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)

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

It is still undecided in clinical medicine if an increased serum CK-MB level indicates irreversible myocardial damage. We measured CK and AST activities on three serum samples obtained during the first 24 hours following admission of patients with a clinical history suggesting myocardial ischemia. Isoenzymes were not separated when CK and AST activities were less than 300 U/L and 35 U/L respectively, but were fractionated when the enzyme activities doubled during the first 24 hours even within their normal ranges. Over a three-year period this doubling occurred in 30 patients, one of whom was admitted twice to the hospital. The serum CK-MB fractions of these patients were 6% or greater in 26 and less than 6% in 5 admissions. The final clinical diagnosis given to the patients on 20 of these 26 admissions was acute subendocardial infarction. None of the five patients with a CK-MB fraction less than 6% had a clinical diagnosis of acute myocardial infarction. A comparative study of 102 patients with higher average enzyme activities but without doubling of both enzymes during a 24-hour period, did not yield a CK-MB of 6% or greater. None of this group of patients was diagnosed clinically as having had acute myocardial infarction.
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PMID:Detection of ischemic myocardial injury in patients with normal, or moderately elevated, serum CK and AST activities. 711 21

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

In twenty-nine patients suffering from acute myocardial infarction changes of concentrations in plasma of creatine kinase, aspartate aminotransferase and lactate dehydrogenase were monitored 1 week following onset of infarction. The temporal characteristics of enzyme changes described are (i) the time lag from onset of chest pain until increasing enzyme concentrations occur, (ii) the time of maximum concentrations, and (iii) the period during which enzyme is released into blood. Three estimates for the extent of the infarct (i) the peak value of the plasma enzyme curves,(ii the value of the cumulated plasma curves, and (iii) the size of the infarct in grams of necrotic myocardial tissue were, as expected, closely correlated. It is concluded, that the three types of quantification of infarct size are of almost identical value for clinical, prognostic usage, From a pathophysiological point of view they are of limited interest being based on assumptions that are either unlikely to occur or cannot be tested in man.
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PMID:Plasma enzymes in myocardial infarction. An appraisal of quantitative, clinical and pathophysiological information. 725 92

An elevation of serum aspartate aminotransferase (GOT) and alanine aminotransferase (GPT) may be produced in patients treated with i.v. full-dose HEPARIN. We studied the influence of low-dose s.c. HEPARIN (5,000 IU X 2) in 34 patients with acute myocardial infarction (AMI) and in 7 with cerebrovascular accidents or calf thrombophlebitis. Twelve patients (all males) with AMI showed a secondary elevation of GOT and GPT at about the sixth or seventh day after the commencement of therapy that persisted throughout the period of treatment. Four patients (two males and two females) with cerebrovascular accidents or thrombophlebitis showed similar increases of GOT and GPT.
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PMID:Hypertransaminasemia with subcutaneous heparin therapy. 732 13

The value of serum creatine kinase B subunit activity (CK B) in the diagnosis of acute myocardial infarction was studied in 238 consecutive cases. All were admitted to a coronary care unit because of suspected acute myocardial infarction. Serum CK B activity was determined by an immunoinhibition procedure, using a CK M subunit inhibiting antibody (anti-M). For the evaluation of serum CK B, patients were classified into acute myocardial infarction and non-acute myocardial infarction groups. This classification was based on electrocardiographic findings, on quantitative determinations of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total serum creatine kinase (CK) activities, and on qualitative electrophoretic determinations of serum CK and serum lactate dehydrogenase (LD) isoenzymes. The prevalence of acute myocardial infarction in the patient material was 0.47. Serum CK B subunit activity was found to be a highly selective indicator of acute myocardial infarction with a predictive value of a positive test result of 0.97 and a predictive value of a negative test result of 0.99. The serum CK B activity increased above the acute myocardial infarction discrimination limit within 12 hours from onset of symptoms. Two non-acute myocardial infarction patients, who were resuscitated after cardiac arrest, had increased serum CK B values caused by the transient presence of CK isoenzyme BB in serum.
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PMID:Serum creatine kinase B subunit activity in diagnosis of acute myocardial infarction. 737 10


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