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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

We evaluated different diagnostic strategies for the early diagnosis of acute myocardial infarction, combining sensitivity and specificity of different markers evaluated singly and using combination testing in parallel and serial modes. Myoglobin, cardiac troponin I (TnI), creatine kinase (CK), and CK-MB mass were tested in blood samples from 26 patients with acute myocardial infarction collected at admission (T0; mean = 3.3 hours from the onset of chest pain) and 3 and 6 hours later. The comparison group was made up of 70 patients with renal failure, skeletal muscle diseases, stable angina, unstable angina, and chest pain of nonischemic origin. Single tests showed different sensitivities in relation to the different release kinetics; myoglobin was the most sensitive (69% at T0) although less specific (46%), and TnI showed the highest specificity (90%) and a sensitivity of 54%. Combination testing in a parallel mode using myoglobin and TnI or CK-MB had the same sensitivity and specificity as myoglobin tested singly. The best combination in a serial mode is myoglobin and TnI (at T0 sensitivity, 54%; specificity, 98%), as confirmed by the analysis of the positive predictive value, the negative predictive value, and the accuracy evaluated as a function of different disease prevalences.
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PMID:Strategies for the early diagnosis of acute myocardial infarction using biochemical markers. 1076 62

This study evaluated the role of serum cardiac troponin I as a biochemical marker for the diagnosis of acute coronary syndromes in the presence of noncardiac diseases. Diagnostic characteristics were examined in 102 consecutive patients who were found to have serum cardiac troponin I levels higher than the upper reference limit of 0.6 ng/mL. Of 102 patients with cardiac troponin I levels of >0.6 ng/mL, 35 did not have the final diagnoses of acute coronary syndromes (myocardial infarction or unstable angina) but had various other final diagnoses, including nonischemic dilated cardiomyopathy, muscular disorders, central nervous system disorders, HIV disease, chronic renal failure, sepsis, lung diseases, and endocrine disorders. The mean value of serum cardiac troponin I in the patients with diseases other than acute coronary syndromes was significantly lesser than in those with acute coronary syndromes (2.0+/-1.9 [SD] v. 24.7+/-28.2 ng/mL; P<.0001). There were significantly fewer histories of chest pain and prior myocardial infarction in patients with diseases other than acute coronary syndromes than in those with acute coronary syndromes (history of chest pain, 3 v. 48 patients [P<.001]; history of prior myocardial infarction, 0 v. 30 patients [P<.001]). In conclusion, elevated serum levels of cardiac troponin I, especially in the lower ranges, should be interpreted with caution, particularly in patients suffering from acute illnesses who lack other diagnostic features suggestive of acute coronary ischemic events.
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PMID:Elevation of serum cardiac troponin I in noncardiac and cardiac diseases other than acute coronary syndromes. 1033 75

The need for point of care testing (POCT) must be seen within the context of the need for biochemical diagnosis of patients suspected of acute coronary syndromes (ACS). The electrocardiogram is the initial test to select patients for thrombolysis and risk stratification. The majority of patients presenting with chest pain do not have AMI and diagnostic sensitivity of the ECG is only 55-75%. This means that biochemical diagnosis to confirm or exclude a diagnosis of acute myocardial infarction (AMI) is required for 90% of patients who present with suspected ACS. This can be achieved using myoglobin, creatine kinase and its MB isoenzyme and the cardiac troponins, cardiac troponin T and cardiac troponin I within 4-12 hours of admission, depending on the markers selected. Measurement of the cardiac troponins is superior to conventional tests as it allows risk stratification in patients with unstable angina in addition to a definitive diagnosis of AMI. Rapid diagnoses can have direct influence on length of stay and admission and discharge policies. The rationale for POCT is the improvement in analytical turnaround time (TAT). A number of systems for POCT have been developed ranging from conventional analysers used next to the patient to whole blood systems using immunochromatography. Laboratory and clinical evaluations of these systems have shown that they are accurate, equivalent to laboratory based diagnosis and can be related to outcome. In a prospective randomised controlled trial of POCT compared to laboratory testing we have shown improved TAT (20 minutes vs. 72 minutes) and significant reduction in hospital stay in patients randomised to POCT. Rapid diagnosis is effective and cost effective for patient management but only within the context of data driven decision-making protocols. The use of POCT will depend on the need for and the ability to achieve a rapid TAT for clinical decision making. POCT for cardiac markers has a definite place in management when very short TAT is required such as the ED. If the laboratory TAT exceeds 25% of the decision time, then POCT will be required. If therapeutic decisions are to be made, only POCT will be able to fulfil the TAT requirement.
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PMID:The need for a point of care testing: an evidence-based appraisal. 1038 4

