Cardiac Troponin I in Standardbred Racehorses

Abstract

We investigated the use of cardiac troponin I (cTnI) assays in horses and their application in detection of exercise-associated myocardial damage. Available assays were designed for use in humans; therefore, study phase I involved analytical validation of current assays in the horse. Linearity, limit of quantification, and short and long-term precision were evaluated using the American Society for Veterinary Clinical Pathology (ASVCP) guidelines, with equine myocardium and serum as test substrates. Two assays, including a high-sensitivity assay, underwent full analytical validation and performed with clinically acceptable accuracy and precision. Linearity was evaluated in 2 additional assays and was found to be within acceptable limits. Equine cTnI was not detected by 1 assay, and recovery was poor in a second. Appropriate choice of validated assays is essential for clinically valid decision making. Validated contemporary and high-sensitivity assays were used in phase II to establish the normal post-exercise cTnI release curve. Moderate increase in cTnI concentration of limited duration was detected within 1 hour post-exercise and peaked at 2-6 hours. Concentrations returned to near baseline within 24 hours. In phase III horses were sampled pre and post-race in conjunction with ECG monitoring to investigate the cTnI exercise response. Associations between resting and post-race cTnI concentration, demographic variables, and race variables were investigated using multivariable linear regression models. Moderate increase in cTnI of limited duration was detected in most horses monitored, but some developed elevations suggesting myocardial damage. Concentrations increased significantly with age and were higher in trotters than pacers. Post-race cTnI concentrations were significantly increased with presence of exercise-associated complex ventricular arrhythmia and finishing distanced relative to either condition alone or the absence of both. Results were consistent with exercise-induced myocardial damage, though causation could not be confirmed and the clinical significance of these findings is unknown. Further longitudinal studies are needed to investigate associations and establish causation. Equine clinicians should be aware of the presence and timing of exercise-associated cTnI release when evaluating horses post-exercise. Some cTnI elevation may be a usual feature of the response to maximal effort in the horse.