Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 64-year-old female patient with a prosthetic mitral valve suffered from recurrent typical angina and dyspnea. Left heart catheterization excluded a dysfunction of the prosthesis and coronary artery disease (CAD). A stress thallium scan demonstrated an ischemic reaction. An antimyosin scintigram was positive, indicating myocytal membrane disruption. Serological tests were suspicious for systemic lupus erythematosus (SLE). Therefore, an endomyocardial biopsy (EMB) was performed and a severe alteration of an intramyocardial artery, comparable with chronic SLE, was diagnosed. EMB is a useful diagnostic tool in patients with typical chest pain, positive thallium and anti-myosin scintigrams, however exclusion of CAD.
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PMID:[Diagnosis by endomyocardial biopsy: angina pectoris as a manifestation of lupus erythematosus]. 175 Feb 31

An ELISA assay with monoclonal antibody (Mab 2F4) raised against human ventricular myosin heavy chains was developed and used to investigate human sera after myocardial infarction. The monoclonal antibody 2F4 was selected for its high affinity to soluble fragments of myosin heavy chains (subfragment-1) and for its appropriate tissue specificity. By including Mab 2F4 in a simple and rapid dot immunobinding assay sera from patients with acute chest pain and of persons without a history of heart disease were tested. Myosin was detected only in the sera of the patients with myocardial necrosis, confirmed by electrocardiographic data. Negative reactions in all control cases were found. The serum myosin fragments reactive with Mab 2F4 were characterized by immunoblot experiments and protein bands in the region about 43 kDa were found. It was concluded that the myocardial infarction can be demonstrated by detection of cardiac myosin heavy chain fragments in the patients' sera.
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PMID:Identification of human ventricular myosin heavy chain fragments with monoclonal antibody 2F4 in human sera after myocardial necrosis. 175 94

A monoclonal solid-phase enzyme immunoassay has been developed for the detection of human serum ventricular myosin light chain-1. Cross-reactivity of this with human skeletal muscle myosin was observed, but the enzyme immunoassay with the sera of patients with acute myocardial infarction gave similar results with radioimmunoassay. The human ventricular myosin light chain-1 levels in the healthy subjects were 0.2-6.6 ng/ml in males and 0.2-4.1 ng/ml in females. Within-run and between-run precision (CVs) of the assays was on the order of 2.3-4.7% and 4.3-8.7, respectively. Sensitivity of the assay was 1.0 ng/ml, and working range was 5-100 ng/ml. In all patients with define acute myocardial infarction, serum ventricular myosin light chain-1 levels increased three- to ten-fold the upper reference range within 6 hr after the onset of chest pains. Two types of subtrend were discovered: its levels remain elevated for 3-4 days and its levels increased and then decreased 1-2 days after the initial rise but became elevated again for the next 4-7 days after the onset of chest pain, which is in contrast to the case with all conventionally used biochemical cardiac markers.
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PMID:Measurement of human ventricular myosin light chain-1 by monoclonal solid-phase enzyme immunoassay in patients with acute myocardial infarction. 189 May 37

A radioimmunoassay for human cardiac myosin light chains (CM-LC) was developed and evaluated as a selective diagnostic test for acute myocardial infarction (AMI). The assay had a sensitivity of 1.0 ng/ml (+/- 2 standard deviations) in serum. Eighty-three patients with confirmed AMI all showed an elevated plasma concentration of CM-LC at some time during the course of their illness. Of 9 patients from whom early blood samples were obtained, 7 had diagnostic concentrations within 6 hours from the onset of chest pain. Only 2 had an elevated total creatine kinase level at this time. CM-LC concentrations peaked on days 2 to 4, but remained elevated in patients with large AMIs for more than 1 week. In preinfarction syndrome, 8 of 15 patients had elevated CM-LC levels at least once. Of 15 patients with stable angina pectoris, only 1 patient, who had congestive heart failure, showed elevated light chain levels. CM-LC levels were not detectable by this method in the sera of healthy persons (n = 72), patients with recent intramuscular injection (n = 3), or those with a variety of systemic illnesses (n = 14). In initial studies using an antiserum having 25% cross-reactivity between cardiac and skeletal muscle myosin light chains, 3 patients who had extensive skeletal muscle damage appeared to have elevated concentrations. Patients with this finding have not yet been examined with a more specific antiserum (8% cross-reactivity).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diagnosis of acute myocardial infarction by detection of circulating cardiac myosin light chains. 649 59

