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)

Different strategies using creatine kinase-MB(mass), myoglobin, and troponin T were compared in 738 patients admitted because of chest pain and an electrocardiogram not diagnostic of acute myocardial infarction. We conclude that a combination of creatine kinase-MB and troponin T during the first 6 hours enables early detection or exclusion of acute myocardial infarction in this population.
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PMID:Comparison between strategies using creatine kinase-MB(mass), myoglobin, and troponin T in the early detection or exclusion of acute myocardial infarction in patients with chest pain and a nondiagnostic electrocardiogram. 1111 15

During the last decade, there have been many studies comparing myoglobin and the troponins to creatine kinase MB. Myoglobin was introduced as an early marker, but most studies have not directly compared it to total creatine kinase in any detail. We retrospectively (9/98-5/99) examined 1772 paired samples from 1572 patients drawn in the emergency department to assess the optimum decision limits, sensitivity, specificity, positive predictive values (PPV), and negative predicitve value (NPV) for creatine kinase and myoglobin in predicting acute myocardial injury. Of the admitted patients, 114 had acute myocardial injury, 166 had angina and 89 had non-cardiac chest pain; 1203 patients were discharged. Initially low creatine kinase (<100 IU/l; minimum 19 IU/l) and myoglobin (<100 microg/l; minimum 9.5 microg/l) results were identified in 63.5% and 88.3% of patients, respectively, emphasizing the importance of serial sampling. Receiver operator characteristic analysis demonstrated optimum decision limits at 100 IU/l and 70 microg/l, respectively. These levels were associated with sensitivity/specificity/PPV/NPV of 66/66/13/96 for creatine kinase and 54/85/22/96 for myoglobin. We conclude that both tests are comparable for initial screening of patients with chest pain in the emergency department. Since creatine kinase is faster, cheaper, and more widely available, it is the test of choice for our institution.
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PMID:Screening for acute myocardial injury: creatine kinase is comparable to myoglobin. 1115 46

In a prospective trial, the diagnostic performance of the second version of the troponin T rapid assay (Trop T; cutoff 0.2 microg/L) was compared with the quantitative cardiac-specific troponin T assay (cTnT ELISA; cutoff 0.1 microg/L) and other established cardiac markers such as CK, CK-MB activity, CK-MB mass and myoglobin. Additionally, a 30-day follow-up was performed to determine the suitability of the Trop T assay and the reference markers for short-term risk stratification. Two-hundred-and-eighty-six consecutive patients with chest pain and suspected acute myocardial infarction (AMI) were enrolled in two CCU departments. Serial blood specimens were taken at admission and at 3, 6, 12, 24, 48, 72 and 96 h after admission. According to the biochemical criterion CK-MB mass, the patients were classified as having AMI in 154 patients (54%), unstable angina (UAP) in 72 patients (27%) and no evidence for acute cardiac ischemia in 55 patients (19%). Analytical method comparison of Trop T with cTnT ELISA (cutoff 0.1 microg/L) showed a good agreement, Trop T yielded only 4% false-negative and 3% false-positive results. The diagnostic performance of Trop T for the detection of AMI was only slightly inferior compared to cTnT ELISA. Beyond 12 h after admission, Trop T and cTnT ELISA maintained a sensitivity close to 100%, whereas the sensitivity of the other cardiac markers decreased sharply. The diagnostic sensitivity of Trop T for the detection of minor myocardial damage in UAP patients was the same as for cTnT ELISA. Death within 30 days' follow-up occurred only in AMI patients with a positive Trop T test result within the first 6 h after admission. The admission Trop T and cTnT ELISA were the only significant biochemical predictors of major cardiac events. In conclusion, these data show that Trop T has similar diagnostic sensitivity as cTnT ELISA and is a useful tool to confirm acute or subacute myocardial infarction. Trop T is an excellent marker in detecting minor myocardial damage in UAP patients and is suitable for short-term risk stratification.
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PMID:Time-dependent diagnostic performance of a rapid troponin T version 2 bedside test in patients with acute coronary syndromes. 1121 49

