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 relations between reciprocal ST segment depression in the electrocardiogram and infarct size and 10 year prognosis were studied in 315 patients who survived for at least 28 days after a first anterior or inferior myocardial infarction. ST depression was more common in inferior infarcts (72%) than in anterior (37%) ones. It occurred more frequently in complicated infarcts and in the presence of considerable ST elevation. Patients experiencing second or third degree heart block were significantly more likely to show reciprocal changes. The rise in peak cardiac enzyme concentration was higher in patients showing ST depression. In patients with ST depression, peak creatine kinase concentration was 46% higher, aspartate aminotransferase was 39% higher, and lactate dehydrogenase 29% higher after correction for site and complications. A discriminant function analysis selected infarct site, peak aspartate aminotransferase, and magnitude of ST elevation as predictors of the occurrence of ST depression. Age, severity, and smoking status did not significantly improve discrimination. Despite larger increases in peak enzyme concentrations patients with ST depression had marginally fewer subsequent episodes of unstable angina or fatal or non-fatal infarction and a marginally lower 10 year death rate. Neither difference was statistically significant. ST depression occurring early in the acute phase of myocardial infarction is likely to be a reflection of electrophysiological changes taking place at the site of the infarct that is manifested in the contralateral surface of the heart. Other causes, however, such as transient ischaemia at the site of the reciprocal changes or extension of the infarct to contiguous areas cannot be excluded in all cases.
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PMID:The aetiology and prognostic implications of reciprocal electrocardiographic changes in acute myocardial infarction. 370 82

Twenty beef calves weighing approximately 180 kg were allotted to 3 groups. In group A, 6 calves were given 25 mg of mycelial monensin/kg of body weight orally and were evaluated at 1, 2, and 4 days for clinical, ECG, clinicopathologic, and pathologic alterations. In group B, 7 calves were given a single dose of monensin (40 mg/kg) and 5 were given a 2nd 40 mg/kg dose on day 7; calves were evaluated at days 1, 2, 4, 7, 8, 9, and 11. In group C, 2 calves served as controls. Monensin-treated calves developed anorexia, diarrhea, and lethargy after day 1. One group B calf died on day 7 with lesions of congestive heart failure. Electrocardiographic abnormalities were not observed in group A calves; in group B, prolongation of Q-T and QRS intervals occurred from days 2 to 11 and first degree heart block was seen from days 7 to 11. Clinicopathologic alterations included: increased serum activities of aspartate aminotransferase and creatine kinase in group B calves after day 2; decreased serum K+, Na+, and Ca2+ concentrations in both groups, and postdosing occurrence of leukocytosis. Calves were euthanatized sequentially and the lesions of monensin toxicosis were present in the heart, skeletal muscles, and rumen in groups A and B. Disseminated pale yellowish-brown areas of necrosis were present in the ventricular myocardium of 6 of 12 group B calves. Gross lesions were not present in the skeletal muscles or rumen. Microscopically, the myocardial and skeletal muscular lesions were characterized by sarcoplasmic vacuolation from mitochondrial swelling and lipid accumulation in calves killed after day 1 in groups A and B, and by myocardial necrosis with contraction bands, but without calcification, in group B calves killed by day 4. Acute rumenitis was present in groups A and B calves. Myotoxic effects of monensin may be related to its action as an ionophore producing altered intracellular ion concentrations and initiating degeneration and necrosis in striated muscle fibers.
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PMID:Clinical, clinicopathologic, and pathologic alterations in acute monensin toxicosis in cattle. 665 Sep 60

Serial estimations of activities of creatine kinase and its MB isoenzyme, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase and of concentrations of alpha(1)-acid glycoprotein were performed in 15 healthy well-trained male marathon runners. Estimations were made initially within three days before a race and then one, 24, and 96 hours after the race. Technetium-99m pyrophosphate myocardial scintigraphy was carried out at the initial prerace assessment and repeated 48 to 96 hours after the race. None of the subjects developed cardiac symptoms during or after the race.Activities of creatine kinase and creatine kinase MB became maximal 24 hours after the race. One and 96 hours after the race two and five subjects, respectively, showed amounts of creatine kinase MB totalling 5% or more of total creatine kinase. Lactate dehydrogenase activity peaked at one hour after the race, and activities of aspartate and alanine aminotransferases peaked at 24 and 96 hours after the race, respectively. Activities of all these enzymes showed a significant increase from prerace values during the rest of the study. Electrocardiographic features noted were similar to those reported elsewhere in athletes under similar conditions. They included first-degree heart block, incomplete right bundle-branch block, left ventricular hypertrophy, pseudoischaemic T-wave changes, and early repolarisation of variant ST-segment elevations in precordial leads. Technetium-99m pyrophosphate myocardial scintigraphy did not show evidence of myocardial damage before or after the race. Alpha(1)-acid glycoprotein concentrations were normal throughout.These data suggest that reliance on standard enzyme estimations and electrocardiographic criteria may yield false-positive indicators of myocardial injury during prolonged strenuous exercise. Technetium-99m pyrophosphate scintigraphy and alpha(1)-acid glycoprotein measurements offer additional information and may usefully be employed in evaluating circulatory collapse associated with such exercise.
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PMID:Abnormal cardiac enzyme responses after strenuous exercise: alternative diagnostic aids. 681 29