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)

New clinical requirements for triaging chest pain patients challenge the abilities of the current cardiac markers. Serial measurements of myoglobin, creatine kinase (CK) isoenzyme MB (CKMB) mass, or CK isoforms in emergency rooms help to rapidly rule out acute myocardial infarction (AMI). However, within the first 3 to 4 h from chest pain onset, their sensitivities are too low to contribute significantly to AMI diagnosis during this period. CKMB and lactate dehydrogenase (LDH) isoenzyme 1 are not heart-specific, which hampers reliable diagnosis in patients with concomitant skeletal muscle damage. By contrast, the regulatory proteins troponin I and troponin T are expressed in three different isoforms: one for slow-twitch skeletal muscle fibers, one for fast-twitch skeletal muscle fibers, and one for cardiac muscle (cTnI, cTnT); cardiac-specific cTnI and cTnT assays are already available for routine use. cTnT and cTnI are the most promising markers for risk stratification in patients with unstable angina pectoris. Recent reports on increased cTnT in patients with renal failure or myopathy without evidence of myocardial injury and undetectable cTnI suggest that cTnT could be reexpressed similar to CKMB and LDH-1 in chronically damaged human skeletal muscle. Therefore, cTnI is probably the most heart-specific marker. Among the recently proposed new markers for early AMI diagnosis: glycogen phosphorylase isoenzyme BB (GPBB), fatty acid binding protein, phosphoglyceric acid mutase isoenzyme MB, enolase isoenzyme alpha beta, S100a0, and annexin V, GPBB is the most promising because it increases as early as 1 to 4 h from chest pain onset and its early release appears to be essentially dependent on ischemic myocardial injury.
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PMID:Progress in myocardial damage detection: new biochemical markers for clinicians. 905 56

The prognosis and extent of injury to the myocardium have previously been assessed by increased serum creatine kinase (CK) MB levels. We report findings from 39 consecutive, acute myocardial infarction (AMI) patients presenting 4.5 h (range, 0.7-12.1 h) after the onset of chest pain. We compared CK MB mass (upper reference limit, 5.0 ng/ml) and cardiac troponin I (cTnI; upper reference limit, 0.8 ng/ml) (Stratus II, Dade International) in serial serum specimens obtained over 36 h after chest pain from AMI patients; within 6 h after onset of chest pain. While the appearance of the kinetics of CK MB and cTnI were similar during the initial 24 h following the onset of chest pain, cTnI was increased significantly (p < 0.05) over CK MB after 9 to 12 h. Half-life determinations (mean+/-S.D.) in 22 of the 39 AMI patients demonstrated a significantly (p < 0.01) shorter half-life in non-Q-wave infarcts [t1/2 6.8 h (+/-5.6)] vs. Q-wave infarcts [t1/2 20.4 h (+/-10.7)]. Further serial time versus marker (mean+/-S.D.) results were significantly correlated (p < 0.001, r = 0.66). Sixteen of twenty patients assessed by echocardiography had an abnormal left ventricular ejection fraction (LVEF); mean 37.6 (S.D. 15.2)%, ranging from 15.4 to 67.6%. LVEF was significantly and inversely correlated to peak CK MB (r = .50, p = 0.03), as well as to peak cTnI (r = 0.46, p = 0.04). Based on these findings, cTnI shows excellent promise as a useful marker of infarct size, for the assessment of left ventricular function, and may potentially replace CK MB as the cardiac-specific marker for AMI detection.
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PMID:Assessment of left ventricular function using serum cardiac troponin I measurements following myocardial infarction. 958 57

