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)

We examined sera from 159 patients with ischemic heart disease and hypertension and from 50 apparently healthy control subjects for content of trace elements, cholesterol, triglyceride, and enzymes. Concentrations of copper, cobalt, cholesterol, and triglyceride were increased in all patients, but calcium was decreased in patients with hypertension, acute myocardial ischemia, and acute myocardial infarction. Also accompanying acute myocardial infarction were decreased concentrations of zinc and iron but increases in nickel, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase. Magnesium concentration was lower in patients with acute myocardial ischemia. In acute myocardial infarction, the concentrations of copper, zinc, and iron were higher after 21-30 h (as compared with the values at 0-10 h), by which time concentrations of calcium, magnesium, cobalt, and alanine aminotransferase had decreased. The variation in concentration of trace elements in serum from cases of ischemic heart disease and hypertension corresponds to the severity of the disorder.
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PMID:Trace elements in serum from Pakistani patients with acute and chronic ischemic heart disease and hypertension. 671 25

Enzyme kinetics for creatine kinase (CK), CK-MB, aspartate aminotransferase (AST), and lactate dehydrogenase (LD) in serum were followed in 14 patients who had suffered acute myocardial infarction and who were given intracoronary streptokinase shortly (mean 4.9 h, SD 2.6 h) after onset of symptoms. In the 10 patients for whom thrombolysis was successful, CK activity peaked earlier (12.8 vs 21.6 h) and at higher values (3548 vs 2436 U/L) than in the four patients for whom the treatment was unsuccessful. The mean maximum rate of increase in CK was threefold greater in the former group (574 vs 169 U/L per hour), but the total amount of CK released into the circulation and the fractional disappearance rates were similar for both groups. The profiles for AST and CK-MB for successfully treated patients closely resembled those for CK. LD, however, peaked significantly later than CK (25.7 vs 12.8 h). Early peaking of CK or CK-MB after nonsurgical reperfusion can be potentially useful as a noninvasive in vitro index to the success of therapy of myocardial infarction with thrombolytic agents.
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PMID:Activities of some enzymes in serum after therapy with intracoronary streptokinase in acute myocardial infarction. 671 33

In a prospective study of 90 consecutive patients with acute myocardial infarction, 15 (28.3%) of 53 patients with an anterior wall infarction developed a left ventricular thrombosis diagnosed by cross sectional echocardiography. Patients received anticoagulants only after a left ventricular thrombosis had been diagnosed. Twenty eight patients had an inferior infarction, but none of these had a left ventricular thrombosis. Five (5.5%) of the 90 patients suffered a cerebrovascular accident, and all had an anterior wall infarction. In four of these five patients a left ventricular thrombosis was confirmed by echocardiography before the cerebrovascular accident. All patients with left ventricular thrombosis had apical akinesis. The incidence of a thrombosis did not differ in patients with a first anterior myocardial infarction and with reinfarctions. Among the 40 patients with a first anterior wall infarction, 12 with a thrombosis had a significantly higher incidence of enlarged heart on chest radiographs and significantly higher serum aspartate aminotransferase enzyme activity than those without. Thus patients with a large anterior wall infarction and with akinesis in the apical region are at high risk of developing a left ventricular thrombosis, which may be a source of peripheral emboli. Left ventricular thrombosis appears to be rare with infarctions in other locations.
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PMID:Left ventricular thrombosis and cerebrovascular accident in acute myocardial infarction. 672 49

Mitochondrial and cytoplasmic isoenzymes of aspartate aminotransferase (AST) were studied in the sera of 42 patients following acute myocardial infarction and compared to creatine kinase (CK), lactate dehydrogenase (LDH) and alanine aminotransferase (ALT). Mitochondrial AST( ASTm ) was detected in 93% (39/42) of patients. Maximum recorded ASTm activity was 59.5 +/- 8.8 U/l and was found 39.4 +/- 3.5 hours after the onset of symptoms (chest pain) of myocardial infarction. In contrast the maximum recorded cytoplasmic AST ( ASTc ) activity was greater (327 +/- 23 U/l) and it occurred earlier (33.5 +/- 2.2 hours) after onset of infarction compared to ASTm . ASTm correlated significantly (p less than 0.05) with ASTc , LDH and ALT but not with total CK or CK-MB. ASTc correlated significantly (p less than 0.05) with total CK, CK-MB and LDH but not ALT. Maximum recorded ASTm activity was significantly associated with the clinical assessment of left ventricular failure ( Killip classification) but not with ventricular arrhythmias. In a subset of 15 patients evaluated with invasive hemodynamic measurements of cardiac output and pulmonary capillary wedge pressure. ASTm correlated significantly (p less than 0.05) and better than CK-MB with the hemodynamic assessment of left ventricular dysfunction. Thus ASTSm can be readily identified in sera of patients after acute myocardial infarction and may be of value in the evaluation of patients with acute myocardial infarction.
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PMID:Mitochondrial and cytoplasmic isoenzymes of aspartate aminotransferase in sera of patients after myocardial infarction. 672 62

