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)

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.
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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.
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PMID:Does acute-phase beta-blockade reduce mortality in acute myocardial infarction by limiting infarct size? 304 3

Determinants of plasma glucose concentrations were studied in patients on admission to hospital with confirmed acute myocardial infarction but without previous glucose intolerance as evidenced by raised concentrations of glycosylated haemoglobin (HbAlc). Mortality in hospital increased significantly with increasing plasma concentrations of glucose in patients with both normal (p less than 0.0001, n = 311) and borderline (p less than 0.02, n = 70) concentrations of HbAlc. There was a weak relation between plasma glucose concentrations and infarct size as estimated by peak aspartate transaminase activity in both HbAlc groups (rs = 0.26, n = 101 and rs = 0.41, n = 35 respectively). A correlation was found between adrenaline and plasma glucose concentrations (r = 0.47, n = 27) and cortisol and plasma glucose concentrations (r = 0.75, n = 19), but the relation of plasma noradrenaline and plasma glucose suggested a threshold effect. Concentrations of adrenaline, but not those of noradrenaline or cortisol, correlated with infarct size as measured both by peak aspartate transaminase activity and cumulative release of creatine kinase MB isoenzyme. Multiple regression analysis showed that concentrations of cortisol, adrenaline, and noradrenaline (but not the concentration of HbAlc, infarct size, or age) are the main determinants of plasma glucose concentration measured in non-diabetic patients when admitted to hospital after acute myocardial infarction.
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PMID:Determinants and importance of stress hyperglycaemia in non-diabetic patients with myocardial infarction. 309 14

We kinetically measured total lactate dehydrogenase (LD, EC 1.1.1.27), total creatine kinase (CK, EC 2.7.3.2), and aspartate aminotransferase (AST, EC 2.6.1.1.) in 16 elite college basketball players, before the competition season and not in close temporal relation to near-maximal exercise, and in 17 healthy non-athlete controls. LD isoenzymes were determined by both electrophoretic and immunoprecipitation methods. CK-MB isoenzyme was measured electrophoretically. We found significantly higher mean LD-1 values and LD-1/LD-2 ratios in the players than the controls: 31.6 (SD 3.7)% vs 25.8 (SD 3.2)% (P less than 0.005) and 1.1 (SD 0.13) vs 0.87 (SD 0.16) (P less than 0.001), respectively. A "flipped" LD pattern (LD-1 greater than LD-2) was found in half the players and in six of the eight black athletes, but in only two of the control group and in none of the black controls. Mean CK activity in serum exceeded normal values in the serum of the athletes and was higher in comparison with the control group [274 (SD 156) vs 103 (SD 82) U/L]. Mean CK was significantly higher in the eight athletes with the flipped LD pattern than in those with LD-1 less than LD-2 [322 (SD 163) vs 180 (SD 98) U/L; P = 0.05], and also in comparison with CK in the two controls with flipped LD pattern. We saw no significant difference in mean CK between the nine players with normal immunochemical LD-1/LD ratios and the seven players with above-normal ratios. CK-MB was not detected in either athletes or controls. None of the players had any clinical or electrocardiographic evidence for myocardial ischemia or infarction. Evidently the flipped LD pattern usually found in patients with acute myocardial infarction and reported in some athletes after extreme exercise such as ultra-marathon running may also be found in athletes who are in their "basal fitness shape" but who are not involved in competitive physical activity.
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PMID:"Flipped" patterns of lactate dehydrogenase isoenzymes in serum of elite college basketball players. 318 Apr 33

Although measurements of creatine kinase isoenzyme 2 (CK-MB) are often used to diagnose acute myocardial infarction, their sensitivity and specificity are less than 100%. Because skeletal muscle contains more CK and less aspartate aminotransferase (AST) than cardiac muscle, the CK/AST ratio might provide a useful adjunct in evaluating the source of a supranormal value for CK. I established the following decision levels in a retrospective study of 342 patients: ratios less than 14 (if total CK was 300-1200 U/L), less than 20 (CK 1201-2000 U/L), or less than 25 (CK greater than 2000 U/L) suggested myocardial infarction, with a sensitivity of 95% and a specificity of 65%. In a validation study with 277 additional patients, liver disease and alcohol abuse caused erroneous results, leading to exclusion of 22% of these patients. In the remaining cases, sensitivity was 94%, specificity 90%. The CK/AST ratios changed little with time, suggesting that a single value would be adequate for evaluating patients with increased CK.
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PMID:Creatine kinase:aspartate aminotransferase activity ratio as an indicator of the source of an increased creatine kinase activity. 319 92

