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)

Elevated cardiac troponin I (cTnI) levels in patients hospitalized with chest pain often lead to a diagnosis of acute myocardial infarction (MI) or unstable angina. However, as we describe in this review, this finding may occur in other conditions, leading to an incorrect diagnosis and other, sometimes invasive, tests. We review briefly cTnI, its release and detection. We describe the various conditions that may cause an elevated cTnI level and give possible explanations for these findings, and we offer some guidelines for diagnosis in patients with an elevated cTnI.
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PMID:Elevation of cardiac troponin I indicates more than myocardial ischemia. 1285 47

Diagnosis of non-ST-elevation acute myocardial infarction (AMI) by a 12-lead electrocardiogram has poor sensitivity and specificity and, therefore, relies on biochemical markers of myocardial necrosis, which can only be reliably detected within 14 to 16 hours from symptom onset. The body surface map (BSM) improves AMI detection but is limited by its interpretation by inexperienced medical staff. To facilitate interpretation, an automated BSM algorithm was developed and is evaluated in this study. One hundred three patients with ischemic-type chest pain were recruited for this study from December 2001 to April 2002. A 12-lead electrocardiogram (Marquette Mac 5K) and BSM (PRIME-ECG) were recorded at initial presentation, and cardiac troponin I and/or creatine kinase-MB levels measured at 12 hours after symptom onset. The admitting physician's 12-lead electrocardiographic (ECG) interpretation, 12-lead ECG algorithm (Marquette 12 SL V233) diagnosis, and BSM algorithm diagnosis were documented for each patient. AMI, defined by elevation of troponin I to >1 microg/L and/or creatine kinase-MB to >25U/L, occurred in 53 patients. The admitting physician diagnosed 24 patients with AMI (sensitivity 45%, specificity 94%), the 12-lead ECG algorithm diagnosed 17 patients with AMI (sensitivity 32%, specificity 98%), and the BSM algorithm diagnosed 34 patients with AMI (sensitivity 64%, specificity 94%). The BSM algorithm improved the diagnostic sensitivity by 2.0 (p <0.001) and 1.4 (p = 0.002) compared with the 12-lead ECG algorithm or the admitting physician, respectively. There was no significant difference in specificity. Thus, the BSM algorithm improves detection of AMI compared with the 12-lead ECG algorithm or physician's 12-lead ECG interpretation.
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PMID:Comparison of the 80-lead body surface map to physician and to 12-lead electrocardiogram in detection of acute myocardial infarction. 1288 26

Human heart-type fatty acid-binding protein (FABP) has a high potential as an early marker for myocardial infarction (MI) being more specific than myoglobin. FABP is a low molecular mass cytoplasmic protein (15 kDa) that is released early after the onset of ischemia and it may be useful for rapid confirmation or exclusion of acute myocardial infarction (AMI). Immunochemically assayed FABP, cardiac troponin I (cTnI) and enzymatically assayed creatine phosphokinase (CPK) were determined serially in plasma and serum samples from 218 patients presenting with chest pain and suspected MI. In the 94 patients with confirmed MI, FABP rose to a maximum level (577.6 +/- 43.8 microg/L) 3 hours after the onset of symptoms and returned to normal within 30 hours. The FABP level peaked 7-9 hours earlier than CPK (2288 +/- 131 U/L) and cTnI (357.1 +/- 23.9 microg/L). CPK took 50-70 hours to return to normal level and cTnI returned to normal level over 70 hours. The areas under the receiver operating characteristic (ROC) curves for FABP were calculated as 0.871 at admission and 0.995 one hour after admission, whereas for CPK the areas were 0.711 and 0.856 and for cTnI the areas were 0.677 and 0.845, indicating that the FABP test gave a better diagnostic classification at the early stage being reached by cTnI (0.995) only 8 hours after admission. For FABP, both sensitivity and negative predictive value (NPV) increased quickly to 100% for samples monitored just one hour after admission. By using only two samples, one at admission and one 1 hour post admission, sequential FABP monitoring can reliably diagnose AMI patients 1 hour after admission and 100% of non-AMI patients can be excluded with no false negative results. The late markers cTnI and CPK have the similar diagnostic performance only 7 hours later. Thus measurement of FABP in plasma or serum allows the earliest immunochemical confirmation or exclusion of AMI.
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PMID:A superior early myocardial infarction marker. Human heart-type fatty acid-binding protein. 1516 Feb 74