Myoglobin has been measured in sera from 305 consecutive patients with suspected acute myocardial infarction (AMI) to study the clinical value in relation to other diagnostic methods. On admission the frequency of false negative (i.e. the diagnostic sensitivity) myoglobin values was 28% in the AMI group as compared with 60% for serum creatine kinase (CK) and 46% for serum aspartate aminotransferase (ASAT). Four hours after admission the corresponding figures were 2, 31 and 29%. This makes the diagnostic sensitivity of the myoglobin test 0.98, which is significantly higher (p less than 0.001) than that of the two enzyme tests. The predictive value of a negative myoglobin test was 0.97 and also significantly higher (p less than 0.001 and p less than 0.01) than for CK and ASAT. S-myoglobin was further related to the number of complications and the prognosis of the patients, and high levels appeared to be an unfavourable sign, particularly in combination with an anterior wall infarct. This study has demonstrated and confirmed the superior diagnostic sensitivity of myoglobin determination in early AMI. The inclusion of S-myoglobin in the routine diagnosis of AMI warrants serious consideration.
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PMID:The value of serum myoglobin determinations in the early diagnosis of acute myocardial infarction. 674 6

The predictive value of a diagnostic test estimates the likelihood for presence or absence of disease in a patient with a positive or negative test result (PVpos or PVneg). We evaluated the predictive values of serum activities of the heart-specific creatine kinase isoenzyme MB (CK-MB), aspartate aminotransferase, lactate dehydrogenase, CK, and ECG in 401 consecutively admitted patients suspected of acute myocardial infarction (AMI). The study showed that CK-MB (PVpos = 0.98, PVneg = 1.00) was better than the other enzymes (single as well as serial) and ECG, evaluated both separately and in combinations. In all cases of AMI CK-MB was positive within 17 hours from admission. Replacement of the standard enzymes with CK-MB provides a faster and safer diagnosis of AMI and reduces hospitalization time considerably for patients without AMI.
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PMID:Optimal diagnosis in acute myocardial infarction. A cost-effectiveness study. 676 24

The possibility of predicting myocardial infarct size from early enzyme measurements was studied using a physiological two compartment distribution model. Based on this the time dependent appearance function in plasma was calculated for creatine kinase, aspartate aminotransferase, and lactate dehydrogenase in 29 patients suffering from acute myocardial infarction. On average, the appearance function of the three enzymes started four hours after the onset of symptoms, and the maximum was reached after 12 hours for creatine kinase, 13 hours for aspartate aminotransferase, and 22 hours for lactate dehydrogenase. The cumulated appearance function was used as an acceptable estimate of infarct size. The prediction of infarct size from defined points of the appearance function curve for each of the three enzymes was attempted according to a set schedule during the first 25 hours after the onset of myocardial infarction. The prediction using creatine kinase was superior to the other enzymes. Even so, a reliable prediction could only be established at the very earliest from nine hours and this is too late, as irreversible loss of myocardium occurs rapidly after the onset of symptoms. This, together with the fact that other models have unacceptable variability of the prediction, lead to the conclusion that enzymatic predictive models are of no practical value in clinical intervention studies to reduce infarct size.
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PMID:Limitation of enzymatic models for predicting myocardial infarct size. 686 May 13

