EQUINE VETERINARY EDUCATION Equine vet. Educ. (2018) 30 (2) 85-87 doi: 10.1111/eve.12715
Critically Appraised Topic When should we measure cardiac troponin I?
A. G. Raftery Weipers Centre Equine Hospital, University of Glasgow, Bearsden Road, Glasgow, Scotland. Corresponding author email:
alexandra.raftery@googlemail.com
Summary
Clinical question 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?
Introduction and history 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).
Search method The search terms ‘horse’ or ‘equine’ and ‘cardiac troponin I’ were entered into Pubmed (
http://www.ncbi.nlm.nih.gov/ pubmed).
Search outcome (1) Quantity of evidence: A total of 54 papers were retrieved; 31 provided useful information and 23 were discarded as irrelevant to the question (16), provided a low level of evidence (six case reports) or a secondary source (one review article).
(2) Quality of evidence: There were eight case–control studies, seven cross-sectional studies, 11 case series and six experimental studies providing moderate evidence for the conclusions.
How has CTnI been validated for use in the horse? Normal values in healthy animals 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 H€
aggstr€ om 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.
Evaluation in horses presenting with myocardial disease 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.
Diagnosis of myocardial damage for horses presenting with other pathologies 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. (1) Haemorrhage: One small case series concluded myocardial injury associated with the presence of dysrhythmias occurs during acute haemorrhage (Navas de Solis et al. 2015).
(2) Colic and/or endotoxaemia: Two case–control, one case series and an experimental study (Nath et al. 2012b; Nostell et al. 2012; Radcliffe et al. 2012; Dıaz et al. 2014) examined horses with colic and/or endotoxaemia. Cardiac troponin I values were increased in the horses likely to be hypovolaemic and/or endotoxaemic (associated with requirement for surgery, negative prognosis, infusion of endotoxin). Increased values were associated with development of ventricular dysrhythmias and decreased cardiac function.
(3) Cardiotoxicity: Seven studies (five experimental, one case series, one case–control) evaluated serum concentrations of CTnI following administration of toxins known to result in cardiac muscle damage (fumosin B1 [Smith et al. 2002]), monensin (Divers et al. 2009; Kraus et al. 2010), rattlesnake envenomation (Gilliam et al. 2012), lasalocid (Decloedt et al. 2012a,b) and rayless goldenrod (Davis et al. 2013). Increased CTnI concentrations are documented alongside decreased cardiac function and presence of dysrhythmias with decreasing frequency of all these markers associated with recovery.
(4) Cardiomyopathy: A case series of horses with atypical myopathy demonstrates concurrent increase in CTnI with abnormal clinical findings and presence of dysrhythmias (Verheyen et al. 2012).
© 2017 EVJ Ltd
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