Preventing and Treating Feline Arterial Thromboembolism (F.A.T.E)
What is F.A.T.E?
Feline arterial thromboembolism or FATE is a deadly complication of heart disease (cardiomyopathy) in cats. It is caused by dislodgment of blood clots formed inside an enlarged chamber, the left atrium. The most common location, where the clot travels to, is the aortic bifurcation. This causes turbulence of blood flow and growth of the thrombus. In severe cases, it causes complete obstruction of blood flow causing pain, tissue injuries and ischemic reperfusion injury. FATE can be seen in ~11% of cats with HCM and carries a poor prognosis. Despite treatment, mortality rate can be as high as 50% in the initial 48 hours. FATE remains one of the most significant contributors to morbidity and mortality in feline medicine.
Research to prevent F.A.T.E
Primary prevention is key to minimize clot formation in the first place. However, this requires prompt recognition of at-risk cats and optimal therapies.
Current guidelines recommend treatment with the antiplatelet drug, clopidogrel, in cats at-risk of FATE. Platelets are small white blood cells responsible for clot formation and our laboratory has demonstrated that platelets are activated or hyperreactive in cats with cardiomyopathies. https://www.frontiersin.org/journals/veterinary-science/articles/10.3389/fvets.2022.892377/full
However, not all cats respond to clopidogrel the same way and a one-size-fits-all approach in primary prevention likely does not provide optimal protection in all at-risk cats. A genetic mutation has been found in cats, which affects their response to the drug, rending it less effective.
Finding the optimal prevention strategy
The optimal therapies to prevent FATE in the first place have not been found in veterinary medicine. However, studies are ongoing to evaluate existing or novel drugs.
Ongoing studies
Novel phosphodiesterase 3 inhibition to tackle immunothrombotic platelet priming and activation in cats
Inhibition of platelet-neutrophil interaction using a shear-induced in vitro model of cardiogenic arterial thromboembolism
In vitro and ex vivo effects of rapamycin on platelet activation and procoagulant platelet formation in cats