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)

Cardiac troponin I (TnI) was tested in 316 consecutive patients with chest pain who were admitted to the emergency department, of whom 62 were discharged with a diagnosis of acute myocardial infarction (AMI). The TnI level was abnormal in 49 patients with AMI compared with 27 for creatine kinase (CK)-MB in the first specimen obtained at admission. All 62 patients with AMI were correctly diagnosed at admission with a combination of TnI and myoglobin testing. The overall peak performance of TnI testing in samples received within 24 hours of admission indicated high sensitivity (97%) and specificity (98%) for the diagnosis of AMI. The TnI was positive in elderly patients with myocardial injury and low CK and normal CK-MB values. These data suggest that testing for TnI could replace CK-MB and, in combination with myoglobin, could facilitate the rapid and effective triage of patients with chest pain in the emergency department.
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PMID:Cardiac troponin I for the diagnosis of acute myocardial infarction in the emergency department. 935 94

Intracoronary thrombosis plays a key role in the pathogenesis of acute myocardial infarction (AMI), and the formation of an occlusive thrombus usually precedes the development of myocardial damage. Therefore we evaluated and compared the early sensitivities of thrombin-antithrombin III complex (TAT), D-dimer, myoglobin, creatine kinase (CK) MB mass concentration, and cardiac troponin T (cTnT) on admission to a coronary care unit (CCU) before heparin or thrombolytic therapy was started. We investigated 31 consecutive patients admitted to CCU for evolving AMI within 6 hours from the onset of infarct-related symptoms; the median delay from chest pain onset to CCU admission was 135 minutes. Of all biochemical markers tested TAT had the highest early sensitivity on admission to the CCU, and TAT was significantly more sensitive than cTnT, CKMB mass, myoglobin, and D-dimer. However, TAT increases give no information about the location of clot formation in the body, and the diagnosis of AMI must be subsequently verified by an increase in more cardiac specific proteins, such as troponins or CKMB.
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PMID:Markers of activated coagulation for early diagnosis of acute myocardial infarction. 946 56

We evaluated whether recent cocaine use alters the specificity of CK-MB, myoglobin, and cardiac troponin I for acute myocardial infarction (AMI) in patients who are seen in the emergency department for chest pain. Patients <60 years old with potential myocardial ischemia underwent a standardized history and physical examination and routine CK-MB assays every 8 to 12 hours and had study serum obtained at presentation for CK-MB, myoglobin, and cardiac troponin I immunoassays, as well as benzoylecgonine, cocaine's main metabolite. We enrolled 97 patients, 19 (20%) of whom had recent used cocaine. Patients with and without cocaine use were similar with regards to sex, race, renal and muscular disease, diabetes, family history, and hypertension and rate of AMI (12% vs 11%, p = 1.0). In patients without MI, the mean myoglobin level was higher in cocaine users than noncocaine users (179 vs 74 ng/ml; Mann-Whitney p = 0.003), but the mean values were similar for CK-MB (2.2 vs 2.1 ng/ml; Mann-Whitney p = 0.58) and for cardiac troponin-I (0.02 vs 0.02 ng/ml; Mann-Whitney p = 0.87). The specificities of the markers in patients with and without cocaine use were as follows: cardiac troponin I, 94% vs 94%, (p = 1.0); CK-MB, 75% vs 88% (p = 0.24); and myoglobin, 50% vs 82%, (p = 0.02), respectively. Our data demonstrate that the specificity of myoglobin was altered by recent cocaine use. The specificity of CK-MB was affected less and the specificity of cardiac troponin I was not affected by recent cocaine use.
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PMID:Effect of recent cocaine use on the specificity of cardiac markers for diagnosis of acute myocardial infarction. 948 72

With the aim to compare the diagnostic efficacy as regards acute myocardial infarction of two rapid dry-strip tests, one with both creatine kinase MB (CK-MB) and myoglobin (C + M) and the other with troponin T, and to test the reliability of bedside diagnosis by the coronary care unit (CCU) nurse, 151 patients with acute chest pain admitted to the CCU were investigated. There was no difference in diagnostic performance between rapid tests and quantitative determinations. With <6-hour duration of symptoms, the sensitivity was better for C + M than for troponin T (72% vs 33%, p < 0.05). With symptoms lasting >12 hours on arrival, troponin T performed better, with 100% sensitivity and a negative predictive value of 100% in the 6-hour retest. For exclusion of damage, the two tests have similar and reliable diagnostic capacities 12 hours after the onset of symptoms. The bedside diagnosis or exclusion of acute myocardial infarction was carried out rapidly (within 20 minutes) and reliably by the CCU nurses.
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PMID:Excellent reliability of nurse-based bedside diagnosis of acute myocardial infarction by rapid dry-strip creatine kinase MB, myoglobin, and troponin T. 953 85

