The release of cardiomyocyte components, i.e. biomarkers, into the bloodstream in higher than usual quantities indicates an ongoing pathological process. Thus, detection of elevated concentrations of cardiac biomarkers in blood is a sign of cardiac injury which could be due to supply-demand imbalance, toxic effects, or haemodynamic stress. It is up to the clinician to determine the most probable aetiology, the proper therapeutic measures, and the subsequent risk implied by the process. For this reason, the measurement of biomarkers always must be applied in relation to the clinical context and never in isolation. There are a large number of cardiac biomarkers, but they can be subdivided into four broad categories, those related to necrosis, inflammation, haemodynamic stress, and/or thrombosis. Their usefulness is dependent on the accuracy and reproducibility of the measurements, the discriminatory limits separating pathology from physiology, and their sensitivity and specificity for specific organ damage and/or disease processes. In recent years, cardiac biomarkers have become important adjuncts to the delivery of acute cardiac care. Therefore, the Working Group on Acute Cardiac Care of the European Society of Cardiology established a committee to deal with ongoing and newly developing issues related to cardiac biomarkers. The intention of the group is to outline the principles for the application of various biomarkers by clinicians in the setting of acute cardiac care in a series of expert consensus documents. The first of these will focus on cardiac troponin, a pivotal marker of cardiac injury/necrosis.

Background: Diagnosis of cardiac ischaemia in patients attending emergency departments (ED) with symptoms of acute coronary syndromes is often difficult. Cardiac troponin (cTn) is sensitive and specific for the detection of myocardial damage but may not rise during reversible myocardial ischaemia. Ischemia Modified Albumin (IMA) has recently been shown to be a sensitive and early biochemical marker of ischaemia. Methods and Results: This study evaluated IMA in conjunction with ECG and cTn in 208 patients presenting to the ED within three hours of acute chest pain. At presentation, a 12-lead ECG was recorded and blood taken for IMA and cardiac troponin T (cTnT). Patients underwent standardised triage, diagnostic procedures, and treatment. Results of IMA, ECG, and cTnT, alone and in combination, were correlated with final diagnoses of non-ischaemic chest pain, unstable angina, ST segment elevation, and non-ST segment elevation myocardial infarction. In the whole patient group, sensitivity of IMA at presentation for an ischaemic origin of chest pain was 82%, compared with 45% of ECG and 20% of cTnT. IMA used together with cTnT or ECG, had a sensitivity of 90% and 92%, respectively. All three tests combined identified 95% of patients whose chest pain was attributable to ischaemic heart disease. In patients with unstable angina, sensitivity of IMA used alone was equivalent to that of IMA and ECG combined. Conclusions: IMA is highly sensitive for the diagnosis of myocardial ischaemia in patients presenting with symptoms of acute chest pain.

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Patients with ESRD with raised cTnT concentrations have increased mortality. Raised concentrations are strongly associated with diabetes, LV dilatation, and impaired LV systolic and diastolic function, but not with severe coronary artery disease.

SUMMARY. Cardiac troponin T (cTnT) and cardiac troponin I (cTnI) were measured in 198 patients with renal dysfunction [132 men: median (range) age 66.1 (8.2-90.3) years]. cTnT was measured by two methods: ELISA and Enzymun (Boehringer Mannheim UK, Lewes, UK), both with a detection limit of 0.05 pg/L in 179 and 78 patients, respectively. cTnI was measured in 80 patients by the OPUS plus and OPUS Magnum systems (Dade-Behring, Milton Keynes, UK) with a detection limit of 0.5 pg/L.Patients were classified as having chronic renal impairment (CRI), chronic renal failure (CRF), acute renal failure including those with multiple organ failure on renal replacement therapy (ARF), and patients with chronic renal failure treated with haemodialysis (HD). Cardiac troponins were detectable in the serum of patients with renal dysfunction. cTnT was detectable in 113/179 (63.1%) and 33/78 (42.3%) by the ELISA and Enzymun methods respectively. cTnI was detectable in 17/80 (21.3%). cTnT (ELISA and Enzymun methods) and cTnI were detectable with increased frequency in the CRF, H D and ARF patient groups compared with the CRI group. Cardiac troponin concentrations did not correlate with serum creatine kinase (CK) activity, CK-MB, or urea or creatinine levels. Serial cardiac troponin measurements may be required to confirm or exclude a diagnosis of acute coronary syndromes in patients with renal dysfunction. Additional key phrases: haemodialysis; multiple organ failureThere is a high prevalence of cardiovascular complications in patients receiving renal replacement therapy.' The precise genesis of these are unknown, but hypertension, problems in fluid and electrolyte balance, metabolic abnormalities, including hyperlipidaemia and a direct toxic cardiomyopathy all contribute.2 We have measured cardiac troponin T (cTnT) and cardiac troponin I (cTnI) in the serum of patients with renal dysfunction to see if cardiac troponins were detectable and if they correlated with any other clinical or biochemical findings. METHODSPatients were classified as having chronic renal impairment (CRI, creatinine 120-200 pmol/L, Correspondence: Dr. P 0 Collinson.

The diagnostic performance of a new enzyme linked immunosorbent assay for the cardiac structural protein troponin T in the differential diagnosis of ischaemic cardiac damage was assessed. A well documented set of patients admitted to the coronary care unit of a district general hospital were studied. At a cutoff value of 0·2μ/L, troponin T measurements 12–24 h after admission or 12–16 to 24–48 h from onset of chest pain showed an overall efficiency of 97 · 6% for diagnosis of proven myocardial infarction. Troponin T was not detectable in patients when ischaemic heart disease could be excluded but was present in four patients with angina. Detectable troponin T in these angina patients was associated with subsequent cardiac events.

Objective: To assess if the combination of cardiac troponin (cTn) and Ischemia Modified Albumin (IMA) can be used for early exclusion of acute myocardial infarction (AMI). Methods: Prospective consecutive admissions to the emergency department (ED) with undifferentiated chest pain were assessed clinically and by electrocardiography. A total of 539 patients (335 men, 204 women; median age 51.9 years) considered at low risk of AMI had blood drawn on admission. If the first sample was less than 12 hours from onset of chest pain, a second sample was drawn two hours later, at least six hours from onset of chest pain. Creatine kinase MB isoenzyme (CKMB) mass was measured on the first sample and CKMB mass and cTnT on the second sample. An aliquot from the first available sample was frozen and subsequently analysed for IMA. If cTnT had not been measured on the original sample cTnI was measured (n = 189). Results: Complete data were available for 538/539 patients. IMA or cTn was elevated in the admission sample of all patients with a final diagnosis of AMI (n = 37) with IMA alone elevated in 2/37, cTn alone in 19/37, and both in 16/37. In 173/501 patients in whom AMI was excluded both tests were negative. In the non-AMI group 22 patients had elevation of both IMA and cTn in the initial sample, suggesting ischaemic disease. Conclusion: Admission measurement of cardiac troponin plus IMA can be used for early classification of patients presenting to the ED to assist in patient triage.