Blood was collected on admission and after 1-2 h in 130 consecutive patients admitted with typical chest pain in order to assess the capacity of myoglobin, fatty-acid-binding protein (FABP), CK-MB mass, and troponin I (TnI) in the early identification of acute myocardial infarction (AMI) without ST elevation. Using the maximum value within 6 h of onset of symptoms, AMI was detected with a 90-95% sensitivity and a 81-94% specificity by FABP at a cut-off level 8-12 midrog/l, or 81-86% and 89-93%, respectively, by myoglobin at a cut-off level 70-90 microg/l. CK-MB mass and TnI had low sensitivity, albeit very high specificity. As almost all AMI patients were identified within 6 h, serial measurements of FABP or myoglobin ruled out AMI with a very high degree of certainty. Due to the low prevalence of AMI (16%), the positive predictive values were modest (47-73%), yet increasing the probability of AMI by a factor 3-4. Myoglobin and FABP are very useful markers in the early triage of chest pain patients.
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PMID:Biochemical markers of ischaemia for the early identification of acute myocardial infarction without St segment elevation. 1132 47

No currently used cardiac-specific serum marker meets all the criteria for an "ideal" marker of AMI. No test is both highly sensitive and highly specific for acute infarction within 6 hours following the onset of chest pain, the timeframe of interest to most emergency physicians in making diagnostic and therapeutic decisions. Patients presenting to the ED with chest pain or other symptoms suggestive of acute cardiac ischemia therefore cannot make a diagnosis of AMI excluded on the basis of a single cardiac marker value obtained within a few hours after symptom onset. The total CK level is far too insensitive and nonspecific a test to be used to diagnose AMI. It retains its value, however, as a screening test, and serum of patients with abnormal total CK values should undergo a CK-MBmass assay. Elevation in CK-MB is a vital component of ultimate diagnosis of AMI, but levels of this marker are normal in one fourth to one half of patients with AMI at the time of ED presentation. The test is highly specific, however, and an abnormal value (particularly when it exceeds 5% of the total CK value) at any time in a patient with chest pain is highly suggestive of an AMI. There have been several improvements of CK-MB assay timing and subform quantification that appear highly useful for emergency physicians. Rapid serial CK-MB assessment greatly increases the diagnostic value of the assay in a timeframe suitable for ED purposes but unfortunately still misses about 10% of patients ultimately diagnosed with acute MI. Assays of CK-MB subforms have very high sensitivity, and, although unreliable within 4 hours of symptom onset, have excellent diagnostic value at 6 or more hours after chest pain begins. Automated test assays recently have become available and could prove applicable to ED settings. The cardiac troponins are highly useful as markers of acute coronary syndromes, rather than specifically of AMI, and abnormal values at any time following chest pain onset are highly predictive of an adverse cardiac event. The ED applicability of the troponins is severely limited, however, because values remain normal in most patients with acute cardiac events as long as 6 hours following symptom onset. Myoglobin appeared promising as a marker of early cardiac ischemia but appears to be only marginally more sensitive than CK-MB assays early after symptom onset and less sensitive than CK-MB at 8 hours or more after chest pain starts. Rapid serial myoglobin assessment, however, appears highly useful as an early marker of AMI. The marker has a very narrow diagnostic window. The clinician is left with several tests that are highly effective in correctly identifying patients with AMI (or at high risk for AMI), but none that can dependably exclude patients with acute coronary syndromes soon after chest pain onset. A prudent strategy when assessing ED patients with chest pain and nondiagnostic ECGs is to order CK-MB and troponin values on presentation in the hope of making an early diagnosis of AMI or unstable coronary syndrome. Although it is recognized that normal values obtained within 6 hours of symptom onset do not exclude an acute coronary syndrome, patients at low clinical risk and having normal cardiac marker tests could be provisionally admitted to low-acuity hospital settings or ED observation. After 6 to 8 hours of symptom duration has elapsed, the cardiac-specific markers are highly effective in diagnosing AMI, and such values obtained can be used more appropriately to make final disposition decisions. At no time should results of serum marker tests outweigh ECG findings or clinical assessment of the patient's risk and stability.
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PMID:Serum markers in the emergency department diagnosis of acute myocardial infarction. 1137 81