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

Eight patients with severe peripheral vascular atherosclerosis scheduled for abdominal aortic surgery were investigated to detect coexisting coronary artery disease. None of the patients had a history of angina pectoris or previous myocardial infarction. Preoperative computerised thallium-201 dipyridamole myocardial scintigraphy was abnormal in all patients, showing either myocardial scar tissue and/or ischaemia with redistribution and/or low washout. In all but one patient, the serum level of creatin kinase was elevated during the first postoperative days. In two patients, the serum concentrations of aspartate aminotransferase and lactate dehydrogenase were elevated. None of the patients showed clinical or electrocardiographical signs of acute myocardial infarction. Thallium-201 dipyridamole myocardial imaging is a new noninvasive method for detection of ischaemic heart disease in patients with severe peripheral atherosclerosis who are unable to perform a bicycle exercise test. The new programme for determination of regional washout appeared to be very precise and may be especially applicable in the case of low washout values.
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PMID:Thallium-201 myocardial scintigraphy during dipyridamole-induced coronary hyperaemia. First experiences with a new regional washout programme. 321 87

The red cell filterability was decreased in patients with acute myocardial infarction (AMI) when compared with healthy controls, 14.6 (12.2-16.3) units and 16.9 (15.6-17.4) units respectively, P50 (P25-P75), p less than 0.001). No significant correlations could be seen within the AMI group between the decrease in filterability and the levels of serum aspartate aminotransferase or serum lactate dehydrogenase. The erythrocyte filterability, however, correlated to the serum concentrations of hepatic enzymes in AMI. The addition of sodium lactate in vitro in physiological concentrations (0.9-3.6 mM/l final concentration) lowered the erythrocyte filterability markedly to 2.7 (0-9.8) units in a dose-dependent manner, supporting the hypothesis that the decrease in erythrocyte filterability in AMI might be caused by an increase in the lactate concentration.
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PMID:Decreased red cell filterability in patients with acute myocardial infarction. 323 50

Myocardial activities of several enzymes were measured in infarcted and non-infarcted areas of heart sections obtained from eight patients who died after acute myocardial infarction. Similar data were obtained from four patients with cardiovascular disorders who died from causes other than myocardial infarction and from six patients without previously known heart disease. It was found that both non-infarcted and infarcted tissue samples contained considerably altered enzyme activities. This finding explains the low correlations between enzymatic and histological estimates of infarct size previously reported. However, when the residual myocardial activities of different enzymes were compared with each other, a close correlation was found between creatine kinase, alpha-hydroxybutyrate dehydrogenase, and aspartate aminotransferase. It appears that the pathological changes in the myocardial activities of these enzymes may be explained by the phenomenon of diluted myocardium. This indicates that myocardial injury, as estimated from plasma enzyme activities, may still be expressed meaningfully in gram equivalents of healthy myocardium.
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PMID:Myocardial enzyme depletion in infarcted human hearts: infarct size and equivalent tissue mass. 324 32

In 727 patients with acute myocardial infarction, different enzyme variables reflecting infarct size were related to the 5-year mortality rate. The maximum activity of serum heat-stable lactate dehydrogenase (LD), analyzed every 12 hours for 48 to 108 hours, was significantly associated with the 5-year mortality rate when patients with a first myocardial infarction were evaluated (p less than 0.001), and similarly (p less than 0.001) when patients with a previous myocardial infarction were included in the analyses. Very similar results were found when the maximum activity of aspartate aminotransferase (ASAT) analyzed once daily for 3 days was related to the mortality rate over 5 years, whereas the maximum activity of creatine kinase (CK) and CK subunit B analyzed every 6 hours for 48 hours in a subset of patients did not predict the outcome to the same extent. The results from LD and ASAT analyses clearly indicated that the association between infarct size and 5-year mortality rate was caused by the much higher mortality rate in patients with larger infarcts during the first year after onset of infarction, whereas after the first year, incidence of death appeared to be independent of the original infarct size. Thus we conclude that although a highly significant relationship between infarct size and overall 5-year survival was found, the mortality rate seemed to be higher in patients with larger infarcts, particularly during the first year after infarction.
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PMID:Five-year mortality rate in relation to enzyme-estimated infarct size in acute myocardial infarction. 331 May 63


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