A monoclonal enzyme immunoassay for measuring human ventricular myosin light chain isotype 1 (HVMLC1) in serum has been developed. To evaluate the method in patients with suspected myocardial injury, we studied 51 patients (16 acute myocardial infarction (AMI), 19 unstable angina pectoris (UAP), 9 stable angina pectoris, 3 nonischemic heart disease, 4 hip surgery patients), and 190 controls (blood donors). Serial blood-samples were drawn from patients; a single blood-sample from controls. The diagnostic value of the HVMLC1 assay was compared with total creatine kinase (CK), CKMB activity, CKMB mass concentration, lactate dehydrogenase isoenzyme 1 (LD1), troponin T (TnT) and mitochondrial-aspartate aminotransferase (m-ASAT). The detection limit of HVMLC1 was 0.4 microgram/l (linear range 0-20 micrograms/l). Sera from 190 reference persons did not contain detectable levels of HVMLC1 (< 0.4 microgram/l; 99% percentile). The coefficients of variation were 13% (1.0 microgram/l) and 3.1% (17.7 micrograms/l). Cross-reactivity with myosin from skeletal muscle was seen. Times to peak value were: CK 19.3 +/- 2.0, LD1 43.4 +/- 3.2, HVMLC1 72.9 +/- 7.0, and m-ASAT 67.3 +/- 5.6 h. Time-curves of HVMLC1 and m-ASAT were similar, whereas time-curves for HVMLC1 and TnT were quite different in most cases. Peak value of HVMLC1 was five times higher than CK peak value and eight times that of LD1. HVMLC1 appeared in the blood within hours after the onset of chest pain and in the majority remained for more than a week after AMI. Among patients with UAP 16% (3/19) had elevated HVMLC1 in serum, whereas elevated TnT was seen in 26% (5/19) and elevated CKMB mass in 26% (5/19). We conclude that the new HVMLC1 assay offers a sensitive diagnosis of myocardial injury. It is characterized by a wide diagnostic time window. The similarity of the HVMLC1 and m-ASAT curves indicates that it may be used to estimate the extent of myocardial necrosis.
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PMID:Human ventricular myosin light chain isotype 1 as a marker of myocardial injury. 817 43

We evaluated the performance and analytical parameters of a one-step magnetic IRMA kit for the measurement of myosin in serum. The method uses two monoclonal antibodies selected for their high affinity to the heavy chains of human ventricular myosin. The first antibody is coupled to a magnetic solid phase and the second one is labeled with 125I. The working range of the IRMA (range of myosin concentrations measured with an imprecision < 10% CV) was 250-3600 microU/L and the sensitivity 20.8 +/- 7.2 microU/L. The between-assay variability, evaluated from replicate measurements in different runs of two serum pools was 14.6 CV% for the first pool (259.1 +/- 37.8 microU/L) and 14.3 CV% for the second pool (442.0 +/- 63.1 microU/L), respectively. To evaluate the clinical usefulness of myosin as a marker of myocardial cell damage, serum myosin was measured in patients with acute myocardial infarction (AMI) (n = 9) or subarachnoid hemorrhage (n = 20). The results obtained with the myosin assay were compared with those of two other markers considered specific for myocardial necrosis (CK-MB and myoglobin). In eight patients with AMI, serum myosin was elevated 24-36 hours after the onset of chest pain and reached a maximum at 4-7 days, returning to control levels at 8-11 days. The one remaining AMI patient showed two subsequent peaks in serum CK-MB and myoglobin concentrations (thus suggesting an extension of myocardial necrosis), the myosin concentrations reaching their peak only after 9 days.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunoradiometric assay of serum myosin as a marker of myocardial cell damage: methodological and clinical evaluation. 832 75

The serum level of human ventricular myosin light chains 1 and 2 was determined by competitive ELISA assay in 56 patients, of whom 26 with acute myocardial infarction (18 with simple AMI and 8 with complex AMI), 10 with unstable angina pectoris and 20 healthy subjects. The serum level of human ventricular myosin light chains 1 and 2 (HVMLC1 and HVMLC2) in healthy subjects was of 6-10 ng/ml. Sensitivity of the assay was 10 ng/ml, and the working range was 10-100 ng/ml. In all AMI patients the HVMLC1 serum level exceeded 2-3 times the reference range within the first 24 hours after the onset of chest pain, the mean (+/- ISD) peak concentration was of 45.7 (+/- 13.6) ng/ml (simple AMI) and 64.22 (+/- 18.5 ng/ml) (severe AMI) 48 hours after infarction and it remained significantly higher than the normal value for another 7-10 days after the onset of infarction. The serum HVMLC2 concentration exceeded 10 ng/ml 48 hours after infarction, with a mean (+/- 1SD) peak concentration of 37.8 (+/- 10.4) ng/ml (simple AMI) and 53.8 (+/- 16.1) ng/ml (complex AMI) 90 hours after the onset of infarction and remained at high values for another 4-7 days. In two of ten patients with unstable angina pectoris LC2 increases above 10 ng/ml. The prolonged release of HVMLC1 and HVMLC2 in serum for 4-7 days after the onset of myocardial infarction may facilitate the retroactive detection of infarction, hence the extension of myocardium necrosis.
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PMID:Level of ventricular myosin light chains 1 and 2 determined by ELISA in serum of patients with acute myocardial infarction. 899 12

