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)

The delay between the onset of symptoms and the call for help is the longest single component of the time taken for patients with acute myocardial infarction to come under coronary care and receive thrombolytic therapy. In order to investigate factors influencing patient delay, visual analogue scores for pain, shortness of breath, and anxiety were obtained retrospectively from 250 patients with acute myocardial infarction, for the time of onset of symptoms, and for the time of the call for help. The predominant symptom was chest pain, followed by anxiety and breathlessness. Although all symptoms increased in severity after their onset, the initiation of a call was largely unexplained in terms of worsening symptoms. Patient delay had a skewed distribution with modal, median and mean values of up to 1 h, 1.5 h, and 11 h respectively. Patient delay was negatively correlated with the pain score at the time of calling, but most of the variance of patient delay could not be explained in terms of symptom scores. However, patient delay was independently and negatively related to maximum serum aspartate aminotransferase. During acute myocardial infarction, patients with higher cardiac enzyme levels experience more pain and delay less. This tendency for patients with more severe infarction and a greater risk of death to call for help sooner is an added reason for administering thrombolytic treatment at the first opportunity: those patients who call early have most to gain from prompt therapy.
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PMID:Association of patient delay with symptoms, cardiac enzymes, and outcome in acute myocardial infarction. 237 99

The Minnesota Heart Survey assessed attack rates of MI in Twin Cities residents ages 30-74 years in 1970 and 1980. The age-adjusted attack rate per 100,000 of definite MI was similar in 1970 (174.2) and 1980 (179.9) p greater than 0.05, using ECG, chest pain, and blood enzyme concentrations of aspartate transaminase and/or lactic dehydrogenase as criteria. The attack rate of definite MI also remained constant when autopsy findings were included in the algorithm, 197.0 in 1970 and 191.4 in 1980 (p greater than 0.05). Adding creatine phosphokinase (CPK) and CPK-MB isoenzyme to the algorithm increased the rate of definite MIs from 209.0 in 1970 to 277.0 in 1980 (p less than 0.001). Interpretation of long-term trends in coronary heart disease morbidity is highly dependent upon variables used to validate cases. Care must be taken to maintain consistent criteria to avoid bias due to improvements in diagnostic techniques over time which increase sensitivity for detection of cardiac ischemia.
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PMID:The effects of diagnostic criteria on trends in coronary heart disease morbidity: the Minnesota Heart Survey. 264 74

Plasma levels of glutamate, alanine, free fatty acids (FFA), citrate, glucose, insulin, lactate, creatine kinase and aspartate aminotransferase were determined frequently during the first 2-48 h after onset of chest pain in 10 patients who developed acute myocardial infarction (AMI) and in 8 who did not (non-AMI). An initial decrease in plasma glutamate and increase in alanine was found in AMI compared to non-AMI patients. The AMI group showed early, moderate rises of plasma FFA and citrate concentrations, positively related to the initial ST-segment elevation and to the enzymatic estimated infarct size. The AMI patients were continuously hyperglycaemic, but their relative insulin response i.e. plasma glucose/insulin ratio was identical to that of non-AMI patients. Lactate values did not differ between the two groups. Via participation in the malate-aspartate shuttle and by shunting pyruvate to alanine instead of lactate, glutamate is of importance for maintaining myocardial glucose utilization. Our finding of initial low plasma glutamate concentrations after onset of myocardial infarction suggests insufficient glutamate supply to the ischaemic myocardium. On basis of this and animal experiments, an external supply of glutamate might be a 'metabolic' treatment of AMI, alternative or additional to glucose-insulin-potassium infusion in order to promote myocardial glucose oxidation.
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PMID:Altered plasma concentrations of glutamate, alanine and citrate in the early phase of acute myocardial infarction in man. 287 95