The aim of this study was to define the use of a new cardiac troponin I (cTnI) assay for emergency patients with chest pain and no specific electrocardiographic changes consistent with the presence of ischemia. Patients (n = 106) admitted in Emergency/Cardiology Departments for chest pain and suspicion of acute coronary syndrome (ACS) were randomized into two diagnosis groups (ACS or non-ACS) by two independent cardiologists. cTnI measurements were performed at admission, and 6 hours and 12 hours later with a new generation assay (Access AccuTnI, Beckman Coulter). Using an upper reference limit of 0.04 microg/l, 27 patients had a cTnI elevation not related to the final diagnosis of ischemia; the positive predictive value (PPV) was 67% with specificity 48%. The decisional value was re-defined and set at 0.16 microg/l, a concentration corresponding to the 99th percentile of the non-ACS patient group. Precision (coefficient of variation) was 8% at this level, PPV 97% and specificity 98%. This new decisional value is now used in our institution and could be included in standard care guidelines to improve the management of patients presenting chest pain in emergency departments.
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PMID:Emergency department triage of patients with acute chest pain: definition of cardiac troponin I decisional value to manage patients without electrocardiographic evidence of ischemia. 1520 94

A number of reports have raised the possibility that myocardial strain could be associated to increased plasma levels of troponin I. A 69-year-old, male, Caucasian, patient was admitted with prolonged chest pain and dyspnoea. The electrocardiogram showed atrial fibrillation with a ventricular rate of about 120 to 150/minute. After treatment with digoxin and amiodarone, the patient returned to sinus rhythm. An elevation in the plasma levels of troponin I was noted, with a maximum value of 0.66 ng/ml. Coronary angiography showed absence of coronary artery atherosclerotic lesions. Atrial fibrillation of recent onset and with a relatively high heart rate may be yet another situation in which acute myocardial strain could be the cause of the abnormal release of cardiac troponin I.
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PMID:Troponin I in atrial fibrillation with no coronary atherosclerosis. 1525 69

Cardiac biomarkers, eg, cardiac troponin, have become the standard test in combination with clinical and electrocardiographic findings for physicians to conduct prompt and effective triage of patients presenting with chest pain. Cardiac biomarkers are protein components of cell structures that are released into circulation when myocardial injury occurs. The purpose of this article is multifold. First, to identify specific cardiac biomarkers and review current guidelines based on study findings on the diagnostic utility of cardiac biomarkers in detecting myocardial infarction. Recent guidelines of the European Society of Cardiology, the American College of Cardiology, the American Heart Association, and the National Academy of Clinical Biochemistry were examined, as well as relevant studies relating to the development of these guidelines. Second, to analyze the clinical significance of cardiac biomarker measurements and the challenges with existing cardiac biomarker assays. Third, to discuss our findings regarding our evaluation of the analytical performance of a chemiluminescent microparticle immunoassay for the quantitative determination of cardiac troponin I in human serum and plasma on an automated immunoassay instrument system (ARCHITECT) to aid in the diagnosis of myocardial infarction.
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PMID:The diagnostic utility of cardiac biomarkers in detecting myocardial infarction. 1589 66