We evaluated the AxSYM troponin I (cTnI) immunoassay for assisting in the detection of acute myocardial infarction (AMI). At four sites, the total imprecision (CV) over 20 days was 6.3-10.2%. The minimum detectable concentration was 0.14 +/- 0.05 microgram/L. Comparison of cTnI measurements between the AxSYM and Stratus (n = 406) over the dynamic range of the AxSYM assay demonstrated good correlation, r = 0.881, with a proportional bias: AxSYM cTnI = 3.50(Stratus cTnI) - 1. 10. The confidence intervals (95%) for the slope and intercept were 3.39-3.64 and -1.32 to -0.95, respectively. The expected cTnI concentration in healthy individuals was </=0.5 microgram/L, whereas the ROC curve-determined cutoff for AMI was 2.0 microgram/L. This gave a diagnostic sensitivity of 91.8% and specificity of 92.4% when tested in serial samples collected within 24 h of admission in 633 patients presenting with chest pain, of which 122 had an AMI. The concordances of the AxSYM cTnI with the Stratus cTnI, OPUS cTnI, and Access cTnI were 95.3%, 95.1%, and 94.3%, respectively, from patients with suspected AMI. The AxSYM cTnI demonstrated excellent clinical specificity, >/=96%, in skeletal muscle injury, chronic renal disease, and same-day noncardiac surgery patients.
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PMID:Multicenter clinical and analytical evaluation of the AxSYM troponin-I immunoassay to assist in the diagnosis of myocardial infarction. 1070 39

In recent years, cardiac troponins have attracted great interest as a marker for myocardial injury. However, there are limited data on strategies for use of creatine kinase (CK)-MB and troponin I (cTnI) in clinical practice. We sought to develop a testing strategy using prospectively collected clinical data including serial CK-MB and cTnI levels from 1,051 patients aged > or = 30 years admitted to a teaching hospital for acute chest pain. Diagnostic performance was evaluated for peak values of CK-MB and cTnI obtained during the first 24 hours for the combined end point of acute myocardial infarction and/or major cardiac events within 72 hours. The overall diagnostic accuracy was similar for both cardiac markers alone, and for the combination of cTnI and CK-MB (receiver-operating characteristic curve 0.84, 0.86, and 0.87, respectively). In the multivariate analysis, models including cardiac markers showed that both CK-MB and cTnI added information to clinical data to predict the combined end point, but cTnI added significantly less. Using recursive partitioning analysis, we developed a strategy that would restrict routine cTnI use to patients with normal CK-MB results and findings on the electrocardiogram consistent with ischemia. This strategy would divide patients with suspected myocardial ischemia into 4 groups with risks for the combined end point of 4%, 13%, 26%, and 85%. Thus, cTnI adds information to CK-MB mass and clinical data for predicting major cardiac events, but this contribution is mainly in patients with evidence of myocardial ischemia on their electrocardiograms.
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PMID:A proposed strategy for utilization of creatine kinase-MB and troponin I in the evaluation of acute chest pain. 1021 79

Patients with acute chest pain suggestive of myocardial ischaemia, and normal or non-diagnostic electrocardiograms, form a difficult subgroup for diagnosis and early risk stratification. We prospectively evaluated the role of troponin T (cTnT), troponin I (cTnI), CKMB mass and myoglobin, in the diagnosis and risk stratification of 214 patients with acute chest pain of < or = 24 h and non-diagnostic or normal ECGs admitted directly to the Cardiac Unit of the Royal Victoria Hospital Belfast from the Mobile Coronary Care Unit or the Accident/Emergency Department. This was a single-centre prospective study, and follow-up (3 months) was complete for all patients. Blood was assessed for quantitative cTnT, cTnI, CKMB mass and myoglobin, and qualitative cTnT on admission and at 12 h. Diagnosis of index event and incidence of new cardiac events (death, non-fatal myocardial infarction, revascularization, or readmission for unstable angina) over 3 months were assessed. Based on standard criteria, myocardial infarction occurred in 37/214 (17%), and unstable angina in 72/214 (34%). At 12 h from admission, cardiac troponins had higher sensitivity for the diagnosis of acute coronary syndromes (myocardial infarction and unstable angina) than conventional markers (cTnI 48%, cTnT 38%, CKMB mass 30% or myoglobin 27%). At 3 months, a new cardiac event had occurred in 42/214 (20%). Significantly higher event rates occurred when any of the biochemical markers was elevated, but the statistical significance was highest for patients with elevated cTnI (p < 0.0001). Whilst gender, history of ischaemic heart disease (IHD), stress test response, cTnT, cTnI, CKMB mass and myoglobin were univariate predictors, cTnI at 12 h and stress test response were the only two independent significant predictors for a subsequent cardiac event at 3 months. Raised cTnI at 12 h after admission had the highest sensitivity for the diagnosis of acute coronary syndromes, and was independently associated with a 2-3 times increased risk of future cardiac events within 3 months among patients with acute chest pain suggestive of myocardial ischaemia but with normal or non-diagnostic ECGs.
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PMID:Diagnosis and risk stratification of patients with anginal pain and non-diagnostic electrocardiograms. 1062 77

