This thesis is an investigation into the possible genetic background underlying the liability of Standardbred racehorses (Std) to atrial fibrillation (AF). Pedigrees of 204 affected Std admitted to the Ontario Veterinary College Teaching Hospital (OVCTH) for treatment of AF born from 1978 to 2007 and of 1,017 randomly selected racing contemporaries (5 for each Std admitted). Estimates of heritability of AF were obtained using a linear threshold animal model. Marginal genetic contributions of ancestors to affected and control cohorts were determined and differences were tested. The estimate of heritability of AF in the Std was 14% on the observed scale. Eleven ancestors had significantly higher contributions to affected cohorts than to controls. Many of these ancestors appeared multiple times in the five-generation pedigrees of affected horses. Results strongly indicate a genetic predisposition to AF in the Std, with the arrhythmia particularly prevalent in one popular sire line.

Observed and expected heterozygosity (H) levels for ten electrophoretic blood marker loci and expected H for seven red blood cell (RBC) anitgen/antibody loci were examined for 20 years in American Standardbred and 30 years in American Saddlebred horses. Standardbreds were classed by gait, Trotter and Pacer, and evaluated separately in most analyses. 4,404 Trotters and 12,271 Pacers were found to have statistically highly significant losses of mean total observed H through time for the ten electrophoretic loci (P<0.005), although in Trotters the loss was more extreme (P<<0.001). Loss of H in 5984 Saddlebreds was not significant (P=0.259). Correlations of RBC expected H through time showed decreases in all three groups.