A reflex algorithm was developed and evaluated for the use of serum cardiac markers for the diagnosis and rule out of acute myocardial infarction (AMI), and risk stratification of unstable angina patients for those who present to emergency departments (ED) with chest pain. The process begins with testing of total CK and myoglobin at admission. Based on these results, the algorithm determines the need for subsequent testing for the CK-MB isoenzyme and cardiac troponin I (cTnI). The algorithm also directs the need for further blood collection and cardiac marker testing at 4, 8, and 12 h after presentation. A total of eleven stopping points were identified. For some of these stopping points, the algorithm concluded that further blood collections and testing was unnecessary and redundant. The algorithm was retrospectively evaluated on 101 non-consecutive chest pain patients who presented to the EDs at three hospitals. For the AMI group (n=34), six of nine possible different stopping points were reached: 64.7% of cases were diagnosed with the first sample at admission, an additional 32.3% after 4 h, and 2.9% at 8 h. The 12-h sample was not necessary for any of the AMI patients. For the non-AMI group (n=67), most reached the stopping point of no cardiac injury or risk. There were five unstable angina patients who had minor myocardial damage on the basis of a marginally increased cTnI. Of these, one patient subsequently suffered AMI, and three others required angioplasty or bypass surgery. Compared to performing four tests on all patient samples, the reflex algorithm would have reduced the number of necessary tests from 442 to 130 (71% reduction) for AMI patients, and 871 to 469 (46% reduction) for non-AMI patients, if prospectively implemented.
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PMID:Reflex testing II: evaluation of an algorithm for use of cardiac markers in the assessment of emergency department patients with chest pain. 1052 62

We evaluated the AxSYM immunoassay for the quantification of cardiac troponin I (cTnI). Total assay imprecision, expressed as coefficient of variation, ranged between 5.6% and 8.3% for commercial control serum samples and between 4.2% and 13.9% for pooled patient samples. Linearity was verified up to 42 micrograms/L. Triglycerides (up to 1,000 mg/dL) did not interfere with the assay, but minor hemolysis and clinically relevant hyperbilirubinemia caused a negative bias. In 186 patient samples, AxSYM cTnI levels correlated significantly with data obtained with the Stratus II cTnI fluorometric enzyme immunoassay but were 3 to 4 times higher on AxSYM than on Stratus II. In 111 healthy blood donors, the reference range for cTnI levels on AxSYM was 0.0 to 0.4 microgram/L. After eccentric isokinetic exercise, healthy volunteers showed a rise in creatine kinase MB mass (AxSYM) but not in cTnI. On AxSYM and Stratus II, cTnI levels increased above the manufacturer's cutoff for acute myocardial infarction in all 17 patients followed up after onset of infarction-related chest pain but in only 1 of 91 control subjects. The AxSYM cTnI assay is a valid alternative for the detection of myocardial injury with diagnostic performance comparable to the established Stratus cTnI assay.
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PMID:Analytic and clinical evaluation of the Abbott AxSYM cardiac troponin I assay. 1058 94