Serum samples from patients admitted to a coronary care unit with a history of acute chest pain suggestive of myocardial infarction in the previous 12 h were obtained on admission and at 6 and 12 h, thereafter. Creatine kinase (CK), CK-MB isoenzyme, CK-MM sub-bands, myoglobin, and lactate dehydrogenase (LD) isoenzymes were examined. Changes were evaluated in relation to the diagnosis obtained from clinical examination, serial electrocardiography and 'routine' cardiac enzymes (CK, aspartate transaminase and alpha-hydroxy butyrate dehydrogenase daily for 3 days following admission). The slope of the logarithms of CK, CK-MB activity and CK-MB concentration in the early post infarct period fully distinguished between infarct and non-infarct patients. Measurement of myoglobin and lactate dehydrogenase isoenzymes was less sensitive. Serial estimation of CK-MM sub-band patterns allowed the time from infarction to be estimated. Serial estimation of CK in the 12 h following admission can be substituted for conventional daily enzyme estimations for the diagnosis of acute myocardial infarction in patients with onset of chest pain within the previous 12 h. This could reduce laboratory and in-patient costs.
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PMID:Early diagnosis of myocardial infarction by timed sequential enzyme measurements. 321 18

In 67 patients with a clinical history of suspected acute myocardial infarction (MI) who developed T-wave inversions in standard ECG and had normal serum aspartate aminotransferase activity (possible MI) the clinical outcome was compared with that in patients fulfilling criteria for subendocardial infarction. Patients with possible MI had a lower mortality (p = 0.02) and also a lower reinfarction rate (p = 0.14) during the first 2 years as compared with those with subendocardial MI. Although patients with subendocardial MI had more problems with chest pain in the acute phase, angina pectoris occurred more frequently in patients with possible MI during a longer follow-up period. Congestive heart failure occurred more frequently in patients with subendocardial MI during initial hospitalization, whereas treatment for heart failure appeared similar in the two groups during a longer follow-up time. We conclude that the clinical course in patients with possible MI, here defined as chest pain and appearance of T-wave inversions without elevation of serum enzyme activity, seems to differ from that in patients with subendocardial MI, particularly regarding long-term survival and incidence of angina pectoris.
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PMID:Appearance of T-wave inversions without raised serum enzyme activity in suspected acute myocardial infarction: clinical outcome in relation to subendocardial infarction. 370 48

Serum kinetics of total creatine kinase (CK), CK-MB isoenzyme, aspartate aminotransferase (AST), lactate dehydrogenase (LD) and alpha-hydroxybutyrate dehydrogenase (HBD) activities were studied in twenty patients with acute myocardial infarction randomly assigned to receive either intracoronary urokinase (group A) or conventional (control) therapy (group B). The temporal characteristics of enzyme changes described were the time lag from onset of chest pain until maximum catalytic concentration value, the rate at which enzymes are released into blood, the peak value of the serum enzyme curves and (d) the fractional disappearance rate (Kd) for each enzyme considered. Thrombolytic treatment induced earlier peak times in group A: for CK, 10.8 vs 27.0 h, for CK-MB, 10.4 vs 23.1, for AST, 13.9 vs 31.3, for LD, 24.4 vs 49.1, and for HBD, 20.5 vs 48.5 (for all enzymes, p less than 0.001). The maximal rate of release for the enzymes was at least twofold greater in group A. Enzyme peak activities and Kd were not significantly different between the groups. The most significant discrimination between the two groups was obtained with AST peak time (Hartz overlap index (Oi) = 0.11) and CK-MB peak time (Oi = 0.12).
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PMID:Serum enzymes in acute myocardial infarction after intracoronary thrombolysis. 376 94

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 levels of creatine kinase, hydroxybutyric dehydrogenase, and aspartate transaminase have been serially measured in the serum of patients undergoing surgery. Serum enzyme levels often rose to a range commonly found after myocardial infarction but fell to normal within 5-10 days. Raised serum enzyme levels have no diagnostic significance in a case of postoperative chest pain until after the fifth postoperative day, but may be significant thereafter.
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PMID:Serum enzyme levels in diagnosis of postoperative myocardial infarction. 507 12

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

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


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