Free radical species have been implicated as important agents involved in myocardial ischemic and reperfusion injuries. Superoxide is capable of mobilizing iron from ferritin and the released iron can cause hydroxyl formation from H2O2. The aim of this study was to evaluate the time-dependent increase in lipid peroxidation assessed by plasma thiobarbituric acid reactive substances (TBARS) and the relationship between lipid-peroxidation and the iron status. Peripheral venous blood samples were obtained from 17 men with acute myocardial infarction (AMI) before thrombolytic treatment (T0) and 1, 2, 3, 4, 8, 12, 16, 20, 24 and 48 hours after commencing fibrinolytic treatment. The concentration of TBARS, the parameters of iron metabolism, serum myoglobin, creatine kinase, and creatine kinase-MB were measured. Early reperfusion was judged by regression of sinus tachycardia (ST) elevation and reduction of chest pain. Recanalization of coronary artery was evaluated by a late coronary angiography 24-96 hours after thrombolysis. After thrombolytic therapy, the TBARS level was raised from 2.98 +/- 0.80 (T0) to 4.57 +/- 1.24 (peak), and decreased to 2.96 +/- 0.40 nmol/mL plasma at T48 (T0 vs peak: P < 0.001, peak vs T48: P < 0.001, T0 vs T48: NS). The mean time of the peak was observed at 9.7 +/- 7.5 hours. The iron increased significantly from 0.67 +/- 0.34 (T0) to 1.15 +/- 0.52 mg/L (peak), and returned to the pre-reperfusion to levels: 0.53 +/- 0.28 UI/L at T48 (TO vs peak: P < 0.001, peak vs T48: P < 0.001, T0 vs T48: NS). The mean time of the peak was observed at 9.4 +/- 7.3 hours. In return, no correlation was found between the increase of plasma creatine-kinase activity, myoglobin and iron or between the biochemical markers and time of fibrinolytic therapy. The results confirmed the importance of the temporal relationship between lipid peroxidation and iron status after thrombolytic therapy. Our results are in agreement with the concept that antioxidant agents used in association with thrombolytic therapy might be useful.
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PMID:Plasma iron status and lipid peroxidation following thrombolytic therapy for acute myocardial infarction. 956 80

The objective of this study was to determine whether two novel rapid bedside assays for whole-blood detection of cardiac troponin T and creatine kinase (CK)-MB mass/myoglobin could rule out or rule in acute myocardial infarction in patients with acute chest pain. Ninety-two patients with chest pain <12 h prior to admission were investigated. No difference in the cumulative sensitivity of the TropT test and the CARDIAC STATus test (CK-MB mass and myoglobin in combination) was found 6 h after admission (94 vs. 97%). The cumulative positive predictive value of the TropT test and CARDIAC STATus test 6 h after admission was 97 and 76%, respectively. The negative predictive value was 97% for the TropT test and 98% for the CARDIAC STATus test at this time point. Our data show that the rapid assays provide diagnostic as well as prognostic information shortly after admission.
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PMID:Clinical application of two novel rapid bedside tests for the detection of cardiac troponin T and creatine kinase-MB mass/myoglobin in whole blood in acute myocardial infarction. 957 Apr 38

New immunochemical assay methods for the cardiac markers creatine kinase (CK) MB mass, myoglobin, troponin T (TnT), troponin I (TnI), fatty acid binding protein (FABP) necessitate re-evaluation of their usefulness in the early diagnosis of myocardial damage. Cardiac markers play an important part in the exclusion of myocardial damage in patients with chest pain and an inconclusive ECG at admission. A serial CK-MB mass determination is particularly suitable for this exclusion of myocardial damage. The sensitivity of TnT shortly after an infarction is comparable with that of CK-MB mass; a single determination on admission is insufficient. The marker myoglobin is of limited value owing to the brief duration of myoglobin rise and insufficient heart specificity. An increased TnT or TnI value in patients with unstable angina pectoris is a prognostically negative sign. It is still not clear how this prognosis can be improved. A negative troponin finding appears not to exclude early complications. The department of Emergency Cardiac Care of the Academic Medical Centre, Amsterdam, the Netherlands, currently prefers the serial measurement of the CK-MB mass, in the future possibly to be supplemented by a troponin determination.
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PMID:[Early exclusion of ischemic myocardial damage made possible by new biochemical cardiac markers]. 985 93

