Republished: Sensitive troponin assays
- Departments of Cardiology and Clinical Blood Sciences, St George's Hospital and Medical School, London, UK
- Correspondence to Dr Paul O Collinson, Departments of Cardiology and Clinical Blood Sciences, St George's Hospital and Medical School, London SW17 0RE, UK;
- Accepted 31 May 2011
Sensitive troponin assays have been developed to meet the diagnostic goals set by the universal definition of myocardial infarction (MI). The analytical advantages of sensitive troponin assays include improved analytical imprecision at concentrations below the 99th percentile and the ability to define a reference distribution fully. Clinically, the improved sensitivity translates into the ability to diagnosis MI earlier, possibly within 3 h from admission and the ability to use the rate of change of troponin (Δ troponin) for diagnosis. Very sensitive assays may, in appropriately selected populations (perhaps with the addition of Δ troponin), allow diagnosis on hospital admission or within 1–2 h of admission. An elevated troponin level occurring in patients without suspected acute coronary syndromes has, in all studies to date in which outcome has been examined, been shown to indicate an adverse prognosis whatever the underlying clinical diagnosis. Failure of elevation means a good prognosis allowing early, safe hospital discharge, whereas a raised value requires investigation and should help prevent clinically significant pathology being overlooked. Sensitive troponins do present a challenge to the laboratory and the clinician. For the laboratory, the diagnosis of MI requires a change in troponin value. For the clinician, the challenge is to shift from a simplistic yes/no diagnosis of MI based on a single troponin value to a diagnosis that utilises early troponin changes as part of the clinical picture, and to relate the new class of detectable troponin elevation in patients with ischaemic myocardial disease to existing clinical guidelines and trial evidence.
- chemical pathology
- colorectal cancer
- gall bladder
- laboratory tests
- molecular biology
- vascular disease
This is a reprint of a paper that first appeared in Journal of Clinical Pathology, October 2011, Volume 64, pages 845–849.
Competing interests None to declare.
Provenance and peer review Commissioned; externally peer reviewed.