Available noninvasive techniques for identifying patients with failed epicardial reperfusion after fibrinolytic therapy are limited by poor accuracy. It is unknown whether combining multiple noninvasive predictors would improve diagnostic accuracy and facilitate identification of candidates for rescue percutaneous coronary intervention. In the Thrombolysis In Myocardial Infarction (TIMI) 14 trial, we evaluated the ability of ST-segment resolution (n = 606), chest pain resolution (n = 859), and the ratio of 60-minute/baseline serum myoglobin (n = 308) to identify patients with angiographic evidence of failed reperfusion 90 minutes after fibrinolysis. Three criteria were prospectively defined: <50% ST resolution at 90 minutes, presence of chest pain at the time of angiography, and myoglobin ratio <4. Patients who met any individual criterion were more likely to have less than TIMI 3 flow and an occluded infarct-related artery (TIMI 0/1 flow) than those who did not meet the criterion (p <0.005 for each). When the 3 criteria were used together (n = 169), patients who satisfied 0 (n = 29), 1 (n = 68), 2 (n = 51), or 3 (n = 21) of the criteria had a 17%, 24%, 35%, and 76% probability of failing to achieve TIMI 3 flow (p <0.0001 for trend), a 0%, 6%, 18%, and 57% probability of an occluded infarct-related artery (p <0.0001 for trend), and a 0%, 1.5%, 2.0%, and 9.5% rate of 30-day mortality (p = 0.05 for trend), respectively. Use of the criteria in combination increased positive predictive values without decreasing negative predictive values. In conclusion, ST-segment resolution, chest pain resolution, and early washout of serum myoglobin can be used in combination to aid in the early noninvasive identification of candidates for rescue percutaneous coronary intervention.
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PMID:Early noninvasive detection of failed epicardial reperfusion after fibrinolytic therapy. 1154 53

Patients admitted with suspicion of an acute coronary syndrome (ACS) still constitute a diagnostic, prognostic and therapeutic challenge for the treating physician. The final diagnosis ranges from a noncardiac diagnosis to a full-blown myocardial infarction (MI). Biochemical markers of myocardial damage are essential for diagnosis and, especially troponin T and troponin I, have been shown to be valuable for early risk stratification and for selection of treatment in ACS. Patients identified to be at low risk of future cardiac events might be discharged early, and unnecessary investigations and treatments avoided. On the contrary, a more intense treatment can be started in patients identified to be at high risk. Unstable angina patients with, compared to without, elevation of troponin, have a more activated coagulation system and more frequently complex lesions and visible thrombus in their coronary arteries. Accordingly, antithrombotic and antiplatelet therapies, i.e. l.m.w heparin and GP IIb/IIIa receptor antagonists, have been proved to have beneficial effects in troponin positive patients, but little or no beneficial effects in troponin negative patients. Also, the beneficial effects of an invasive compared to a noninvasive approach seem to be much more pronounced in troponin positive patients. In patients with ST-elevation MI, an elevated troponin T level at admission are associated with an increased mortality. However, the therapeutic implications of this finding remain speculative. Patients admitted with chest pain and left bundle branch block (LBBB) and who develop an MI have a poor prognosis. Current guidelines in acute myocardial infarction state that these patients should receive thrombolysis. Despite that, only a minority of these patients do receive thrombolysis, most probably because of the great diagnostic uncertainty. Rapid testing with a cardiac marker, e.g. myoglobin, would most probably increase the proportion of patients with chest pain and LBBB who receive appropriate reperfusion treatment.
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PMID:Markers of myocardial damage in acute coronary syndromes--therapeutic implications. 1155 49

