 72.9 +/- 7.0, and m-ASAT 67.3 +/- 5.6 h. Time-curves of HVMLC1 and m-ASAT were similar, whereas time-curves for HVMLC1 and TnT were quite different in most cases. Peak value of HVMLC1 was five times higher than CK peak value and eight times that of LD1. HVMLC1 appeared in the blood within hours after the onset of chest pain and in the majority remained for more than a week after AMI. Among patients with UAP 16% (3/19) had elevated HVMLC1 in serum, whereas elevated TnT was seen in 26% (5/19) and elevated CKMB mass in 26% (5/19). We conclude that the new HVMLC1 assay offers a sensitive diagnosis of myocardial injury. It is characterized by a wide diagnostic time window. The similarity of the HVMLC1 and m-ASAT curves indicates that it may be used to estimate the extent of myocardial necrosis.
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PMID:Human ventricular myosin light chain isotype 1 as a marker of myocardial injury. 817 43

In a randomized, double-blind, placebo-controlled trial, the effects of combined treatment with the antioxidant vitamins A (50,000 IU/day), vitamin C (1,000 mg/day), vitamin E (400 mg/day), and beta-carotene (25 mg/day) were compared for 28 days in 63 (intervention group) and 62 (placebo group) patients with suspected acute myocardial infarction. After treatment with antioxidants, the mean infarct size (creatine kinase and creatine kinase-MB gram equivalents) was significantly less in the antioxidant group than in the placebo group. Serum glutamic-oxaloacetic transaminase decreased by 45.6 IU/dl in the antioxidant group versus 25.8 IU/dl in the placebo group (p < 0.02). Cardiac enzyme lactate dehydrogenase increased slightly (88.6 IU/dl) in the antioxidant group compared with that in the placebo group (166.5 IU/dl) (p < 0.01). QRS score in the electrocardiogram was significantly less in the antioxidant than in the placebo group. The following levels increased in the antioxidant group versus the placebo group, respectively: plasma levels of vitamin E increased by 8.8 and 2.2 mumol/L (p < 0.01), vitamin C increased by 12.6 and 4.2 mumol/L (p < 0.01), beta-carotene increased by 0.28 and 0.06 mumol/L (p < 0.01), and vitamin A increased by 0.36 and 0.12 mumol/L (p < 0.01). Serum lipid peroxides decreased by 1.22 pmol/ml in antioxidant versus 0.22 pmol/ml in the placebo group (p < 0.01). Angina pectoris, total arrhythmias, and poor left ventricular function occurred less often in the antioxidant group. Cardiac end points were significantly less in the antioxidant group (20.6% vs 30.6%, respectively). These results suggest that combined treatment with antioxidant vitamins A, E, C, and beta-carotene in patients with recent acute myocardial infarction may be protective against cardiac necrosis and oxidative stress, and could be beneficial in preventing complications and cardiac event rate in such patients.
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PMID:Usefulness of antioxidant vitamins in suspected acute myocardial infarction (the Indian experiment of infarct survival-3) 931 5

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


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