The enzyme activities of creatine kinase (CK), its isoenzyme MB (CK-MB) and of lactate dehydrogenase isoenzyme 1 (LD-1) have been used for years in diagnosing patients with chest pain in order to differentiate patients with acute myocardial infarction (AMI) from non-AMI patients. These methods are easy to perform as automated analyses, but they are not specific for cardiac muscle damage. During the early 90's the situation changed. First creatine kinase MB mass (CK-MB mass) replaced the measurement of CK-MB activity. Subsequently cardiac-specific proteins troponin T (cTnT) and troponin I (cTnI) appeared on the scene, displacing LD-1 analysis. However, troponin concentrations in blood increase only from four to six hours after onset of chest pain. Therefore a rapid marker such as myoglobin, fatty acid binding protein or glycogen phosphorylase BB could be used in early diagnosis of AMI. On the other hand, CK-MB isoforms alone may also be useful in rapid diagnosis of cardiac muscle damage. Myoglobin, CK-MB mass, cTnT and cTnI are nowadays widely used in diagnosing patients with acute chest pain. Myoglobin is not cardiac-specific and therefore requires supplementation with some other analyses such as troponins to support the myoglobin value. Troponins are very highly cardiac-specific. Only the sera of some patients with severe renal failure, which requires hemodialysis, have elevated cTnT and/or cTnI without there being any evidence of cardiac damage. On the other hand, the latest studies have shown that elevated troponin levels in sera of hemodialysis patients point to an increased risk of future cardiac events in a similar manner to the elevated troponin values in sera of patients with unstable angina pectoris. In addition, the bedside tests for cTnT and cTnI alone or together with myoglobin and CK-MB mass can be used instead of quantitative analyses in the diagnosis of patients with chest pain. These rapid tests are easy to perform and they do not require expensive instrumentation. For routine clinical laboratory practice we suggest that in diagnosis of patients with chest pain, myoglobin and CK-MB mass measurements should be performed whenever they are requested (24 h/day) and cTnT or cTnI on admission to the hospital and then 4-6 and 12 hours later.
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PMID:Laboratory diagnosis of patients with acute chest pain. 1090 53

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

It has been shown that the 2-h Stratus II delta creatine kinase-MB (CK-MB) is more sensitive and is equally specific compared to a 2-h Stratus II CK-MB and to a 2-h Stratus II delta cardiac troponin-I (DeltacTnI) for identification of acute myocardial infarction and adverse outcome (AO). Because the newest generation of Stratus (Stratus CS) cTnI assay has an analytical sensitivity of 0.03 ng/mL, compared to 0.35 ng/mL for the first generation assay, we undertook a small pilot study of 120 chest pain patients to compare sensitivities and specificities for 30-day AO of the Stratus CS DeltacTnI immunoassay to the DeltaCK-MB and DeltacTnI, as measured by the Abbott Axsym immunoassay, and to the DeltaCK-MB, as measured by the Stratus CS. A Stratus CS DeltacTnI > or = +0.02 ng/mL in 2 h was more sensitive (61.9%) than an Axsym DeltaCK-MB > or = +1.3 ng/mL (38.1%; p = 0.03), a Stratus CS DeltaCK-MB > or = +0.4 ng/mL (38.1%; p = 0.03), and an Axsym DeltacTnI > or = +0.3 ng/mL (33.3%; p = 0.03) for 30-day AO. There were no differences in specificities. Our data support enhanced identification of ACS with a second generation cTnI assay. Pending larger studies, patients with a rise in DeltacTnI of > or = +0.02 ng/mL in 2 h, as measured by the Stratus CS immunoassay, should receive consideration for aggressive anti-ischemic therapy and further diagnostic testing prior to making an exclusionary diagnosis of non-ischemic chest pain.
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PMID:Improved identification of acute coronary syndromes with second generation cardiac troponin I assay: utility of 2-hour delta cTnI > or = +0.02 ng/mL. 1185 18