Chest pain is one of the most important reasons of Emergency Department arrivals (5% of total). As it is not possible to rule-in all patients claiming chest pain, it has been proposed to create new departments to monitor these patients during some hours, in order to exclude or confirm an acute coronary syndrome. These departments are named Chest Pain Units (CPUs). The Chest Pain Unit has been created since June 1998 in Alessandria Hospital "SS. Antonio e Biagio e C. Arrigo". Chest Pain Unit patients presenting in Emergency Department with an unclear defined chest pain are submitted to a continuous ECG monitoring of S-T trend for 24 h. Moreover, cardiac markers such as myoglobin, mass CK-MB and Troponin-I are tested at arrival and Troponin-I is tested again serially 3, 6, 9, 18 h after the first sampling. It is really important to be able to measure these markers of myocardial damage with robust and quick methods. A point-of-care analyzer is available in our chest pain unit and enables our department to obtain results in a very short time at low cost and with quality similar to that of clinical chemistry laboratories' instruments. This easy-to-use analyzer can be run by nurses without interfering in their normal activities. The presentation of our experience will be completed by describing all patients admitted in our Chest Pain Units from January to June 1998.
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PMID:Chest pain unit and decentralized testing of cardiac markers. 1155 56

Rapid, efficient, and accurate evaluation of chest pain patients in the emergency department optimizes patient care from public health, economic, and liability perspectives. To evaluate the performance of an accelerated critical pathway for patients with suspected coronary ischemia that utilizes clinical history, electrocardiographic findings, and triple cardiac marker testing (cardiac troponin I [cTnI], myoglobin, and creatine kinase-MB [CK-MB]), we performed an observational study of a chest pain critical pathway in the setting of a large Emergency Department at the Veterans Affairs Medical Center in 1,285 consecutive patients with signs and symptoms of cardiac ischemia. The accelerated critical pathway for chest pain evaluation was analyzed for: (1) accuracy in triaging of patients within 90 minutes of presentation, (2) sensitivity, specificity, positive predictive value, and negative predictive value of cTnI, myoglobin, and CK-MB in diagnosing acute myocardial infarction (MI) within 90 minutes, and (3) impact on Coronary Care Unit (CCU) admissions. All MIs were diagnosed within 90 minutes of presentation (sensitivity 100%, specificity 94%, positive predictive value 47%, negative predictive value 100%). CCU admissions decreased by 40%. Ninety percent of patients with negative cardiac markers and a negative electrocardiogram at 90 minutes were discharged home with 1 patient returning with an MI (0.2%) within the next 30 days. Thus, a simple, inexpensive, yet aggressive critical pathway that utilizes high-risk features from clinical history, electrocardiographic changes, and rapid point-of-care testing of 3 cardiac markers allows for accurate triaging of chest pain patients within 90 minutes of presenting to the emergency department.
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PMID:Ninety-minute accelerated critical pathway for chest pain evaluation. 1156 82

Diagnosis and risk stratification of patients with acute coronary syndromes remain extremely important in order to avoid unnecessary hospitalizations on the one hand, and to improve prognosis of these patients on the other. For diagnosis of acute coronary syndromes, an ECG should be obtained at rest, troponin T and I should be measured on admission and again 6 to 12 h later, and myoglobin or CK-MB should be determined in patients with recent syndromes and those with recurring ischemia. Risk should be assessed upon admission and repeatedly during the hospital stay. Early risk indicators are: age, male sex, previous manifestation of coronary artery disease, history of left ventricular dysfunction or congestive heart failure and ongoing chest pain, as well as ST depression, transient ST segment elevation, and elevated levels of troponin T or I. Longer term risk assessment in unstable coronary artery disease includes rest and stress echocardiography, exercise ECG, thallium scintigraphy, as well as coronary angiography and left ventriculography. Markers of high long-term risk are old age, prior history of myocardial infarction, diabetes, elevated levels of C-reactive protein, and the extent of coronary artery disease and left ventricular dysfunction.
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PMID:Diagnosis and risk stratification in patients with acute coronary syndromes according to ESC guidelines. 1156 70


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