Elsevier

Clinical Biochemistry

Volume 33, Issue 3, April 2000, Pages 161-166
Clinical Biochemistry

Review
Present issues in the determination of troponins and other markers of cardiac damage

Presented in part at the IFCC-WorldLab Congress held in Florence, June 1999; Workshop on Biochemical markers of acute coronary disease—recent analytical developments.
https://doi.org/10.1016/S0009-9120(00)00063-1Get rights and content

Abstract

Objective: To review some of the recently proposed improvements and the corresponding apparent issues in the field of biochemical markers of cardiac damage.

Conclusions: The continuous development of new analytical tools for the biochemical evaluation of patients with suspected myocardial injury brings without doubt new challenges of careful technological evaluation, implementation, and standardization but it may also provide a unique opportunity to markedly enhance our diagnostic performance in the clinical setting of acute coronary syndrome.

Section snippets

Background

T he field of biochemical markers of cardiac damage is in a dynamic state, with new applications continually appearing and new assays and markers being developed. The availability of innovative procedures to detect myoglobin, cardiac troponin I (cTnI) and troponin T (cTnT), and creatine kinase (CK)-MB mass concentration instead of isoenzyme activity represents a major opportunity to improve significantly clinical assessment of the acute coronary syndrome 1, 2.

Myoglobin was the first

The ongoing issues

These significant and sudden advancements in the development of new biochemical assays for myocardial damage have led to some analytical and interpretative problems (20). There are problems in test standardization, imprecision, and of preanalytical variability; problems also arise with turnaround time and evaluation of point-of-care testing (POCT) devices as a possible alternative in particular situations. We lack accurate economic analyses that consider costs in relation to expected benefits,

Cardiac POCT

Use of POCT devices is another means to deliver emergency cardiac marker results. Advocates of this approach point out the speed and convenience of such testing. POCT devices are now available for myoglobin, CK-MB mass, cTnI, and cTnT (54). These make use of anticoagulated whole blood and provide results within 15 min. Elimination of the need to deliver samples to the central laboratory and centrifugation enables shorter processing time. However, unit costs for POCT are higher than for tests

Improving sensitivity of cardiac troponin assays

An interesting area of further analytical development that may have some clinical utility would be to improve the level of analytical sensitivity of the troponin assays in an attempt to investigate some of the situations in which subtle degrees of myocardial injury may be cumulative, and in which early detection may be helpful. This effort was recently furthered by two investigations by Missov and a group of Sanofi scientists 65, 66 using a new generation, highly sensitive immunoassay for cTnI

References (67)

  • A.S. Jaffe

    Troponin, where do we go from here?

    Clin Lab Med

    (1997)
  • M. Panteghini

    Biochemical assessment of myocardial damage with new diagnostic tools

    Cardiologia

    (1999)
  • A.H.B. Wu

    Biochemical markers of cardiac damagefrom traditional enzymes to cardiac-specific proteins

    Scand J Clin Lab Invest

    (1999)
  • J. Mair

    Myoglobin

  • M. Panteghini et al.

    The sensitivity of cardiac markersan evidence-based approach

    Clin Chem Lab Med

    (1999)
  • R.H. Christenson et al.

    Evidence based approach to practice guides and decision thresholds for cardiac markers

    Scand J Clin Lab Invest

    (1999)
  • F.S. Apple

    Acute myocardial infarction and coronary reperfusion. Serum cardiac markers for the 1990s

    Am J Clin Pathol

    (1992)
  • J. Mair et al.

    Equivalent early sensitivities of myoglobin, creatine kinase MB mass, creatine kinase isoform ratios, and troponin I and T for acute myocardial infarction

    Clin Chem

    (1995)
  • K.J. Dean

    Cardiac troponin T as a marker of myocardial injury

  • F.S. Apple

    Cardiac troponin I

  • A. Lavoinne et al.

