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

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

Incidence rates of electrocardiographic changes during Caesarean section vary from 25 to 60%. To date, no investigator has identified myocardial ischaemia resulting from these changes. We investigated patients undergoing elective Caesarean section using peripartum Holter monitoring and serum analysis of cardiac troponin I (cTnI). Twenty-six patients presenting for elective Caesarean section were studied. Peroperative Holter monitoring continued for 12 h postoperatively, at which time blood samples for cTnI levels were taken. Significant ST changes were recorded in 42% of patients peroperatively and 38.5% of patients postoperatively. Forty-two per cent of patients experienced peroperative chest pain requiring opioid analgesia. Chest pain was significantly associated with abnormal electrocardiogram (ECG) findings. Ischaemic levels of cTnI were recorded in two patients. This study reports, for the first time, myocardial ischaemia (7.69% of patients) arising in conjunction with the ECG changes seen during elective Caesarean section. We also report episodes of significant postoperative ST-segment changes.
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PMID:Myocardial ischaemia in normal patients undergoing elective Caesarean section: a peripartum assessment. 1170 37

This study was undertaken to evaluate the diagnostic accuracy and practicality of Emergency Department (ED) testing for cardiac biomarkers in the diagnosis of acute coronary syndromes. All patients presenting with chest pain to the ED of a community-based tertiary care facility over a 16-day period (N = 205) had blood drawn and tested for cardiac troponin I, myoglobin, and CK-MB by a quantitative, point-of-care instrument system (Stratus CS). Point-of-care cardiac testing expedited diagnosis by decreasing the turn-around time by 55% compared to the central laboratory. The extreme sensitivity of the cardiac troponin I assay integral to this system was responsible for the high diagnostic accuracy (100% sensitivity; virtually 100% specificity, compared with the final assigned diagnosis). The assay also identified a clinically significant "high-risk" zone for near-future cardiac events: 17 patients were identified and four of these progressed to further cardiac events in the next 9 months. Further studies to explore the clinical implications of this high-risk zone are warranted.
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PMID:Evaluation of quantitative cardiac biomarker point-of-care testing in the emergency department. 1180 49

The diagnosis of myocardial infarction (MI) is established in patients with chest pain and equivocal electrocardiogram changes by demonstrating a rise in blood levels of creatine kinase MB (CK-MB) and/or an increase in cardiac troponin I (cTnI) or cardiac troponin T (cTnT). Previous studies have shown that levels of CK-MB are increased in the left ventricle of individuals with heart disease; however, it has not been established whether there are differences in the ventricular myocardium concentrations of cTnI in diseased compared to healthy hearts. Using a simple extraction technique, concentrations of CK-MB and cTnI were measured in the left ventricle (LV) of six hearts obtained at autopsy from individuals ranging in age from 25 to 79 yr, with and without evidence of cardiac disease. The results show an 86-fold higher concentration of CK-MB and 7.7-fold lower concentration of cTnI in left ventricular myocardium of older men with and without cardiac disease, compared to that of younger men (< age 35 yr) without heart disease. These data suggest that age may need to be considered when setting cutoff limits for these markers for the diagnosis of myocardial infarction.
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PMID:Differences of creatine kinase MB and cardiac troponin I concentrations in normal and diseased human myocardium. 1184 17

Acute coronary syndromes remain the leading cause of mortality in the United States and represent an enormous cost to the health care system. Despite decades of investigation into the diagnosis of acute myocardial infarction (MI), the diagnostic process is still quite complex because the majority of patients with chest pain fall in the low or medium risk category with atypical symptoms and nonspecific electrocardiogram (ECG) changes. Cardiac biochemical markers play an important role in helping physicians make the diagnosis and stratify the risk to patients. However, the ideal cardiac marker and the best diagnostic approach to patients with chest pain in the Emergency Department (ED) remain elusive. Currently, among many cardiac markers, cardiac troponin I seems the most cardiac-specific in the diagnosis of acute MI. This article is focused on reviewing the characteristics of different cardiac markers and comparison of their usages in the diagnosis of acute MI. However, since this field is large and rapidly expanding, it is impossible to cover every aspect of cardiac markers. As the search for the most efficacious, specific and cost-effective means to approach patients with chest pain continues, further prospective, randomized, multicenter trials are needed to confirm the value of troponins and other diagnostic strategies in the early diagnosis of acute MI.
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PMID:A review of clinically relevant cardiac biochemical markers. 1210 1

