Recently sudden cardiac death (SCD) during exercise has received a lot of attention and has resulted in pre-participation screenings of human athletes in several countries. Among the reported diseases the screenings have also identified inherited rhythm disturbances as cause for cardiovascular incidences in at least 9% of the cases. Sudden death during exercise occurs also in horses, and 20-68% of such cases do not have structural lesions sufficient to account for death on necropsy and a cardiac origin is hypothesized.
Sudden deaths occurring during public events have a highly negative impact on the public perception about high performance sports, both in humans and in horses, and raise concerns about animal welfare especially in the racing industry. This bad publicity might affect the economy of the racing industry, an important economic factor for many European areas. Moreover, rider safety is also important in other equine disciplines and in leisure activities.
The inherited disturbances in the cardiac rhythm can be caused by mutations in ion channel encoding genes, resulting in altered expression of the channels or changes in their ability to conduct ions across the cell membrane. Drugs can also affect ion channel function. Several drugs have been withdrawn from the human drug market because of cardiac side effects and new drugs are tested for interactions with cardiac ion channels before release. But numerous drugs known in human medicine to induced cardiac arrhythmia are still widely used in veterinary medicine.
One of the known syndromes that is linked to an altered function of cardiac ion channels is the Long QT syndrome (LQTS). On the ECG it is recognized by an increased duration of the time interval between two deflections, namely the Q and T wave. Our objectives were to investigate whether LQTS exists in horses and whether this syndrome can explain some of the cases of SCD in horse.
In conclusion, we have found that the ion channels that account for approx. 80% of the LQTS cases in humans are functionally important for repolarisation in equine hearts, and we have verified that at least one equine drug results in a significant prolongation of the QT interval, suggesting that acquired LQTS exists in horses. But further investigations will have to show whether a prolonged QT interval in horses is associated with an increased risk of cardiac arrhythmia as in humans. But, our study raises the question about safety pharmacology in veterinarian medicine. Finally, our results suggest that there is a hereditary component of SCD in horses and that it is important to identify if certain genes can be linked to SCD. Overall, the impact of the project will increase animal welfare and rider safety, but also initiates studies on SCD, drug safety and on cardiac electrophysiology.
