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)

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

Early sensitivities of creatine kinase (CK), CKMB (activity and mass), CKMM and CKMB isoform ratios, myoglobin, cardiac troponin I (cTnI), and cardiac troponin T (cTnT) were compared to find the most sensitive serum marker for acute myocardial infarction (AMI) during the first hours after onset of chest pain. In a prospective study we investigated 37 consecutive patients with AMI who were admitted to the coronary care unit within 4 h after onset of chest pain. Blood samples were drawn every hour for the first 10 h after admission. CKMB mass concentrations, CKMM and CKMB isoform ratios, myoglobin, cTnI, and cTnT increased significantly (P < or = 0.0067) earlier than CK and CKMB activity and were also significantly (P < or = 0.046) and markedly more sensitive on admission. Differences in early sensitivities of myoglobin, CKMB mass, CK isoform ratios, cTnI, and cTnT were small and not significant. Therefore, turnaround time and practicality for emergency determination of methods, specificities of markers, the required specificity in the individual patient, and costs mainly determine the choice among myoglobin, CKMB mass, CK isoforms, cTnI, and cTnT.
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PMID:Equivalent early sensitivities of myoglobin, creatine kinase MB mass, creatine kinase isoform ratios, and cardiac troponins I and T for acute myocardial infarction. 765 36

It is important to establish as soon as possible whether patients who present with chest pain are having an acute myocardial infarction (AMI). Ideally, sensitive and specific serum myocardial markers could provide the basis for early detection as well as determine the status of reperfusion following thrombolytic therapy. The present study examined the utility of cardiac troponin I (cTnI), CK-MB, and myoglobin for the sensitive and specific detection of AMI in 98 consecutive patients presenting to the emergency department (ED) with chest pain. In addition, cardiac troponin T (cTnT), CK-MB, and myoglobin samples were measured over a 90 min time period following thrombolytic therapy in nine separate AMI patients to assess reperfusion. In the ED study, CK-MB, myoglobin, and cTnI were equally sensitive (100%) for the detection of AMI in patients who presented 7.4-14 h after onset of chest pain. However, cTnI was the most specific serum marker (specificity 91.9% compared to CK-MB 85.6%, myoglobin 61.4%). Five of the six non-related AMI patients who had an elevated cTnI had clinically documented myocardial involvement. In the reperfusion study, cTnT, CK-MB and myoglobin, relative increases were greater in reperfused compared to non-reperfused patients. Within the reperfused group, the relative increase of cTnT was greater than CK-MB and myoglobin at 90 min following thrombolytic therapy. These findings show the clinical utility of cardiac-specific troponins as markers for the early detection of AMI and monitoring of reperfusion following thrombolytic therapy.
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PMID:Cardiac troponin, CK-MB and myoglobin for the early detection of acute myocardial infarction and monitoring of reperfusion following thrombolytic therapy. 766 79

Patients with cocaine-related chest pain with electrocardiographic (ECG) abnormalities are often admitted to rule out acute myocardial infarction (AMI). Cardiac troponin I and T should be superior to measurement of creatine kinase (CK)-MB for detecting cardiac injury in patients with coexisting skeletal muscle injury. We prospectively evaluated 19 consecutive patients with acute chest pain related to cocaine use who were hospitalized to rule out AMI. The admission ECG was abnormal in 16 of 19 patients. Total CK and CK-MB were elevated during the hospital course in 14 and 3 patients, respectively. Cardiac troponin I and cardiac troponin T levels were within normal limits in all patients demonstrating that recent myocardial injury did not occur. Clinically, no patient had an AMI. Cocaine-induced thoracic skeletal muscle injury or transient cocaine-induced coronary vasospasm should be considered as alternative sources of chest pain in these patients.
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PMID:Cardiac troponin I and T concentrations in patients with cocaine-associated chest pain. 879 78

Serial plasma concentrations of myoglobin, creatine kinase MB (CK-MB) isoenzyme, and cardiac troponin I (cTnI) were measured in 25 patients with a confirmed diagnosis of acute myocardial infarction (AMI), and 74 patients who were suspected of AMI but were subsequently ruled out for this diagnosis. The cutoff concentration for the cTnI assay was optimally determined to be 2.5 ng/mL. Of the three markers, myoglobin had the highest clinical sensitivity (50 percent) when blood was collected between 0 to 6 h after the onset of chest pain. Assays for all serum markers used had high clinical sensitivity (> 93 percent) 6 to 24 h after onset. The CK-MB remained highly sensitive for 48 h, while cTnI was sensitive for up to 72 h. Between 72 and 150 h, cTnI had a clinical sensitivity of 70 percent as compared to 21 percent and 18 percent for myoglobin and CK-MB, respectively. The clinical specificity of cTnI for non-AMI patients was equivalent to CK-MB and significantly higher than for myoglobin. The clinical efficiency of cTnI for all samples was better than either CK-MB or myoglobin, owing mainly to the wider diagnostic window. The specificity of cTnI for 59 patients with chronic renal failure, skeletal muscle trauma and disease was better than all of these markers including cardiac troponin T (cTnT). Results of this study show that cTnI is an effective marker for the retrospective diagnosis of AMI, and consideration should be given to its use in place of CK-MB.
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PMID:Comparison of myoglobin, creatine kinase-MB, and cardiac troponin I for diagnosis of acute myocardial infarction. 880 Apr 29

