Cardiac Troponin in Cerebral Injury: Understanding your Laboratory Reports

Abstract

Cardiac troponin (cTn) is now the ‘gold standard’ biochemical test for the diagnosis of acute coronary syndrome (ACS). This clinical spectrum of ischemic heart disease includes stable and unstable angina through to acute myocardial infarction (AMI). The growing evidence base for the diagnostic and prognostic use of cTn in ACS has resulted in the redefinition of AMI [1]. With increasing popularity owing to ease of measurement, the presence of a tick box on a laboratory request form and a reduction in test price, cTn is a common request in many clinical scenarios outside the remit of ACS. This has resulted in the identification of a plethora of elevated cTn in other conditions, often creating clinical confusion. With the redefinition of AMI, many emergency physicians could not adequately distinguish between a primary acute coronary syndrome and secondary ischemic or nonischemic disease states [2], plainly from ignoring the clinical history. A common misconception is that elevated cTn indicates AMI. It does not. All cTn elevations indicate myocardial cell necrosis [3] but not the pathological mechanism of release. Anecdotal data from a London teaching hospital demonstrate as many as 30% of all medical noncardiac admissions with elevated serum cTn do not have a final diagnosis of ACS [2]. Cardiac troponin T (cTnT) and cardiac troponin I (cTnI) are expressed in the cardiac myocyte. A small circulating pool exists in the cytosol, but greater than 90% is bound to the thin filament of the contractile apparatus. The cardiac isoforms are distinctly different in amino acid sequence from those expressed in skeletal muscle. Monoclonal antibodies have been raised against cTnT and cTnI and form the basis of immunoassay tests that have been in commercial use since the early 1990s [4]. Patients presenting to the emergency department with an acute cerebral injury may be cognitively impaired or exhibit severe speech