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)

86 patients with ischaemic heart-disease were assessed for the presence of the MB isoenzyme of creatine kinase (C.K.-MB). Raised C.K.-MB levels with normal total C.K. were found in 10 patients with a clinical picture, but no electrocardiographic evidence, of acute myocardial infarction. 4 of these patients later had an infarction, but the remaining 6 have remained undiagnosed. Of 26 patients with unstable angina, 11 (42%) had high levels of C.K.-MB in the presence of normal total C.K. Of 50 patients with effort angina and a positive ergometric stress test, 3 (6%) with crescendo angina had high C.K.-MB levels in the presence of normal total C.K. In patients with angina, myocardial necrosis was excluded by normal serum-myoglobin levels. In both groups with angina, those with raised C.K.-MB levels had a more severe clinical picture, greater depressions of the ST segment, and lower threshold to ergometry. Raised C.K.-MB levels may indicate myocardial ischaemia.
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PMID:The MB isoenzyme of creatine kinase as an indicator of severity of myocardial ischaemia. 8 64

The reliability of serum myoglobin as a marker for acute myocardial infarction was evaluated in 157 consecutive coronary-care admissions. Admission myoglobin was elevated in 47 of 52 patients with acute infarction. Excluding those patients who presented later than 24 hr after symptom onset, only one patient with acute infarct had a normal admission myoglobin. In 22 of 105 patients with no infarct, myoglobin was elevated in association with angina, congestive heart failure, arrhythmias, and renal insufficiency. The detection of acute infarction by serum myoglobin measurement equals that of serial serum creatine phosphokinase isoenzymes (CPK-MB) by electrophoresis, but an elevated myoglobin is not specific for what is now considered clinically significant myocardial infarction.
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PMID:Assessment of serum myoglobin as a marker for acute myocardial infarction. 43 Jan 83

A radioimmunoassay was developed to determine serum myoglobin (SMb). 50 healthy persons showed values between 0 and 90 ng/ml. Serial tests of 10 patients following acute myocardial infarction or during angina pectoris (AP) indicated that SMb reached pathological values before CK and CK-MB (average 250 +/- 95 ng/ml at the time of hospitalisation which corresponds to 3.3 +/- 1.4 h after beginning of angina pectoris). At hospitalisation the simultaneously determined CK was within normal limits and reached pathological values only 6.2 +/- 1.9 h after the onset of angina. Maximum of SMb was 506 +/- 194 ng/ml occurring 8.8 +/- 2.8 h after beginning of AP, maximum of CK was 905 +/- 475 mU/ml occurring 20.0 +/- 7.8 h after AP. CK-MB and CK differed only slightly in their time course. One patient with severe AP had pathologically increased SMb values whilst all other enzymes were completely normal. Methodical and clinical results are discussed.
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PMID:[Radioimmunoassay for human myoglobin: methodology and diagnostic significance in myocardial infarction (author's transl)]. 43 Oct 32

Myoglobin and the enzymatic activity of creatine phosphokinase CK), MB-isoenzyme of CK (CK-MB), aspartate aminotransferase (GOT), alanine aminotransferase (GPT) and lactic acid dehydrogenase (LDH) were serially determined in 10 patients with acute myocardial infarction. Additionally the same parameters were assessed in 5 patients with angina pectoris for 24 hours after bicycle ergometry. 10 in-patients served as controls. Myoglobin was determined by radioimmunoassay and the other enzyme activities according to the current kinetic methods. Comparison of myoglobin with the enzymatic parameters showed that the myoglobin peak occurs 5.6 hours after the beginning of the sampling period, i.e. 7.3 hours earlier than CK and CK-MB and 11.6 hours earlier than GOT. In analogy to this finding the descending limb of the myoglobin curve was significantly earlier at a level of one third of the peak value, i.e. 8.2 hours earlier than CK-MB, 18.8 hours earlier than CK and 27.3 hours earlier than GOT. No signs of myocardial necrosis in terms of myoglobin or enzymatic activity could be detected after bicycle ergometry. It is concluded that myoglobin is a more sensitive parameter for assessment of the acute phase in patients with myocardial infarction than the usualy enzymatic parameters.
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PMID:[Plasma myoglobin level as a course criterium in patients with acute myocardial infarct]. 53 58

