When should we measure cardiac troponin I?

In horses (population) does measurement of cardiac troponin I (intervention) improve ability to diagnose myocardial disease (outcome) with respect to: (1) presence and (2) severity when compared with clinical evaluation and ECG? Cardiac troponin I (CTnI) is part of the troponin complex integral to myocardial contraction. During myocyte necrosis or membrane damage CTnI leaks into the circulation and is detectable in the serum (gold standard to detect myocardial injury in man [Anon 2014], correlated to severity and prognosis in dogs and man [Fonfara et al. 2010]), but provides no information on the mechanism of injury. Genetic sequencing of equine CTnI confirms that use of commercial human immunoassays is appropriate (Rishniw and Simpson 2005). The search terms ‘horse’ or ‘equine’ and ‘cardiac troponin I’ were entered into Pubmed (http://www.ncbi.nlm.nih.gov/pubmed). Multiple studies have generated reference ranges for CTnI from clinically healthy horses (Phillips et al. 2003; Van Der Vekens et al. 2015a,b). In the majority of these studies a clinical examination and ECG were not performed and therefore cardiac disease could have been overlooked. Importantly, there were significant differences between values obtained from different assays in different laboratories that precludes quantifiable comparison between published studies (Serra et al. 2010; Van Der Vekens et al. 2015a). Mild and transient increases (up to 14 h) in CTnI are documented after intense exercise (Begg et al. 2006; Holbrook et al. 2006; Nostell and Häggström 2008; Slack et al. 2012; Flethøj et al. 2016) and fetal reference range is higher (Herman et al. 2014), but with no other age-effect noted. General anaesthesia (Slack et al. 2011) and polysaccharide storage myopathy (PSSM) (Naylor et al. 2012) do not increase CTnI. The half-life of CTnI (0.47 h) (Kraus et al. 2013) is short, therefore effect of unknown variables can easily be assessed by their removal. A diagnostic test should undergo an independent, blind comparison with a reference standard (for CTnI, clinical evaluation and an ECG). These four studies of horses presenting for cardiac disease separately to healthy animals (case–control studies) may overestimate the accuracy of the test (due to bias, Table 1). The findings of these studies are consistent and conclude an increase in CTnI with primary active myocardial disease, but not necessarily with secondary disease where myocyte injury may not always occur. A wide of range of pathologies have been evaluated for evidence of myocardial injury providing a population with less bias as these horses may have not presented with symptoms of cardiac disease. There is a clear and well documented relationship between myocardial injury and increased CTnI in horses. There may be a correlation between both the degree and duration of this increase and severity of injury/prognosis but further work is required to define this relationship. CTnI should be measured in all horses presenting with myocardial disease and in any pathology where myocardial injury can occur. No conflicts of interests have been declared.