Heritability of sudden cardiac death in Thoroughbred racehorses.

BACKGROUND: Sudden cardiac death (SCD) is an important cause of exercise-associated fatalities in Thoroughbred racehorses. Equine deaths share similarities with fatalities in human athletes that result from inherited cardiac disease. Whilst genetic causes have been postulated in horses, these have not been confirmed and heritability of SCD has not previously been estimated in Thoroughbred racehorses. OBJECTIVES: To determine the heritability of SCD in a sample population of Thoroughbred racehorses. STUDY DESIGN: Retrospective case-control study. METHODS: Steward and post-mortem reports of Thoroughbred racehorses in Australia between 2007 and 2020 were reviewed to identify horses with SCD. Control horses were randomly selected from races in which SCD occurred or from races on the date of the case fatality. A five-generation integrated pedigree chart was collected for each horse. Estimates of heritability were obtained using an animal model in the ASReml-R program with variance components estimated assuming SCD was normally distributed, and on the logit transformed scale. Inbreeding coefficients were calculated and the risk of producing SCD-affected progeny was calculated for stallions that sired ≥5 individuals in the case-control population. RESULTS: Ninety-three horses with SCD and 465 control horses were identified. Heritability on the underlying scale was 0.15 ± 0.09 (logit animal) and 0.24 ± 0.12 (normal animal). Inbreeding coefficients were not significantly different between groups. Of the 16 first generation sires that appeared ≥5 times in the case-control data set, two sires more frequently produced affected progeny (OR 7.95-10.41). MAIN LIMITATIONS: Challenges in definitively confirming SCD may lead to misclassification of some cases. Some control horses may have not been exposed to environmental influences of SCD. Case numbers are low and the studied population may not represent the entire Thoroughbred genetic pool. CONCLUSION: The heritability of SCD in this population was relatively low. However, individual stallions appear more likely to produce affected progeny. Further studies are required to understand the genetic and environmental influences that contribute to disease expression.

Associations between postrace atrial fibrillation and measures of performance, racing history and airway disease in horses.

BACKGROUND: Atrial fibrillation (AF) is the most common performance limiting arrhythmia in racehorses. High dose exercise and airway disease promote AF in humans. Few studies have investigated epidemiological factors associated with AF in horses. OBJECTIVES: Explore variables relating to performance, exercise volume and postrace endoscopic findings in horses with AF. ANIMALS: A total of 164 horses with poor race performance and postrace AF were compared to 321 horses with poor performance without AF (PP) and 314 horses performing to expectation (TE). METHODS: Horse-level and race-level variables for horses racing in Australia and Hong Kong from 2009 to 2021 were compared using univariable and multivariable logistic regression. Postrace endoscopic exercise-induced pulmonary hemorrhage (EIPH) and tracheal mucus accumulation (TMA) grades for AF and PP horses were compared using chi-squared analysis. RESULTS: Variables that were significant in the multivariable model of AF compared to TE were distance (lengths) behind the winner, (odds ratio [OR]; 95% confidence interval [95% CI], 1.41 [1.32-1.51], P < .0001), cumulative prize money per start before the event (OR [95% CI] 1.02 [1.01-1.03], P = .01) and age (OR [95% CI] 0.72 [0.55-0.92], P = .01). More AF horses had EIPH grade ≥ 3 (23/109; 21.1%) than PP horses (7/213; 3.3%; OR [95%CI] 7.9 [3.3-20.2], P < .0001). CONCLUSIONS AND CLINICAL IMPORTANCE: Acute race performance was substantially impaired by AF but career earnings before the event were not inferior. Exercise volume did not promote AF. Higher grades of EIPH found in AF horses suggests a mechanistic relationship between these conditions.

Assessment of P Wave Indices in Healthy Standardbred Horses.

P wave indices are used as non-invasive electrocardiographic markers of atrial remodelling in humans. Few studies have investigated their use in animals. The aim of this study was to measure P wave duration and P wave dispersion (Pd) in healthy standardbred horses and investigate variables that might influence these measurements. A 12-lead electrocardiogram was recorded at rest and P wave indices were calculated in 53 horses. A general linear model was used to investigate the main effects: age, bodyweight, sex, resting heart rate, presence of a murmur, exercise status and the number of years raced. There were significant associations with exercise status for both the maximum P wave duration and Pd, with both values being increased in strenuously exercising versus non-active horses. Furthermore, a significant moderate positive correlation was identified between the duration of exercise (number of years raced) and both Pmax and Pd. No other significant associations were identified. These findings are similar to those reported in elite human athletes versus sedentary individuals. The increases in these P wave indices most likely occur due to prolongation and heterogeneity in atrial conduction time, which are associated with structural and electrical remodelling, and may explain the increased risk of atrial fibrillation in athletic horses.

Risk Factors for Exercise-Associated Sudden Cardiac Death in Thoroughbred Racehorses.

Cardiac arrhythmias resulting in sudden cardiac death (SCD) are an important cause of racehorse fatalities. The objective of this study was to determine risk factors for SCD in Thoroughbreds by evaluating a sample with a policy of mandatory post-mortem following racing or training fatalities. Risk factors were compared between case horses with SCD (n = 57) and control horses with other fatal injury (OFI, n = 188) by univariable and multivariable logistic regression. Survival in years for horses with SCD was compared to OFI using the Kaplan−Meier method with log rank test. The following variables were most important in the multiple logistic model: Horses with SCD were more likely to die during training than during racing, SCD (42/57, 74%) vs. OFI (82/188, 44%; odds ratio [OR], 95% confidence interval [CI], 2.5, 1.2−5.4; p = 0.01), had fewer lifetime starts, median (interquartile range [IQR]), SCD (3.0 [0.0−9.0]) vs. OFI (9.0 [0.0−22.8]; OR, 95% CI, 0.96, 0.9−1.0; p = 0.02 and were less likely to be entire (uncastrated) males, SCD 9/57 (16%) vs. OFI (46/188, 25%; OR, 95% CI, 0.47, 0.1−0.9; p = 0.03). Survival in years (median (IQR)) for horses with SCD was 3.6 (3.1−4.4), which was shorter than OFI (4.5 [3.1−6.0], hazard ratio, 95%CI, 1.6,1.2−2.3; p < 0.001). SCD occurs more commonly in training than racing, which suggests exercise intensity is less important in precipitating this fatality. In this study, SCD occurred early in the careers of affected horses.