To evaluate myocardial cell damage in relation to spontaneous and exercise-induced ischaemia, release of myoglobin, creatine kinase (CK) and its isoenzyme MB (CK-MB) into the serum was estimated in 10 patients with severe stable angina. All patients had a positive exercise test, significant stenosis of one or more of the main coronary arteries and more than five ischaemic attacks per week. ST-segment monitoring was performed for 36 h. During the last 24 h of that period (period A) serial blood samples were analysed for myoglobin, CK and CK-MB using sensitive assays. Three days later (period B) the patients performed an exercise test at 0815 h, with ST-segment monitoring and blood sampling carried out as described for period A. During period A, 47 ischaemic episodes (100% silent) with a total duration of 599 min were noted in four patients. Forty-seven ischaemic episodes (94% silent) with a total duration of 804 min, were observed in seven patients during period B. Release of myoglobin, CK, and CK-MB did not increase in relation either to spontaneous or exercise-induced ischaemia. Thus even frequent and prolonged episodes of transient myocardial ischaemia (symptomatic or asymptomatic) in patients with severe stable angina pectoris does not seem to cause irreversible myocardial damage.
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PMID:Lack of indication of myocardial cell damage after myocardial ischaemia in patients with severe stable angina. 155 15

The hemagglutination test was used to measure the content of myoglobin (MG) in the blood serum in 92 patients suffering from coronary heart disease (myocardial infarction, unstable and stable angina pectoris). The content of MG turned out a safe indicator attesting to acute myocardial infarction. In complications and spreading of necrosis, the MG level was returning to normal slowly. In patients with angina pectoris, the MG level did not on the average differ from control. However, in patients with unstable angina pectoris, there was an increase of the MG content after long-term attacks and in the development of small-focal necroses in the myocardium.
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PMID:[The comparative value of myoglobin determination in patients with different forms of ischemic heart disease]. 175 8

In 1984-88 the authors examined in 813 subjects with the chest pain syndrome of varying aetiology (acute myocardial infarction, myocarditis, pericarditis, vertebrogenic algic syndrome, embolism of the pulmonary artery, patients lacking detectable organic causes of pain) the trend of myoglobin serum levels. They found significantly elevated values only in patients with myocardial infarction and myocarditis whereby the two diseases differ in particular as regards the shape of the curve of myoglobin values. In chest pain with another aetiology the myoglobin levels rose only rarely or not at all. From the differential diagnostic aspect it is particularly valuable that myoglobin was not elevated in any patient with embolism of the pulmonary artery and only very rarely in angina pectoris. Where in exceptional instances the myoglobin levels were elevated in patients with other investigated causes of chest pain, this increase was always due to another basic disease (right-sided cardiac failure, renal insufficiency, neuromuscular disease), whereby for these conditions prolonged persistence of the elevated serum myoglobin values was typical and the levels were never above 8 nmol/l.
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PMID:[The significance of myoglobin determination in the differential diagnosis of chest pain syndrome]. 205 2

ELISA using the test systems and a complex of equipment manufactured by Flow Company was employed to study over time the content of fibronectin, fibrinogen, products of its degradation and myoglobin in 178 patients suffering from coronary heart disease (stable and progressive angina pectoris, acute myocardial infarction). The concentration of myoglobin, fibronectin, fibrinogen and products of its degradation was established to depend on the gravity of coronary heart disease and the tame elapsed since the disease onset. In patients with progressive disease, there was an increased consumption of fibronectin which may be due both to its expenditure during blood coagulation and fulfillment of angioprotective function because of exacerbation of systemic atherosclerosis.
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PMID:[The content of fibronectin, fibrinogen, its degradation products and myoglobin in patients with ischemic heart disease]. 209

The detection rate was examined for ECG (EchoECG) equivalents of clinical coronary heart disease (CHD) forms, such as angina pectoris, focal myocardial dystrophy, small and large myocardial infarction, at various levels of the peak activity of blood creatine phosphokinase in the acute period of the disease. A series of investigations revealed in the acute period the time when myoglobin, CPK, CPK MB, AST, and LDH attained their maximal blood content, which were directly related to the molecular weight of proteins. The findings allowed the author to consider a relationship between the values obtained by diagnostic techniques and the time course of an infarct process, the mass of ischemic necrosis and its topography in the myocardium.
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PMID:[Correlations of laboratory and instrumental method parameters in the diagnosis of acute ischemic lesion of the myocardium]. 229 Feb 68

The serum level of myoglobin (Mb) was determined in 11 male patients with chronic ischemic heart disease (angiographically studied) by the mean of an enzyme immunoassay (EIA). By a second EIA we could detect in all our patients autoantibodies (autoAB) to Mb. While the level of Mb in all cases was normal (less than 100 ng/ml) we found differences in the level of autoAB to Mb (normal value 90-100%). 7 patients with unstable Angina pectoris exhibited decreased levels of autoAB to Mb (65%). In 4 patients with stable Angina pectoris autoAB to Mb were 93%. The physiological role of the autoAB to Mb remains still unclear. The simultaneous determination of Mb and the autoAB to Mb may be helpful in differential diagnosis of stable and unstable Angina pectoris.
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PMID:Determination of serum level of myoglobin and plasma level of autoantibodies to myoglobin in patients with angina pectoris. 246 75


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