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

A 79-year-old female was admitted to our hospital because of a malignant pleural effusion following mastectomy 4 years ago. In the patient's history arterial hypertension and previous inferior myocardial infarction have been known. Two doses of 20 mg mitoxantrone were installed intrapleurally at an interval of 4 weeks. Six hours after the second mitoxantrone application and the patient had increasing dyspnea with consecutive left heart failure, pulmonary congestion, and a drop of blood pressure. The white-cell count was 14800/mm3. The levels of creatinine phosphokinase (CPK), lactate dehydrogenase (LDH) and serum aspartate aminotransferase (SGOT) were in the normal range. Transthoracic echocardiography showed concentric left ventricular hypertrophy and a markedly decreased fractional shortening, but no left ventricular dilatation. The electrocardiogram showed newly appeared down-sloping ST-segments and inverted T-waves. Clinical recovery was achieved after 6 days by application of oxygen, dobutamine and furosemide followed by angiotensin converting enzyme inhibition and digitalis. In the echocardiographic control examination 14 days later left ventricular function had normalized. The changes of electrocardiogram normalized 4 weeks later.
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PMID:[Mitoxantrone-induced acute left heart failure after intrapleural administration]. 937 56

A 52-year-old Indian woman with underlying diabetes mellitus and hyperlipidemia, presented with generalized musculoskeletal pain and oliguria for three days. The patient was taking 80 mg of simvastatin initiated 20 days earlier after cardiac catheterization for an inferior myocardial infarction. Laboratory investigations revealed the following serum levels: creatine kinase 81,620 U/L, aspartate aminotransferase 2497 U/L, alanine aminotransferase 1304 U/L, blood urea nitrogen 21.7 mmol/L, creatinine 447 micromol/L, Free T4 12.6 pmol/L, and thyroid stimulating hormone (TSH) 22.7 microIU/L. Simvastatin was discontinued and the patient received forced alkaline diuresis. Her hypothyroidism was treated with thyroxin, which was continued upon discharge, and her renal function recovered within two months. This case report discusses the incidence of rhabdomyolysis in a patient with primary hypothyroidism receiving large doses of simvastatin.
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PMID:Severe rhabdomyolysis and acute renal failure secondary to use of simvastatin in undiagnosed hypothyroidism. 1911 32

A 52-year-old Indian woman with underlying diabetes mellitus, hyperlipidemia and undiagnosed hypothyroidism presented with generalized musculoskeletal pain and oliguria for three days. The patient was taking 80 mg of simvastatin (initiated 20 days before) after cardiac catheterization for an inferior myocardial infarction. Laboratory evaluation revealed the following serum levels: creatine kinase, 81,660 U/L; aspartate aminotransferase, 2,497 U/L; alanine aminotransferase, 1,304 U/L; blood urea nitrogen, 88 mg/dL; creatinine, 5.1 mg/dL; free thyroxine (FT(4)), 12.6 Pmol/L and thyroid stimulating hormone, 22.7 uIU/L. Simvastatin was discontinued and the patient was administered forced alkaline diuresis. Her hypothyroidism was treated with thyroxine, which was continued after discharge. Her renal function recovered within two months. This case report discusses the higher incidence of rhabdomyolysis in patients with undiagnosed hypothyroidism receiving large doses of simvastatin.
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PMID:Severe rhabdomyolysis and acute renal failure secondary to the use of simvastatin in undiagnosed hypothyroidism. 2036 19