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)

Autoimmune responses to myoglobin were studied in patients with myocardial infarction at different disease stages. It was revealed that during myocardial infarction, the clone of lymphocytes reacting with myoglobin was activated. Besides, these patients showed sensitized T lymphocytes with high cytotoxic activity, lymphotoxins and leukocyte migration inhibition factor, attesting to the development of the delayed type hypersensitivity to myoglobin. It was demonstrated that lymphotoxin assay in the blood might be of importance for differential diagnosis of acute myocardial infarction and angina pectoris with a long-term painful syndrome.
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PMID:[Autoimmune reactions to myoglobin in myocardial infarct patients]. 633 8

The myoglobin concentration, creatine kinase and creatine kinase sub-unit B activity were estimated in fourteen patients with ischaemic heart disease before and after exercise induced angina pectoris. No changes in these parameters were found.
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PMID:Myoglobin concentration, creatine kinase, and creatine kinase sub-unit B activity in serum after myocardial ischaemia. 652 13

Thirteen patients with severe stable angina pectoris were studied by coronary sinus catheterization. In all patients, severe chest pains were produced by atrial pacing. The chest pains had disappeared within 10 min after pacing. Simultaneous arterial (a) and coronary sinus (cs) blood samples were taken before, during and after pacing and analyzed for myoglobin and lactate. The a-cs difference of myoglobin tended to become more negative after pacing, although the change was not significant. However, the change in negative direction post-pacing of the a-cs myoglobin difference was quantitatively correlated with the change in negative direction of the a-cs lactate difference during pacing in the individual patients. This suggests that short-term myocardial ischaemia without signs of established myocardial infarction may provoke myocardial myoglobin release.
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PMID:Myoglobin release in patients with angina pectoris following short-term ischaemia by pacing to angina. 654 Jan 52

Thirty-one patients with acute myocardial infarction (AMI) or doubtful AMI, admitted to the coronary care unit (CCU), were selected for study of serum myoglobin (Mb). In 22 cases with AMI a sequential study of serum Mb shows that it begins to rise 2-3 hours after the onset of the AMI. The average value for the first blood sample taken within 12 hours after the onset was 268.7 +/- 57 ng/ml (ranging from 86-800), and the elevation within 24 hours averaged 2.4-5.0 times the normal value. They were distinctly higher than those of SGOT (0.6-2.1), CPK (2.0-3.4) and LDH (0.6-1.9). Taking into account the peak values determined within 12 hours, Mb showed a 100% correlation with the diagnosis, CPK 85.7% (12/17), GOT 35.9% (6/17) and LDH showed a 13.3% (2/15) correlation. In patients with angina pectoris and old MI, serum Mb was within the normal range, suggesting that the determination of serum Mb is of practical value in the differential diagnosis of angina pectoris and AMI.
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PMID:The value of radioimmunoassay of myoglobin in the diagnosis of acute myocardial infarction. 698 88

We have studied 135 subjects of whom 100 were normal individuals; 10 with diagnosis of acute myocardial infarction (AMI); 10 with angina pectoris; 10 undergoing cardiac catheterism; 5 who underwent open heart surgery. To verify the radioimmunoassay usefulness of CPK cardiac isoenzyme (CK-RIA), of lactate dehydrogenase [LDH (H4)], of myoglobin (MG) in the diagnosis of ischemic disease, we have determined for serum samples: LDH (H4) by radioimmunoassay and HBDH by biochemical assay; CK by biochemical assay; CK-MB by biochemical and radioimmunological assay; MG by radioimmunoassay. The results indicate MG as a sensitive marker for the diagnosis of AMI. In fact serial serum determinations in patients with AMI showed myoglobin levels in 60% of the cases within 1 h after the onset of pain. The CK-RIA is the most sensitive test to evaluate infarct size and LDH (H4) conditioned by the amount of intracellular lactate is an useful test to evaluate myocardial anoxia.
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PMID:[Critical analysis of the radioimmunological methods of determining creatine kinase isoenzyme MB (CK-MB), myoglobin (MG) and of LDH (H4) in ischemic cardiopathy]. 724 91