Current changes of the healthcare environment have promoted the creation of chest pain centers in the emergency departments for rapid triage of patients admitted for cardiac evaluation. Because of the inefficiency of electrocardiogram for the diagnosis of acute myocardial infarction, blood cardiac markers play an important role in the decision making process. Current commercial cardiac tests available include creatine kinase, its MB isoenzyme, MB isoforms, lactate dehydrogenase and its isoenzyme-1, myoglobin, cardiac troponin T and troponin I. The diagnostic efficacy of each of these assays is reviewed. Their appropriate use depends on when the specimens are collected for testing after the onset of myocardial infarction. Since not all patients seek medical attention at the time symptoms appear, the applicability of these markers differs in each case. Based on the time after the onset of chest pain, a utilization strategy of the cardiac markers is proposed. With this protocol, the triage of patients can be optimized resulting in the efficient treatment of patients and large savings in cost.
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PMID:Strategic utilization of cardiac markers for the diagnosis of acute myocardial infarction. 880 Apr 30

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

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

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

Differential diagnosis of patients who present with chest pain remains problematical. It has been shown that 11.8-7% of patients with acute myocardial infarction (AMI) are sent home from the emergency department (ED). Audit of our own ED has shown the incidence of missed prognostically significant myocardial damage to be 6.7%. Diagnostic criteria for AMI have classically been based on the triad of history, ECG and measurement of cardiac enzymes. The choice of 'cardiac enzymes' has been dictated by the evolution of laboratory techniques, commencing with measurement of aspartate transaminase and progressing to measurement of creatine kinase (CK) and its MB isoenzyme (CK-MB). Measurement of CK-MB has been shown by both clinical studies and rigorous statistical analysis to represent the best test for the diagnosis of AMI. The advent of real time immunoassay together with advances in therapeutic options for management of acute coronary syndromes (ACS) has resulted in a paradigm shift in the approach to laboratory testing. Immunoassay for CK-MB (CK-MB mass measurement) is diagnostically superior to CK-MB activity measurement and is the test of choice for 'classical' AMI. Development of immunoassays for the cardiac troponins, i.e. cardiac troponin T (cTnT) and cardiac troponin I (cTnI), has enhanced diagnostic specificity. These measurements are completely specific for cardiac damage, allow quantitation of the extent of infarction and are diagnostically superior to CK-MB measurement. Applications of this specificity have included the differential diagnosis of CK elevation in arduous physical training, detection of myocardial damage after DC cardioversion and prediction of ejection fraction. Of more interest is the utility of these markers in management of patients presenting without clear electrocardiographic changes. Diagnosis and management of patients presenting with ST segment elevation has been clarified by large clinical trials of thrombolytic agents. In such patients, thrombolysis is the treatment of choice. Patients presenting with ST segment elevation represents the minority of patients with probable ACS 9.6% of all patients presenting to our hospital. The majority require risk stratification into high- and low-risk groups. It is here that cardiac troponins have a major role. The measurement of cTnT has been shown in a large number of studies to enable risk stratification of patients with unstable angina. The combination of cTnT, admission ECG and stress ECG can be used for a comprehensive risk stratification of patients with unstable angina. The combination of cTnT, admission ECG and stress ECG can be used for a comprehensive risk stratification which can be completed by 24 h from admission, as well as allowing a safe discharge policy from the ED. Measurements of cardiac troponins can also be used to predict prognosis in patients with other diagnostic categories. Patients with cardiac failure can be risk stratified according to cTnT status. cTnT status on admission allows subdivision into high- and low-risk groups in patients presenting with ST segment elevation. Certainly, cTnT measurement can be incorporated into a clinical decision-making strategy to assign patients to investigation and management pathways. There is evidence that cTnT may be useful to guide therapeutic options. The major issue is one of cost. In the U.K. model of managed care with undemanding diagnostic standards, the role of cTnT will be to enhance clinical decision-making strategies, to provide accurate diagnosis and to reduce lengths of stay. This can be shown to have potential for major improvements in cost efficiency. Improvements in diagnostic accuracy can reduce inappropriate long-term drug therapy. In systems with a more aggressive laboratory investigation strategy, rationalization of test numbers will provide an immediate cost reduction while improving quality. Finally, use of point-of-care testing (POCT) means that biochemical testing can be pe
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PMID:Troponin T or troponin I or CK-MB (or none?). 985 34


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