    Serum cardiac troponin I and T in early posttraumatic rhabdomyolysis

    Clin Chem

    (1998)
  • J.T. Martins et al.

    Comparison of cardiac troponin I and lactate dehydrogenase isoenzymes for the late diagnosis of myocardial injury

    Am J Clin Pathol

    (1996)
  • C.W. Hamm

    Cardiac-specific troponins in acute coronary syndromes

  • W. Rottbauer et al.

    Troponin Ta diagnostic marker for myocardial infarction and minor cardiac cell damage

    Eur Heart J

    (1996)
  • M. Plebani et al.

    Troponin Istructure, physiology and its role in risk stratification of angina patients

  • M. Panteghini

    IFCC Committee on standardization of markers of cardiac damagepremises and project presentation

    Clin Chem Lab Med

    (1998)
  • A.H.B. Wu et al.

    Characterization of cardiac troponin subunit release into serum after acute myocardial infarction and comparison of assays for troponin T and I

    Clin Chem

    (1998)
  • P. Datta et al.

    Comparison of immunoreactivity of five human cardiac troponin I assays toward free and complexed forms of the antigenimplications for assay discordance

    Clin Chem

    (1999)
  • A.G. Katrukha et al.

    Troponin I is released in bloodstream of patients with acute myocardial infarction not in free form but as complex

    Clin Chem

    (1997)
  • I. Giuliani et al.

    Determination of cardiac troponin I forms in the blood of patients with acute myocardial infarction and patients receiving crystalloid or cold blood cardioplegia

    Clin Chem

    (1999)
  • P.H. McPherson et al.

    Characterization and measurement of troponin I, troponin T and troponin complexes in blood from AMI patients

    Clin Chem

    (1997)
  • A. Bereznikova et al.

    Monoclonal antibodies affected by cardiac troponin I phosphorylationis part of troponin in the blood of myocardial infarction patients phosphorylated?

    Clin Chem Lab Med

    (1999)
  • A. Katrukha et al.

    Stability of human cardiac troponin I (cTnI) in homogenates of necrotic tissue of human cardiac muscle

    Clin Chem

    (1998)
  • Cited by (36)

    • A voltammetric immunosensor based on nanobiocomposite materials for the determination of alpha-fetoprotein in serum

      2011, Biosensors and Bioelectronics
      Citation Excerpt :

      The demand of rapid and high-throughput technology to quantitatively measure a number of proteins precisely and simultaneously in medical diagnosis and biological research is increasing (Apple et al., 2007; Bondar et al., 2007). In this context, immunologic assays, based on the highly specific molecular recognition of antigens by antibodies, have become fundamental analytical methods in several fields (Knopp, 1995; Panteghini, 2000; Ring et al., 2001; Trull, 2001; Belloque et al., 2002; Worwood, 2002). These techniques have proved to be successful for rapid screening purposes allowing to obtain excellent detection limits in complex matrices with reduced or no sample treatment.

    • Incidence of elevation of cardiac troponin I prior to and following routine general anaesthesia in dogs

      2010, Veterinary Anaesthesia and Analgesia
      Citation Excerpt :

      Due to its cardiac muscle specificity and its very low concentrations in the serum of normal individuals, cTnI has a high sensitivity even for minor levels of myocardial injury. These aspects make cTnI a very powerful biomarker of myocyte injury (Panteghini 2000; Collison et al. 2006). cTnI is highly conserved across species and assays used to detect human cTnI have been validated in the dog (Cummins & Cummins 1987; Schober et al. 1999; Sleeper et al. 2001).

    • Biochemical markers of myocardial injury

      2004, British Journal of Anaesthesia
      Citation Excerpt :

      It is not surprising that absolute values obtained using different manufacturers’ assays may not be comparable, and may differ numerically by up to 20-fold. There is also evidence that some cTnI assays were inadequately appraised before their introduction into routine clinical use.102 The situation for cTnT assays is much clearer than that for cTnI.

    View all citing articles on Scopus
    View full text