86


EQUINE VETERINARY EDUCATION / AE / FEBRUARY 2018


TABLE 1: Horses presenting with myocardial disease Reference


Van Der Vekens et al. (2015b)


Level of evidence Case–control


Population


Thirty-five healthy horses, 23 suspected primary, 41 suspected secondary myocardial disease


Van Der Vekens et al. (2015a)


Nath et al. (2012a) Case–control Case–control with


Twenty-three healthy horses, 72 with myocardial disease (primary and secondary)


Eighteen healthy horses. 49 with cardiac disease (7 with myocardial, 25 with structural, 17 with lone dysrhythmia)


Trachsel et al. (2013) Case–control


Fifteen healthy, 7 with mitral regurgitation


Conclusions


CTnI > 0.095 ng/mL in primary myocardial damage (sensitivity: 90.5%, specificity 100%). No significant differences with secondary myocardial disease


CTnI > 0.035 ng/mL sensitivity 70%, specificity 91% (1/3 assays tested)


CTnI > reference range in all horses with myocardial disease (7/7) and a proportion of horses with structural heart disease (7/25) or a lone dysrhythmia (2/17)


No ↑ CTnI with mitral regurgitation even when chamber enlargement


Conclusion


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.


Authors’ declaration of interests No conflicts of interests have been declared.


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