A 75-year-old African American man with a history of gastroesophageal reflux reported chest pain during an episode of intravascular hemolysis. Although the electrocardiogram and echocardiogram were unchanged from baseline, cardiac troponin I was persistently elevated. Cardiac catheterization showed no critical disease, and the elevated troponin was attributed to interference by free hemoglobin and/or bilirubin. Hemoglobinemia and hyperbilirubinemia may produce either false-positive or false-negative troponin levels, depending on the assay used and the form or subunit of troponin measured. In the presence of hemolysis, troponin levels must be interpreted with caution.
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PMID:Elevated troponin levels associated with hemolysis. 1623 15

Point-of-care testing (POCT) is defined as testing at or near the site of patient care. POCTdecreases therapeutic turnaround time (TTAT), increases clinical efficiency, and improves medical and economic outcomes. TTAT represents the time from test ordering to patient treatment. POC technologies have become ubiquitous in the United States, and, therefore,so has the potential for speed, convenience, and satisfaction, strong advantages for physicians, nurses, and patients in chest pain centers. POCT is applied most beneficially through the collaborative teamwork of clinicians and laboratorians who use integrative strategies, performance maps, clinical algorithms, and care paths (critical pathways). For example, clinical investigators have shown that on-site integration of testing for cardiac injury markers (myoglobin, creatinine kinase myocardial band [CKMB],and cardiac troponin I [cTnI]) in accelerated diagnostic algorithms produces effective screening, less hospitalization, and substantial savings. Chest pain centers, which now total over 150 accredited in the United States, incorporate similar types of protocol-driven performance enhancements. This optimization allows chest pain centers to improve patient evaluation, treatment, survival, and discharge. This article focuses on cardiac biomarker POCT for chest pain centers and emergency medicine.
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PMID:Point-of-Care Testing and Cardiac Biomarkers: The Standard of Care and Vision for Chest Pain Centers. 1627 18

Recently, a rapid bedside assay for quantitative determination of cTI and CPK-MB has been developed that provides a positive or negative result in 10 to 15 minutes allowing for a better therapeutic approach. The objective of our study was to validate the diagnostic usefulness of cardiac troponin I in patients with chest pain. We determined sensitivity, specificity, positive and negative predictive values in 40 patients that arrived to the hospital with chest pain. These patients were assigned to four different groups: Group A: Patients with acute myocardial infarction. Group B: Patients with unstable angina and normal ECG. Group C: Patients with atypical chest pain and normal ECG. Group D: Control. Eighteen (45%) patients were woman and 22 (55%) were men; age 54.1 +/- 26, range 32 to 85 years. In Group A, sensitivity, specificity, positive and negative predictive values for cTI were 95%, for CPK-MB, they were 40, 50, 90, 7.1%. For Group B, cTI: 64, 90, 90, 64%; CPK-MB: 50, 90, 87, 56%. Group C, cTI and CPK MB 25, 95, 50, 86%. Group D, cTI and CPK-MB: 50, 95, 50, 95%. This study suggests that the rapid bedside qualitative test through cardiac troponin I assessment is a test with higher predictive value for early diagnosis of acute myocardial infarction than CPK-MB.
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PMID:[Usefulness of rapid bedside assay of cardiac troponin I and creatine phosphokinase-MB in acute ischemic coronary syndromes]. 1674

A 70-year-old female was admitted for syncope preceded by chest pain. On admission ECG showed signs of myocardial ischaemia and cardiac troponin I (cTnI) was mildly elevated. Acute coronary syndrome without ST elevation was diagnosed. During hospitalization transthoracic echocardiography (TTE) revealed the presence of a round echogenic pedunculated mass adherent to the aortic valve. Cardiac catheterization revealed normal coronary arteries. According to the hypothesis that the lesion could be responsible for both acute coronary syndrome and syncope, surgical intervention was scheduled. The mass was removed and the histological examination revealed a cardiac papillary fibroelastoma (CPF). CPF is the most common tumour of the cardiac valves, it is often found incidentally but it can cause myocardial infarction, sudden death, syncope and stroke; its embolization is the most common complication. For symptomatic patients surgical excision is curative.
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PMID:Cardiac papillary fibroelastoma presenting with acute coronary syndrome and syncope. 1686 62


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