These data indicate that cardiac stress may occur in horses associated with endurance exercise. Future studies utilising echocardiograpy to assess cardiac function in horses with increased cTnI are warranted.

This study evaluated the effects of exercise on cardiac troponin I (cTnI) concentrations in healthy, adult horses. Fifteen fit, healthy horses determined to have a normal cardiovascular system completed a standardized exercise test on a high-speed treadmill. Heparinized blood was collected for plasma cTnI concentrations before maximal exercise, and 1, 3, 6, 9, 12 and 24 h post-exercise. The cTnI concentrations were measured with a commercial system (Stratus CS, Dade Behring, Inc.). Results were analysed by a multivariate ANOVA, where indicated post hoc analysis was done by Tukey-Kramer HSD and significance was placed at p , 0.05.All horses had elevations in cTnI concentrations after maximal exercise. Values for cTnI trended higher at 3 h (0.066^0.011 ng ml 21 ) and 6 h (0.062^0.011 ng ml 21 ) post-exercise compared with pre-exercise (0.039^0.007 ng ml 21 ), although this did not reach statistical significance. Mean cTnI concentrations were within our normal reference range at all time points, although four individuals were above our normal range after exercise.These data show that short-term, high-intensity exercise induces a small rise in plasma cTnI in normal horses. This should be kept in mind when evaluating cTnI concentrations in horses that have recently completed intense exercise. In addition, these data suggest that 3-6 h after intense exercise may be the optimal time for measurement of cTnI concentrations in horses with suspected exercise-induced myocardial damage.

Background: Myocarditis is thought to occur secondary to equine influenza virus (EIV) infections in horses, but there is a lack of published evidence. Hypothesis/Objectives: We proposed that EIV challenge infection in ponies would cause myocardial damage, detectable by increases in plasma cardiac troponin I (cTnI) concentrations. Animals: Twenty‐nine influenza‐naïve yearling ponies: 23 were part of an influenza vaccine study (11 unvaccinated and 12 vaccinated), and were challenged with 108 EID50 EIV A/eq/Kentucky/91 6 months after vaccination. Six age‐matched healthy and unvaccinated ponies concurrently housed in a separate facility not exposed to influenza served as controls. Methods: Heparinized blood was collected before and over 28 days after infection and cTnI determined. Repeated measures analysis of variance, chi‐square, or clustered regression analyses were used to identify relationships between each group and cTnI. Results: All EIV‐infected ponies developed clinical signs and viral shedding, with the unvaccinated group displaying severe signs. One vaccinated pony and 2 unvaccinated ponies had cTnI greater than the reference range at 1 time point. At all other times, cTnI was <0.05 ng/mL. All control ponies had normal cTnI. There were no significant associations between cTnI and either clinical signs or experimental groups. When separated into abnormal versus normal cTnI, there were no significant differences among groups. Conclusions and Clinical Importance: This study demonstrated no evidence of severe myocardial necrosis secondary to EIV challenge with 108 EID50 EIV A/eq/Kentucky/91 in these sedentary ponies, but transient increases in cTnI suggest that mild myocardial damage may occur.