40 patients with acute myocardial infarction had serial determinations of CK, CKMB and an addition of serum myoglobin (SMb) by radioimmunoassay. In 10 patients with normal values on admission SMb rose earlier than CK and CKMB. In another 20 patients SMb was pathologically increased while CK and CKMB were normal and in 10 patients all parameters were elevated on admission. In all 40 patients SMb was significantly elevated in between 10 hrs after beginning of angina, and peak myoglobin occurred 10 hrs before CK and CKMB. In 10 patients peak SMb correlated with infarct size as determined by angiocardiography in the chronic stage (r = 0.863; p less than 0.01). Peak SMb also correlated with infarct size as estimated by CK release (r = 0.73; p less than 0.001). Thus determination of SMb is a sensitive method in diagnosing early myocardial infarction, and peak serum myoglobin allows early prediction of infarct size.
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PMID:[Early prediction of infarct size by serial determination of serum myoglobin (author's transl)]. 726 33

We have studied 28 patients undergoing coronary angiography by the Judkins technique to determine whether serum myoglobin (MG) might be useful as an indicator of myocardial injury during routine cardiac catheterization and coronary angiography. MG was measured immediately before and after the procedure, and 4 hr later. The study population failed to show a rise of MG outside the normal range in spite of angina, hypotension, or severe coronary disease. Four patients premedicated with intramuscular pentobarbital (positive control) showed a consistent rise, with a range 1.5--3 times normal (p less than 0.001). We conclude that injury to myocardial or peripheral tissues occurring during coronary angiography does not raise myoglobin in venous blood above normal levels in the absence of myocardial infarction or preoperative intramuscular injection. Myoglobin, therefore, provides a useful test for the exclusion of myocardial infarction following coronary angiography.
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PMID:Behavior of serum myoglobin during cardiac catheterization: concise communication. 727 20

Radioimmunological determination of serum myoglobin in 115 patients is reported. Frankly pathological values were noted in 45/55 subjects with a diagnosis of acute myocardial infarct, whereas 7 displayed only a slight rise, and the remaining 3 proved to be false negatives. Pathological values were observed only 2 hr after the commencement of pain, with maxima after 6-20 hr (mean 10 hr). Values returned tonormal 37 hr after the onset of pain. In patients with angina pectoris, myocardial ischaemia, and pulmonary oedema not due to acute infarct, there was only a slight increase in serum levels, while pathological values were never noted in patients with precordial pain of non-cardiac origin.
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PMID:[Diagnostic value of serum myoglobin]. 743 69

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 aim of our study was to evaluate the clinical relevance of serum troponin I (TnI) as a marker of ischemic myocardial injury by using an automated fluoroenzymometric assay. The reference range for serum TnI was established by measuring serum TnI concentrations in blood from 75 healthy donors. The concentration was then compared with serum creatine kinase (CK) activity, CK-MB mass, and myoglobin concentrations in 20 patients with myocardial infarction diagnosed according to the WHO criteria, 20 patients with chest pain of nonischemic origin, 9 patients with unstable angina, 11 with stable angina, 11 patients with chronic muscular diseases, 6 patients with muscular trauma without chest contusion, and 13 patients with chronic renal disease. We found that: (a) 99% of the blood donors had TnI concentrations <0.26 microgram/L (detection limit of the assay in our study); (b) TnI values in acute myocardial infarction (AMI) patients 4 h after onset of chest pain showed a sensitivity of 0.769 and a specificity of 1.0 at a decisional concentration for AMI of 1 microgram/L, even in the presence of severe skeletal muscle injuries or renal diseases; (c) the increase in TnI concentrations after infarction (interquartile range 3.25-6 h) and the peak occurred later (interquartile range 11.5-24 h) than the rise found in myoglobin and CK-MB, but the increase persisted much longer (>96 h); (d) receiver-operating characteristic curve analysis showed the high diagnostic accuracy of TnI in diagnosing AMI even in patients in whom traditional biochemical markers are adversely influenced by underlying clinical situations.
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PMID:Fluoroenzymometric method to measure cardiac troponin I in sera of patients with myocardial infarction. 878 5


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