Incidence, recurrence, and outcome of postrace atrial fibrillation in Thoroughbred horses.

BACKGROUND: Atrial fibrillation (AF) impacts performance and horse and jockey safety. Understanding the outcomes of AF identified postrace will better inform regulatory policy. HYPOTHESIS/OBJECTIVES: To investigate the outcomes after episodes of AF identified postrace and determine whether affected horses are at increased risk of additional episodes compared to the general racing population. ANIMALS: Total of 4684 Thoroughbred racehorses. METHODS: Race records for Thoroughbred horses racing in Hong Kong from 2007 to 2017 were reviewed. Horses that performed below expectation were examined by cardiac auscultation and ECG. Incidence and recurrence of AF were compared between horses with and without a history of AF and between horses with paroxysmal and persistent episodes using Fisher's exact test. RESULTS: There were 96 135 race starts during the study. Atrial fibrillation was identified in 4.9% of horses, with an overall incidence of 2.7 episodes per 1000 starts. The incidence of AF in horses after any previous episode (12.8 per 1000 starts) was higher than for horses with no previous episode (2.4 per 1000 starts; odds ratio [OR], 5.3; 95% confidence interval [CI], 3.8-7.6). Recurrence was seen in 64% of horses previously treated for persistent AF, which was higher than recurrence in horses with paroxysmal AF (23%; OR, 5.9; 95% CI, 1.6-21.2). Median duration between episodes was 343 days (range, 34-1065). CONCLUSIONS AND CLINICAL IMPORTANCE: Thoroughbreds are at increased risk of recurrent AF after both paroxysmal and persistent episodes, but the duration of time between episodes varies widely. These findings support a substantial burden of AF among individual Thoroughbred racehorses.

Clinicopathologic evidence of myocardial injury in horses with acute abdominal disease.

OBJECTIVE: To determine whether there is evidence of myocardial injury in horses with acute abdominal disease. DESIGN: Prospective case series. ANIMALS: 18 healthy horses and 69 horses with acute abdominal disease. PROCEDURES: 18 healthy horses had been admitted to the hospital for investigation and were assigned to group 1. Horses examined for acute abdominal disease were assigned to 3 groups: strangulating obstruction, nonstrangulating obstruction, or inflammatory disease (groups 2, 3, and 4, respectively). Heart rate, Hct, and blood lactate and cardiac troponin I (cTnI) concentrations were measured at initial examination. Myocardial function was assessed by echocardiographic measurement of fractional shortening and left ventricular ejection time (LVET). Heart rhythm was evaluated via ECG. RESULTS: The proportion of horses with high (> 0.03 ng/mL) cTnI concentration was significantly greater among horses with strangulating (9/25 [36%]) or inflammatory (9/19 [47%]) lesions, compared with healthy horses (0/18). The proportion of horses with high cTnI concentration was significantly greater among nonsurvivors (12/24 [50%]) than among survivors (10/45 [22%]). Serum cTnI concentration was positively correlated with Hct, heart rate, and blood lactate concentration and negatively correlated with LVET. CONCLUSIONS AND CLINICAL RELEVANCE: Evidence of myocardial injury was observed in horses with acute abdominal disease, and this injury was associated with severity of illness. Recognition of myocardial injury could improve treatment of acute abdominal disease in horses.

Use of stored equine colostrum for the treatment of foals perceived to be at risk for failure of transfer of passive immunity.

OBJECTIVE-To assess the use of stored equine colostrum for the treatment of foals perceived to be at risk for failure of transfer of passive immunity (FTPI). DESIGN-Cohort study. ANIMALS-232 Thoroughbred foals and 191 Thoroughbred mares (41 mares gave birth to 1 foal on 2 occasions). PROCEDURES-Postpartum, presuckle colostrum samples were collected from mares; samples with a colostral refractive index (cRI) > or = 23% were frozen (-20 degrees C [-4 degrees F]) and stored for > or = 7 days but < 2 years. Foals of dams that produced colostrum with a cRI value < 20% were treated with > or = 300 mL of stored colostrum that was thawed and administered via nasogastric tube on 1 to 4 occasions within 6 hours after parturition. Serum samples were obtained from colostrum-treated and nontreated foals 24 hours after treatment or suckling, respectively, for determination of serum IgG (sIgG) concentration. RESULTS-8 foals and their respective dams were excluded from the analyses. For the remaining 30 treated and 194 nontreated foals, mean +/- SD sIgG concentration was 1,597 +/- 574 mg/dL. Thirteen (5.8%) foals had sIgG concentrations < 800 mg/dL, of which 1 (0.4%) had an sIgG concentration < 400 mg/dL. Nine of these foals had suckled mares producing colostrum with a cRI value > or = 20%, and 2 foals had been treated with stored colostrum. CONCLUSIONS AND CLINICAL RELEVANCE-Treatment with stored colostrum appeared to be effective for prevention of FTPI in at-risk foals. However, foals were still at risk for FTPI despite suckling of or treatment with colostrum with adequate cRI values.