Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On the basis of a small number of patients with the tentative diagnosis acute myocardial infarction the diagnostic valency of the glycogen phosphorylase was tested. A separation between severe stenocardia and myocardial infarction is possible. After simplification of the methodology the glycogen phosphorylase might substitute in higher specifity the creatinine kinase.
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PMID:[Determination of glycogen phosphorylase B--a contribution to the enzymatic diagnosis of acute myocardial infarct]. 74 75

Methods are described (a) for the estimation of glycogen phosphorylase activity (EC 2.4.1.1) in human blood serum based on the chemical determination of liberated orthophosphate or on the enzymic determination of glucose 1-phosphate in a coupled assay system and (b) for the electrophoretic separation of isophosphorylases I, II, and III in human. Glycogen phosphorylase activities ranging from 1.5 to 18 mU/ml were found in the serum of patients with acute myocardial infarction. In contrast, no glycogen phosphorylase activity was detected in the serum of healthy persons. The enzyme appears in the serum 4 hours after the onset of the infarction and reaches a maximum after 20 to 30 hours. Acrylamide gel electrophoresis of serum after a myocardial infarction revealed only muscle isophosphorylase I, the isoenzyme characteristic of the heart. No phosphorylase activity was detected in serum of patients with angina pectoris, endocarditis, and uncomplicative congestive heart failure. From these findings it appears that the new serum enzyme test may prove to be a valuable addition to presently existing methods for the early differential diagnosis of acute myocardial infarction.
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PMID:The assay of glycogen phosphorylase in human blood serum and its application to the diagnosis of myocardial infarction. 112 38

A method for measuring blood serum glycogen phosphorylase (GP) activity is described, informative at early stages of myocardial infarction. The method is sensitive and available for clinical biochemistry laboratories. It consists in preliminary purification of GP from serum proteins and metabolites by affinity chromatography in micro-columns and subsequent measurement of the activity in the eluate. The procedure involves selective GP sorption on starch, washing, and subsequent desorption with glycogen solution. GP activity is measured by the kinetic spectrophotometric technique, based on enzymic measurement of glucose-1-phosphate, the product of glycogen consumption reaction, at a wavelength of 340 nm. Conditions of serum GP chromatographic purification are modified in the suggested procedure, this improving the sensitivity of the enzyme measurement. Blood serum GP activities were measured in patients with various cardiac diseases--myocardial infarction (15 cases), angina of rest and effort (53), essential hypertension (30). Different methods of GP activity measurements are considered. Recommendations on the use of the described method, a sensitive test for the diagnosis of myocardial infarction, are given.
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PMID:[The determination of the glycogen phosphorylase activity in blood serum]. 171 85

With a new immunoenzymometric assay we measured human glycogen phosphorylase isoenzyme BB (GPBB) in 116 healthy individuals, 14 patients with stable angina, 107 nontraumatic chest pain patients on admission to the emergency department [45 acute myocardial infarction (AMI), 49 unstable angina, 13 other diseases], and in serial samples from 41 AMI patients. GPBB was compared with creatine kinase (CK), CKMB mass, myoglobin, and cardiac troponin T. Receiver-operating characteristic plots demonstrated the significantly greater (P < or = 0.012) discriminatory power of GPBB to detect acute ischemic coronary syndromes compared with all other tested markers. GPBB was the most sensitive marker for detection of AMI during the first 4 h after onset of chest pain, and only GPBB was increased above the upper reference limit (7 micrograms/L) on admission in patients who had unstable angina at rest and reversible ST-T alterations. This and the high early sensitivity of GPBB are most likely explained by its function as a key enzyme of glycogenolysis.
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PMID:Immunoenzymometric assay of human glycogen phosphorylase isoenzyme BB in diagnosis of ischemic myocardial injury. 760 Jun 98

The acute coronary syndromes represent a continuum of myocardial ischemia ranging from angina, reversible tissue injury --> unstable angina, frequently associated with minor myocardial damage --> myocardial infarction and extensive tissue necrosis. Historically, coronary artery disease assessment has been mainly binary, using WHO criteria of symptoms, electrocardiography, and biochemical markers. The creatine kinase-MB isoenzyme (CK-MB) has been a benchmark for markers, but it is not specific for myocardium. Cardiac-specific isoforms of troponin T and I have emerged as sensitive myocardial infarction (MI) indicators and, importantly, for risk stratification of acute coronary syndrome patients. In addition to markers of myocardial cell necrosis, markers of plaque disruption (C-reactive protein and serum amyloid A), "angry" platelets (P-selectin), ischemia (glycogen phosphorylase-BB isoenzyme), and the procoagulant state and thrombosis (soluble fibrin) have potential use. Also, CK-MB and myoglobin have been combined with clinical indicators for monitoring reperfusion after thrombolytic therapy. Biochemical markers will continue to be an important clinical adjunct for MI diagnosis, risk assessment, and reperfusion monitoring in the future.
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PMID:Biochemical markers of the acute coronary syndromes. 970 95

The diagnosis of myocardial damage is preferably based on measurement of the cardiac-specific troponins. However, there is an emerging need for early, specific cardiac markers. One potential candidate is the glycogen phosphorylase BB isoenzyme (GPBB). We investigated the use of a new, commercially available GPBB ELISA assay in 61 patients presenting with an acute coronary syndrome (37 acute myocardial infarction, 24 unstable angina pectoris) in comparison to established cardiac markers such as troponin T, creatine kinase isoenzyme MB (CKMB) mass, and myoglobin. Blood samples were obtained on arrival, as well as 1, 2, 3, 4, 8, 12 and 24 h later. GPBB plasma concentrations were elevated in 90.9% of patients 1 h after onset of chest pain and increased to 100% at 4-5 h. Within the first 6 h, GPBB showed the highest sensitivity (95.5-100%) and high specificity (94-96%) compared to myoglobin (85-95% sensitivity) and CKMB mass (71.4-91.3% sensitivity). As expected, troponin T showed high specificity (100%) and sensitivity >95% later in the time course (>or=3 h). In un-stable angina pectoris patients, a very high rate of elevated GPBB was observed (93.9% at 3 h) compared to myoglobin (66.7%). Cardiac troponin T and CKMB were only elevated in 33.8% and 55.0% of these patients, respectively. In conclusion, GPBB is a promising marker for the early diagnosis of acute coronary syndromes and could probably act as a marker of ischemia. However, further studies on specificity and development of a fast, automated assay are necessary before GPBB can be recommended as a routine diagnostic tool.
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PMID:Glycogen phosphorylase BB in acute coronary syndromes. 1630 72

The aim of the study was to evaluate whether markers of myocardial injury and ischemia are helpful in detecting coronary artery disease (CAD) in patients with stable angina. Venous blood was obtained before and after a bicycle exercise test in 47 outpatients with suspected CAD for measurement of cardiac troponin I (cTnI), heart-type fatty acid binding protein, and glycogen phosphorylase BB. Patients with a coronary artery stenosis >/=70% in diameter (n = 33) were compared with patients with coronary narrowing <50% (controls, n = 14). None of the markers increased after bicycle exercise testing. cTnI measured before and after exercise was higher in the CAD group than in controls (p <0.001). The area under the curve for diagnosis was greater when the cTnI value was detectable than with stress testing alone. In conclusion, baseline cTnI was of value in detecting CAD and also during follow-up in predicting the need for further revascularization.
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PMID:Usefulness of detectable levels of troponin, below the 99th percentile of the normal range, as a clue to the presence of underlying coronary artery disease. 1771 17