Cardiac troponins in intensive care

The cardiac troponins are integral components of the myofibrillary apparatus and they regulate muscle contraction. The measurement of cardiac troponins has replaced other biomarkers for the specific detection of myocardial necrosis and for the diagnosis of myocardial infarction. The tissue specificity plus sensitivity of the measurement technology has meant that cardiac damage can be detected in circumstances other than conventional acute coronary syndromes. The ability to specifically detect cardiac damage as part of multiple organ failure in intensive care patients has been shown to provide prognostic information, but it is unclear whether this is a dependent or an independent marker of outcome

Cardiac troponins as biomarkers of drug and toxin induced cardiac toxicity and cardioprotection

Cardiac troponin T and I (cTnT, cTnI) are sensitive biochemical markers of myocardial cell necrosis and have been adopted as the gold standard tests for acute myocardial infarction. Subtle elevations in cTn above the detection limits of the currently available commercial assays confers poor prognosis. These markers are superior to classical enzyme markers of necrosis due to their cardiospecificity. The diagnosis of drug-induced cardiac toxicity using the classical enzymes is problematic due to the high elevations of these markers in skeletal muscle necrosis. cTnT and cTnI are now being adopted as sensitive biomarkers of drug-induced cardiac toxicity

Biomarkers of cardiovascular damage and dysfunction – An overview

Acute coronary syndromes (ACS) are due to the rupture or erosion of atheromatous plaques. This produces, depending on plaque size, vascular anatomy and degree of collateral circulation, progressive tissue ischaemia which may progress to cardiomyocyte necrosis and subsequent cardiac remodelling. Cardiac biomarkers can be used for diagnosis and assessment of all of these stages. Markers to detect myocardial ischaemia at the pre-infarction stage are potentially the most interesting but also the most challenging. An ischaemia marker offers the opportunity to intervene to prevent progression to infarction. The challenges with potential ischaemia markers are specificity and the diagnostic reference standard for assessment. To date, only one, ischaemia modified albumin, has reached the point where clinical studies can be performed. The measurement of the cardiac troponins, cardiac troponin T and cardiac troponin I, has become the diagnostic standard as the biomarker of myocardial necrosis. The sensitive nature of troponin measurement has also revealed that myocardial necrosis is also found in a range of other clinical situations. This illustrates the need to use all clinical information for diagnosis of acute myocardial infarction. The measurement of B type natriuretic peptides can be shown to be diagnostic and prognostic for both acute ACS and detecting the sequelae of post infarction myocardial insufficiency. The role of the B type natriuretic peptides in detection of cardiac failure, acute and chronic, is well defined. Their role in ACS remains the subject of further studies

Clinical effect of recalibration of the Roche cardiac troponin T assay

Objective: To assess the effect of recalibration of the Roche 3rd-generation cTnT assay with recombinant human cardiac troponin T (cTnT) standards on clinical decision limits. Materials and Methods: Serum samples from 77 patients (66 ± 16 years) admitted to the coronary care unit were assayed using the 2nd- and 3rd-generation cTnT assays. Results: There was excellent agreement (r = 0.99 Spearman, 95% CI 0.99–1.0; p ≤ 0.0001, n = 153) between the 2nd- and 3rd-generation cTnT assays across the analytical range, but there was a curvilinear relationship between values. There was concordance between the 2nd- and 3rd-generation cTnT values in the range from 0 to 0.2 µg/l. Above 0.2 µg/l, however, there were increasing but predictable differences. Conclusion: There was no statistical difference between the 2nd- and 3rd-generation cTnT assays, demonstrated by a linear relationship below 0.2 µg/l. This confirms that the 3rd-generation assay was calibrated to that of the 2nd-generation assay in the range of 0–0.2 µg/l. The detection limit and upper reference limit of normal will be unaffected by this change in calibration. A non-linear relationship at higher 2nd-generation concentrations (0.2–25.0 µg/l) was observed. Clinical decision limits up to 0.2 µg/l, associated with increased cardiac risk, are unaffected by the assay calibration, but values greater than 0.2 µg/l are affected

Biomarkers of cardiovascular damage

Acute coronary syndromes (ACS) are due to the rupture or erosion of atheromatous plaques. This produces, depending on plaque size, vascular anatomy and degree of collateral circulation, progressive tissue ischaemia which may progress to cardiomyocyte necrosis. This may then result in cardiac remodelling. Serum biomarkers are available which can be used for diagnosis of all of these stages. Markers to detect myocardial ischaemia at the pre-infarction stage are potentially the most interesting but also the most challenging. An ischaemia marker offers the opportunity to intervene to prevent progression to infarction. The problems with potential ischaemia markers are specificity and the reference diagnostic standard against which they can be judged. To date, only one, ischaemia-modified albumin(R), has reached the point where clinical studies can be performed. The measurement of the cardiac troponins, cardiac troponin T and cardiac troponin I, have become recognised as the diagnostic reference standard for myocardial necrosis. The sensitive nature of these tests has also revealed that myocardial necrosis is also found in a range of other clinical situations, highlighting the need to use all clinical information for diagnosis of acute myocardial infarction. The measurement of B-type natriuretic peptides can be shown to be diagnostic and prognostic in both ACS and detecting the sequelae of post-infarction myocardial insufficiency. The role of the B-type natriuretic peptides in detection of cardiac failure, both acute and chronic, is well defined but remains the subject of further studies, in ACS