Study of Causes and Diagnosis of Sudden Death in Racehorses (15-08)
Francisco A. Uzal, DVM, M.Sc., Ph.D., DACVP
Robert Poppenga, DVM, Ph.D., DABVT
Santiago S. Diab, DVM, DACVP
Ashley Hill, DVM, MPVM, Ph.D.
Rick Arthur, DVM
The number of equine sudden death cases in apparently healthy horses in California has increased over the past two years. This has created national and international negative attention on California horse racing, as sudden death adversely affects racehorse welfare, jockey safety and public perception of horseracing. Despite thorough post-mortem examinations and diagnostic work-ups, a definitive cause of death could not be established in approximately 50% of the cases of sudden death, although heart failure is suspected to be responsible for a large number of these deaths. Heart failure may be due to administration of substances such as cobalt (long known to cause cardiomyopathies in humans), vitamin B12 or levothyroxine (T4 thyroid hormone). However, no scientific evidence is available to support the claim that many of those horses die of heart failure and/or that those deaths are associated with the use of any particular substance.
This study facilitated the microscopic examination of the hearts of horses with sudden death and an equivalent number of horses euthanized due to catastrophic leg injuries (control group) in an attempt to find a correlation between sudden death and the presence of microscopic lesions in the heart.
Sudden death is a devastating event that severely affects all members of the equine industry and the public. This study found that non-inflammatory cardiomyocyte injury (myofibrillar degeneration and contraction band necrosis) was the most important lesion found at a higher prevalence in sudden death horses than in control animals. Inflammatory lesions, fibrosis and miscellaneous lesions were found at similar prevalence in sudden death and control horses. A baseline cardiac necropsy protocol was established. Finding specific lesions in the heart of at least some of those horses will provide a diagnostic tool to determine the mechanism of death in future cases of sudden death.
Additionally, no significant differences in T3, T4 or liver cobalt concentrations were found between study and control horses, which suggests that at least in the group of horses studied, these substances were not associated with the cause of sudden death. If future studies are able to determine if the administration of cobalt, vitamin B12 and/or levothyroxine are a contributing factor additional preventive tools could be developed to avoid future sudden deaths.
Identification of Asymptomatic Heart Disease in Racing Thoroughbreds and Impact on Performance and Risk for Sudden Cardiac Death (14-04)
Joshua Stern, DVM, Ph.D., DACVIM
Subtle evidence of heart disease may be subclinical in high-level athletes until evaluated after extreme exercise. Changes in blood parameters that indicate heart disease, cardiac arrhythmias and heart function as seen by cardiac ultrasound may all be indicative of subtle but significant heart dysfunction after exercise. This concept, termed exercise-induced cardiac fatigue, has been documented in performance horses but never evaluated in racing Thoroughbreds as a possible explanation for poor performance and sudden cardiac death.
This was the first study to document the cardiac biomarker, cardiac troponin I, electrocardiogram (EKG) and cardiac functional change that is expected in high-level competing Thoroughbreds. This study establishes expected changes in each of these variables and simultaneously identified that outliers exist within the population. These findings may be useful to identify screening tests that could be applied to Thoroughbred racehorses to identify those at risk of heart injury and even sudden cardiac death. With the recently reported increase in sudden death after racing, evidence for possible testing strategies is of paramount importance. This study suggests that a larger data set with long-term follow-up looking at pre- and post-race EKG parameters, as well as cardiac troponin-I, may represent a method to detect horses at risk for cardiac events.