To evaluate the sensitivity of the serum cardiac troponin I level in detecting stress test-induced myocardial ischemia, the authors conducted a prospective study including patients admitted for chest pain to the telemetry floor of Our Lady of Mercy Medical Center at Bronx, NY. Consecutive 134 telemetry patients that agreed to participate in this study were included. All of these patients had a nuclear stress test and were divided into various groups based on the prestress test probability of having coronary artery disease. To assess serum cardiac troponin I levels, blood samples were drawn before and after stress testing and compared with the stress test results. Overall, 30 patients (22%) had reversible perfusion defects on stress images, and none (0%) had increased serum cardiac troponin I levels. One patient of 18 patients (6%) in group C with negative stress test results had an elevated serum cardiac troponin I level after the stress test, but none of group A or group B patients had elevated troponin I levels. These data show that serum cardiac troponin I levels do not increase with stress test-induced myocardial ischemia.
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PMID:Does the serum cardiac troponin I level increase with stress test-induced myocardial ischemia? 1214 81

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

Human albumin has the ability to bind cobalt at the N-terminus. The exposure of circulating albumin to ischemic tissue alters the ability of albumin to bind cobalt, probably through a mechanism involving free-radical production. The Albumin Cobalt Binding (ACB) test measures the alteration in albumin metal binding, and elevation of the ACB test is thought to be an early indicator of myocardial ischemia. In a previous multicenter study of chest pain patients presenting to the emergency department (ED), this test demonstrated high negative predictive value and sensitivity in the sample collected at presentation for predicting cardiac troponin I (cTnI)-negative or cTnI-positive results 6-24 h later. Since the completion of that report, the European Society of Cardiology (ESC) and the American College of Cardiology (ACC) have redefined the criteria for the diagnosis of acute myocardial infarction (AMI). The data from the multicenter ACB study were re-examined using the new diagnostic criteria for AMI to determine if combining the ACB test with troponin improved the sensitivity of either assay used alone for early diagnosis of AMI. Assay values were compared to either the final discharge diagnosis made at each site or to a diagnosis of AMI using the strict application of the ESC/ACC guidelines. Using the criterion of physician's discharge diagnosis and using blood collected at ED presentation, the cTnI test alone had a sensitivity of 23.9%, and the ACB test alone had a sensitivity of 39.1%, but the sensitivity significantly increased to 55.9% (p < 0.001 over cTnI alone) when both tests were used in combination. The sensitivity of the combination of ACB and cTnI tests at the 1- to 6-h time-point was 86.7% and at the >6- to 12-h time-point was 93.5%, but they were not significantly improved over the cTnI test alone. In conclusion, using the new ESC/ACC criteria, the combination also resulted in a statistically significant higher diagnostic sensitivity on blood collected at presentation. These data indicate a possible role of the ACB test in the early triage of patients with chest pain.
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PMID:Analysis of the Albumin Cobalt Binding (ACB) test as an adjunct to cardiac troponin I for the early detection of acute myocardial infarction. 1221 87

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

One hundred asymptomatic high-risk renal transplant candidates were screened for asymptomatic coronary artery disease using stress cardiac isotopic imaging. The cardiac markers, serum cTnT, cTnI, and CKMB, were collected pre and post stress testing. Of the 99 patients whose cardiac scans were technically satisfactory, 32 were normal, 49 had a definite imaging abnormality and the scan was indeterminate in the remaining 18 patients. Based on these results, patients were stratified into either normal, indeterminate or abnormal scan groups. They then were analyzed to detect any correlations between cardiac perfusion defects and either elevated pre-stress cardiac markers or consistent changes 24h after stress testing. While the mean pre-stress serum values for both cardiac troponin T (0.117 +/- 0.12 microgram/L) and cardiac troponin I (0.235 +/- 0.89 microgram/L) were increased in the abnormal cardiac scan group, only the cTnT value proved to differ significantly from the normal group (p < 0.01). For the indeterminate group neither marker was different from the normal scan group. Only an elevated serum cTnT > 0.1 microgram/L (OR 3.042, p = 0.030) proved to discriminate an abnormal scan in this population. It is concluded that the increase in pre-stress serum cTnT encountered in patients with chronic renal failure, with or without evidence of overt, symptomatic coronary artery disease, may represent a combination of subclinical myocardial damage and a prolonged half-life of the marker in the serum. Because of the frequency of elevated serum concentrations of cTnT and, to a lesser degree cTnI, the physician should exercise caution when interpreting a single elevated Troponin value during the evaluation of chest pain in patients with end-stage renal disease. A cTnT > 0.1 microgram/L increases the likelihood of finding significant coronary artery disease three fold in high-risk ESRD patients being evaluated for renal transplantation.
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PMID:Relationship between elevated serum troponin values in end-stage renal disease patients and abnormal isotopic cardiac scans following stress. 1261 33


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