Current findings from the American College of Emergency Physicians (ACEP) are that no serum marker reliably identifies or excludes acute myocardial infarction (AMI) within 6 h of symptom onset. The ACEP recommends repeat serum marker testing 6-10 h after symptom onset for CK-MB mass and subform, and 8-12 h after symptom onset for cardiac troponin I and T before making an exclusionary diagnosis of non-AMI chest pain. A new approach for identifying myocardial necrosis is to rely on time changes in the serum marker value over an abbreviated time interval (slope or delta values) as opposed to the traditional approach of relying on a value exceeding the threshold of normalcy. As assays become ever more sensitive and precise, this approach has the potential for both reliably identifying and excluding AMI (and subsets of high-risk unstable angina) at earlier time intervals with no loss in specificity. This article discusses some of the experimental evidence for this delta approach and some preliminary evidence for the potential of utilizing second-generation cTnI assays for the identification of acute coronary syndromes. Finally, we discuss a unique way of viewing receiver-operating characteristic (ROC) curves as catalogs of likelihood ratios, which we believe will be more useful to the clinician in the proper interpretation of serum marker values.
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PMID:Improved identification of acute coronary syndromes with delta cardiac serum marker measurements during the emergency department evaluation of chest pain patients. 1221 83

Cardiac troponin(cTn) is a sensitive marker for acute myocardial infarction(AMI). However, some cases of renal failure have been reported to show false positive results for cardiac troponin T(cTnT). Recently, it has been reported that heart-type fatty acid-binding protein(H-FABP) is a sensitive marker for AMI in the early phase. We evaluated the usefulness of cardiac troponin I(cTNI) using serum samples from patients(age 57-96) confirmed to have AMI with chest pain(n = 48), unstable angina pectoris(n = 11), cardiac failure(n = 5), others with high creatine phosphokinase(CK) activity(n = 81) and renal failure(n = 28), by comparing among cTnT(qualitative and quantitative), H-FABP, CK and creatine phosphokinase isoenzyme MB(CK-MB) activity. The diagnostic validity of cTn was assessed by receiver operating characteristic(ROC) curve analysis. The cut off value for AMI of cTnI was 0.8 ng/ml, cTnT was 0.16 ng/ml and H-FABP was 19.0 ng/ml. The overall diagnostic sensitivity of cTnI was 83.1%, and 84.8% for cTnT (quantitative), 72.3% for cTnT(qualitative), 64.8% for H-FABP, 81.8% for CK and 59.3% for CK-MB. The overall diagnostic specificity of cTnI was 90.9%, and 81.3% for cTnT(quantitative), 60.5% for cTnT (qualitative), 53.2% for H-FABP, 52.9% for CK and 87.7% for CK-MB. The overall diagnostic efficiency of cTnI was 86.5%, and 82.7% for cTnT(quantitative), 63.6% for cTnT(qualitative), 59.8% for H-FABP, 69.0% for CK and 71.9% for CK-MB. False positive results for cTnI were found in a few cases with renal failure. cTnT(qualitative) showed false positive results in 22/28 with serum creatinine over 2.1 mg/dl due to renal failure. In conclusion, cTnI detection is considered a useful and sufficiently sensitive marker for AMI.
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PMID:[Usefulness of cardiac troponin I in patients with acute myocardial infarction]. 1245 79


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