PhD candidate University of Adelaide Kew, Victoria, Australia
Abstract:
Background: Athletic horses have a high prevalence of cardiac arrhythmia in the absence of structural heart disease. The underlying triggers and substrate for arrhythmia in this species are not well studied.
Hypothesis: Thoroughbred racehorses will have myocardial fibrosis, increased myocyte diameter, and a greater density of fibroblasts compared to untrained horses.
Animals: Thoroughbred racehorses, comprising 15 that died from sudden cardiac death (SCD) and 18 that died from other fatal injuries (OFI), were compared to 10 healthy untrained (UT) wild horses.
Methods: Cardiac tissues were sampled during post-mortem. OFI and UT were age matched to the SCD group. Two atrial and three ventricular sites were stained with Sirius red for assessment of myocardial fibrosis and triple antibody stain (WGA, vimentin, and GS-IB4) for myocyte diameter and fibroblast density. Measurements were made by a blinded operator using automated analysis with commercial software. Results were tested for normality using the Shapiro-Wilk test and differences assessed with one-way ANOVA with multiple comparisons.
Results: SCD had a greater fibrosis proportion compared to UT at 4/5 examined sites. UT had reduced myocyte diameter at 5/5 sites compared to SCD or OFI. There were no significant differences between SCD and OFI for either fibrosis proportion or myocyte diameter and there were no differences between any group for fibroblast density.
Conclusions and clinical importance: Thoroughbred racehorses have histological myocardial hypertrophy. Myocardial fibrosis is pronounced in SCD, and this could be a substrate for arrhythmia. The absence of increased fibroblast density might suggest underlying chronic fibrotic remodelling.