We investigated the early diagnostic utility, including incremental value, of the serum cardiac markers creatine kinase (CK), CK-MB (mass and activity measurements), cardiac troponin T, and myoglobin in the diagnosis of acute myocardial infarction (AMI) in patients presenting to a major teaching hospital with chest pain and non-diagnostic electrocardiographs (ECG). The reference diagnosis of acute myocardial infarction was made by a single, independent cardiologist using World Health Organization criteria. CK and CK-MB mass were the only significant predictors of AMI at presentation to the Emergency Department. Logistic regression analysis revealed that CK did not significantly predict (P = 0.23) myocardial infarction once CK-MB mass was in the model. Using test results on follow up, in addition to presentation CK-MB mass, change in CK-MB mass was the only other significant independent predictor of AMI. Likelihood ratios for various levels of the significant markers in the logistic regression are given. In conclusion, CK-MB mass measurement was the only useful serum cardiac marker for the diagnosis of AMI in patients presenting with chest pain with non-diagnostic ECGs.
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PMID:Biochemical markers of acute myocardial infarction: strategies for improving their clinical usefulness. 963 5

We isolated and purified myoglobin (MYO) from human fresh skeletal muscle and prepared monoclonal and polyclonal antibody from it. A sandwich dot-immunogold filtration assay (DIGFA) for the detection of MYO was developed by using affinity purified sheep anti-MYO antibody as the first antibody for coating nitrocellulose membranes (NCMs; the support) and colloidal gold labelled monoclonal antibody (H3) as the second antibody (an indicator). The test can be completed in 3 min without incubation or any equipment. A reddish dot, indicating positivity, is obvious to the naked eye. No interferences from bilirubin, hemoglobin, rheumatoid factors and lipid were found. In order to use undiluted serum, the detection limit was set at 100 microg of MYO/l. Concentrations up to 30,000 microg/l can be measured without getting a "hook" effect. Serum MYO levels in 53 patients with acute myocardial infarction (AMI), 100 healthy individuals, seven patients with chest pain but without myocardial ischemia and in 39 patients with renal insufficiency were measured simultaneously by DIGFA and enzyme-linked immunosorbent assay (ELISA). All serum samples from patients had MYO concentrations above 100 microg/l by ELISA and were positive by DIGFA. Serum creatinine values were related to MYO test results. Healthy individuals had MYO levels below 85 microg/l by ELISA and were negative by DIGFA.
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PMID:Qualitative bedside assay of increased human serum myoglobin by sandwich dot-immunogold filtration for the diagnosis of acute myocardial infarction. 965 43

Acute chest pain patients without ECG-signs of acute myocardial infarction (AMI) on admission need to be earlier and better diagnosed to reduce use of expensive intensive care beds and to treat more patients with acute recirculation therapy. We investigated whether total CK-activity, CK-MB mass, CK-MB2, myoglobin, cardiac troponin I (cTnI) and T (cTnT) measured in venous blood on admission and after 1 and 2 h could be used to identify or exclude acute myocardial damage (AMD) in 22 acute chest pain patients without ECG-signs of AMI admitted to hospital within 6 h after onset of pain. Increases in CK-MB mass, CK-MB2, myoglobin and cTnI identified AMD in three patients classified retrospectively as AMI. Likewise, CK-MB mass, CK-MB2, cTnI and cTnT increased with time in three of seven patients classified as having unstable angina pectoris. CK-MB2 and cTnI increased with time in two patients with tachycardia belonging to the other heart disease group. The remaining seven patients of the non-heart disease group showed no change in any of the cardiac markers. Thus, early serial measurements of selected cardiac markers appear useful in identifying or excluding AMD 3 h after admission in these acute chest pain patients.
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PMID:Serial measurements of cardiac markers to rule in or out acute myocardial damage less than 3 h after admission in acute chest pain patients without ECG-signs of acute myocardial infarction. 974 21


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