Despite the availability of diagnostic modalities such as transesophageal echocardiography, computed tomography or magnetic resonance imaging up to 30% of patients with acute aortic dissection remain undiagnosed before death. A novel immunoassay of serum smooth muscle myosin heavy chain was recently developed as a potential diagnostic tool for the detection of aortic dissection. The immunoassay was applied in two patients with an acute chest pain syndrome but no initial clinical suspicion of aortic disease. In both patients myocardial ischemia was ruled out by laboratory, electrocardiographic and echocardiographic examinations. In the first patient both dilation of the aorta and long-standing arterial hypertension were known; however, it was not before 48 h until dissection was suspected and a spiral-CT was performed demonstrating a localized ascending aortic dissection. At this time (48 h after onset of symptoms) the smooth muscle myosin heavy chain concentration in the serum was close to normal. In the other patient there was neither a suggestive history nor any clinical sign of aortic dissection. Widening of the abdominal aortic wall on an ultrasound examination was the key to the incidental diagnosis of a clinically unsuspected type B dissection. The serum test 12 h after onset of pain revealed elevated (diagnostic) serum levels of smooth muscle myosin heavy chains. Both cases exemplify important gaps in the diagnostic strategy for the detection of acute aortic dissection. A novel immunoassay for smooth muscle myosin heavy chains provides rapid and reliable diagnostic information especially in patients without clinically suspected aortic dissection and may avoid limitations in the diagnostic work-up of patients with acute aortic disease, if used early in the evaluation of patients with chest pain syndromes.
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PMID:[Increased serum concentration of myosin heavy chain in aortic dissection: discussion of 2 cases]. 932 78

In patients with chest pain at rest but no ST-segment elevation on the electrocardiogram, the diagnoses of unstable angina and non-Q-wave myocardial infarction (MI) are usually considered together because they cannot be differentiated clinically or angiographically. Since the extent of myocardial necrosis is an important determinant of the risk of death, it is important to identify serum markers with which to predict prognosis, in order to initiate appropriate medical treatment and/or invasive procedures in these patients. Cardiac troponin-I (cTnI), one of the subunits of the troponin regulatory complex, binds to actin and inhibits interactions between actin and myosin. The presence of elevated cTnI in serum is a significant prognostic indicator in patients with unstable angina and non-Q wave MI. Its independent prognostic potential persists even after adjustment for independent baseline variables known to be significantly associated with an increased risk of cardiac events. The use of cTnI in the triage of patients with unstable coronary disease may identify those at greater risk for adverse cardiac events.
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PMID:The role of cardiac troponin-I (cTnI) in risk stratification of patients with unstable coronary artery disease. 992 48

We report on a case of embryonal rhabdomyosarcoma in an 11-yr-old boy investigated for mild chest pain after trauma. Chest radiography showed a massive right pleural effusion. Cytological analysis of the pleural fluid demonstrated the presence of malignant small undifferentiated cells. The rhabdomyoblastic nature of the cells was confirmed by positive immunostains of HHf35 actin, desmin, and skeletal muscle myosin; histological examination of a core biopsy confirmed the diagnosis of rhabdomyosarcoma. Computed tomography and gallium scan revealed the presence of an extensive anterior and lower chest wall mass involving the mediastinum, as well as retroperitoneal lymphadenopathy. Massive pleural effusion is a frequent presentation in malignant disease, but is rare in rhabdomyosarcoma. The immunochemical stain studies performed on cytological smears in this case proved to be very useful for making the definitive and accurate diagnosis. Diagn. Cytopathol. 1999;21:125-128.
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PMID:Rhabdomyosarcoma in a child with massive pleural effusion: cytological diagnosis from pleural fluid. 1042 51


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