Are troponins confusing?

Abstract

The cardiospecificity and sensitivity of cardiac troponin measurement has proved to be a two edged sword for the laboratory and the clinician The ability to measure the cardiac specific markers, cardiac troponin T (cTnT) and cardiac troponin I (cTnI) (the cardiac troponins), has produced a paradigm shift in the assessment of patients with suspected acute coronary syndromes (ACS). Elevations of creatine kinase (CK) and its MB isoenzyme (CK-MB) resulting from skeletal muscle damage can now reliably be distinguished from those caused by acute myocardial infarction (AMI).1 In the ACS patient, measurement of cTnT and cTnI identified prognostically significant myocardial damage when myocardial infarction was excluded by conventional tests.2 This confirmed and extended previous work showing that minor but non-diagnostic elevations of CK-MB in ACS patients indicated myocardial damage and were prognostic.3 The evidence that cTnT and cTnI elevations predict prognosis in patients with and without ST elevation ACS is comprehensive and led to the proposed redefinition of AMI.4 This recognised cTnT and cTnI measurement as the biochemical diagnostic “gold standard”. The role of cardiac biomarkers to guide treatment has also been recognised and incorporated into management guidelines.5 The cardiospecificity and sensitivity of cardiac troponin measurement has proved to be a two edged sword for the laboratory and the clinician. The laboratory must now produce analytically precise and accurate cardiac marker measurements by immunoassay on a 24 hour, seven day a week basis. The individual laboratory methods for cTnI show differing sensitivities and do not give equivalent answers.1 The clinician has found that evidence of cardiac damage can be readily (and unsurprisingly) detected in a range of other clinical conditions.6,7 Is this a problem of the test or the clinical interpretation of the test result? There is no evidence that these are “false …