Diagnosis of injury to the myocardium is facilitated by information on the activities of creatine kinase (EC 2.7.3.2) MB isoenzyme (CK-MB) and lactate dehydrogenase (EC 1.1.1.27) isoenzyme 1 in serum, thee isoenzymes being present in higher activities in the myocardium than in other tissues or in normal serum. The temporal relationships of these isoenzymes, total creatine kinase, total lactate dehydrogenase, and aspartate aminotransferase (EC 2.6.1.1) are highly sensitive and specific for acute injury to the heart, particularly acute myocardial infarction. Chronic heart diseases, electric cardioversion for heart rhythm disturbances, coronary catheterization, and exercise usually do not produce increases of CK-MB, although abnormal aspartate aminotransferase, creatine kinase, lactate dehydrogenase, and lactate dehydrogenase isoenzyme 1 activities are seen in some individuals. Many other causes of increased activities of these enzymes and isoenzymes in serum are unrelated to injury to the heart. Because CK-MB is present in the skeletal muscle in low activities, substantial injury to skeletal muscle can increase CK-MB activities in the blood to abnormal values. Pulmonary embolism can mimic myocardial infarction in its clinical presentation. In patients with an accurately known time of onset of symptoms and serial enzyme analysis every 12 h during the first 48 h, acute myocardial infarction can be distinguished from pulmonary embolism by determinations of creatine kinase, CK-MB, aspartate aminotransferase, and lactate dehydrogenase isoenzyme 1 in serum.
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PMID:Serum enzymes and isoenzymes in the diagnosis and differential diagnosis of myocardial ischemia and necrosis. 699 25

It is demonstrated that plasma elimination constants for rapidly eliminated circulating tissue enzymes can be obtained from plasma time-activity curves if a slowly eliminated reference enzyme is simultaneously sampled. Enzyme and reference enzyme must be released together into the plasma. From the elimination constants thus obtained enzyme release into the plasma can be calculated as a function of time. The method can be applied during continuous release of enzyme into the plasma. The validity of the method is tested in the dog by intravascular infusion of a preparation of cytoplasmic enzymes, obtained by incubating dog liver under anoxic conditions. Alanine aminotransferase (ALT) was used as reference enzyme. Infused quantities of aspartate aminotransferase (AST), glucosephosphate isomerase (GPI) and ALT can be estimated with coefficients of variation (CV) of respectively 10, 19 and 7.6%. Application of the method to plasma time-activity curves of enzymes in patients after acute myocardial infarction (AMI), with alpha-hydroxybutyrate dehydrogenase (HBD) as reference enzyme, results in the following values for the fractional catabolic rate constants (FCR) of AST, GPI, creatine kinase (CK) and its isoenzyme CK(MB): FCRAST = 0.093 +/- 0.006 h-1; FCRGPI = 0.27 +/ 0.03 h-1 (mean +/- SE, n = 14); FCRCK = 0.20 +/) 0.02 h-1 (n = 30); FCRCK(MB) = 0.34 +/- 0.08 h-1 (n = 16). These values are considerably higher than mentioned by most authors, and this indicates that enzyme release after AMI has been underestimated. After AMI, enzymes are released in quantities proportional to the enzyme content of human heart tissue. Average release of CK conforms to this rule but large variations for individual patients are observed. Accurate estimates of the quantities of enzymes released into the plasma can be made for slowly eliminated enzymes by the use of fixed mean values for elimination constants. The results presented to this study indicate that tissue enzymes released from infarcted myocardium in patients after AMI are recovered quantitatively in the plasma. Local inactivation of enzymes or inactivation during the transport from heart to plasma is not significant in such patients.
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PMID:Quantitative analysis of plasma enzyme levels based upon simultaneous determination of different enzymes. 708 66

The cardiac rate and rhythm were studied by 24-hour ambulatory electrocardiographic recording in 44 patients before, during, and after being discharged from hospital following an acute myocardial infarction. The first recordings were started 48 hours before discharge, the second on the morning of the day of discharge, and the third 48 hours after discharge (at home). While in hospital and after returning home the heart rate fell during sleep but there was no diurnal variation in the frequency of ventricular extrasystoles. Daytime heart rate and both the frequency and grade (severity) of ventricular arrhythmias were significantly raised 48 hours after discharge. The frequency of ventricular extrasystoles during sleep was also increased in the 48 hours post-discharge recording. Rises in heart rate and frequency and severity of ventricular extrasystoles were observed on the morning of the day of discharge, increasing up to the time of leaving hospital, but during the journey home they all diminished. No relation was found between ventricular arrythmias during early convalescence and (i) ventricular arrhythmias during the acute phase of acute myocardial infarction (including ventricular fibrillation); (ii) peak aspartate aminotransferase; (iii) the level of anxiety; or (iv) the personality type. Six patients taking beta-blocking drugs behaved similarly. Five patients taking anxiolytic drugs has significantly raised frequency of ventricular extrasystoles during each 24-hour electrocardiogram. In spite of the above findings, at the time of leaving hospital after acute myocardial infarction there does not appear to be a serious risk from the development of major cardiac arrhythmias.
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PMID:Cardiac arrhythmias 48 hours before, during, and 48 hours after discharge from hospital following acute myocardial infarction. 719 70


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