We have evaluated the analytical and clinical performance of an automated immunoassay for serum cardiac troponin I (Bayer Immuno 1TM, Bayer Diagnostics, Tarrytown, NY). The between batch imprecision was found to be between 1.2 and 3.2% over the concentration range 2.5 - 34.0 microg/L. The analytical range obtained from duplicate analysis of patient samples and defined as a coefficient of variation of 10% or less was 0.3 - 200 microg/L. The detection limit was found to be less than 0.1 microg/L. A method comparison with the Dade Stratus method (Dade Behring, Wilmington, DE) yielded regression statistics with a slope of 0.705 and an intercept of -0.260. An analysis of samples from 40 patients with renal failure demonstrated six with detectable levels of troponin I (0.2 - 1.9 microg/L). Samples from patients with paraproteinaemia did not demonstrate detectable troponin I (from n = 30); however, two patients with elevated rheumatoid factor titers (from n = 20) demonstrated a detectable amount of troponin I (0.1 and 0.2 microg/L). In a study of 100 patients admitted with acute chest pain and a diagnosis of unstable angina, 6 were subsequently diagnosed as having suffered a myocardial infarction. On admission the sensitivity and specificity of the troponin I results were 26.7% and 94.7%, respectively, moving to 100% and 83% 12 hours after admission.
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PMID:Evaluation of a new troponin I method on the Bayer Immuno 1 immunoassay analyser. 1059 58

To help guide physicians in their evaluation of patients with acute coronary syndromes, we investigated whether elevated cardiac troponin I in patients presenting with unstable angina predicts ischemia on stress testing. Elevated cardiac troponin I in patients who present with chest pain and normal creatine kinase levels is associated with ischemia on stress testing, as well as with future cardiac events.
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PMID:Does elevated cardiac troponin I in patients with unstable angina predict ischemia on stress testing? 1060 19

Patients who have low-risk clinical features and negative cardiac troponin levels may be suitable for early discharge after a brief period of observation in the emergency department (ED). Little is known about the prevalence and severity of coronary artery disease in such patients, although this has implications for follow-up. Subjects included 570 patients who were at < or =7% risk of acute myocardial infarction (AMI), remained clinically stable (defined as the absence of new ischemic changes on their electrocardiograph, signs or symptoms of heart failure, the development of a cardiac arrhythmia or hypotension requiring either inotropes or volume repletion) and had cardiac troponin I (cTnI) levels <0.2 microgl(-1) during the initial 12 hours of hospitalization. Clinical features were documented and those undergoing stress tests and/or coronary angiograms had these graded by 2 independent observers. Overall, 190 (33.3%) of this population, who might be considered suitable for early discharge, had objective evidence of coronary artery disease. Patients with chest pain who are at low risk of AMI, remain clinically stable and have negative cTnI over the initial 12 hours of observation are a heterogeneous population, some of who have threatening coronary disease. This does not preclude early discharge from the ED but emphasizes the need for careful assessment and follow-up.
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PMID:Coronary artery disease in patients with chest pain who have low-risk clinical characteristics and negative cardiac troponin I. 1123 54

Myocardial infarction is a common cause of morbidity and mortality in patients with chest pain. The presence of human cardiac troponin I (cTnI) in serum is considered to be a highly specific biochemical marker of acute myocardial infarction. In this study we compare the performances of the Abbott AxSYM, Behring Opus Plus, DPC Immulite and Ortho-Clinical Diagnostics Vitros ECi for the measurement of cTnI. The first two methods use a fluorogenic enzyme-linked immunoassay. whereas the last two use chemiluminescent immunometric assays. All procedures are completely automated. Total percentage coefficients of variation using pooled sera ranged from 5.9 to 6.5% for the AxSYM, 14.4 to 25.6% for the Opus, 6.9 to 9.8% for the Immulite and 4.5 to 5.2% for the Vitros ECi method. The closest correlation between methods, obtained from 120 fresh serum samples, was observed between the Vitros ECi and the Immulite methods, with r=0.99, and the regression line was Immulite cTnI 1.505 (95% confidence interval 1.474-1.536) x Vitros cTnI--0.154 (-0.702 to 0.394). Receiver operating characteristic curves were nearly identical for all assays, and the areas under the curves were 0.972, 0.927, 0.967 and 0.969 for the AxSYM, Opus, Immulite and Vitros ECi methods, respectively. There was a significant difference between the AxSYM and Opus methods (P= 0.036).
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PMID:Comparison of Abbott AxSYM, Behring Opus Plus, DPC Immulite and Ortho-Clinical Diagnostics Vitros ECi for measurement of cardiac troponin I. 1126 55


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