Evolving FATE: A New Lens on the Pathogenesis and Management of Feline Cardiogenic Arterial Thromboembolism

Abstract

Feline cardiogenic arterial thromboembolism (FATE) remains one of the most devastating complications of feline cardiomyopathies, with high mortality and recurrence rates. Despite its clinical importance, significant knowledge gaps persist in our understanding of FATE's pathogenesis and optimal management strategies. Our review aims to address these gaps by providing a comprehensive overview of the current understanding of FATE, including disease mechanisms, risk factors, emerging diagnostics, and preventative strategies. Importantly, we identify key areas such as immunothrombosis, procoagulant platelets, platelet heterogeneity, and altered fibrinolysis where future research may yield novel biomarkers and therapeutic targets to improve outcomes in affected feline patients.

Keywords: clopidogrel resistance; echocardiogram; point of care testing; saddle thrombus.

Figure 1

Diagram summarizing the sequence of events leading to cardiogenic arterial thromboembolism. Aggregates of blood cells and fibrin polymers settle to form an intracardiac thrombus inside a diseased and enlarged left atrium (LA). The thrombus then dislodges, travels through the left ventricle (LV) and aorta (Ao) to embolize to distal arteries. The thrombus embolizes most commonly to the aortic bifurcation, causing partial or complete obstruction. Stenosis of the vascular lumen creates blood flow turbulence, which facilitates further thrombus growth. Arterial thrombosis leads to impedance of blood flow, tissue ischemia, necrosis, ischemic reperfusion injuries, and multiple organ failure.

Figure 2

Summary of Virchow’s triad and known causes and knowledge gaps of derangements of each component, which includes systemic hypercoagulability, blood flow stasis, turbulence, and endothelial injury. NETs—neutrophil extracellular traps, vWF—von Willebrand factor.

Figure 3

Representative images of echocardiograms in cats with hypertrophic cardiomyopathy. (A) Right parasternal short-axis view of the left ventricle (LV). Note the marked thickening of the LV free wall (* indicates the papillary muscle). (B) M-mode of the LV at the level of the papillary muscle in a normal cat and a cat with HCM. Note the significant reduction in LV diameter during diastole. (C) Right parasternal short-axis view at the level of the left atrium (LA) demonstrating marked LA enlargement (Ao = aorta). (D) An organized thrombus (arrow) is visible in the LA with marked chamber enlargement in an asymptomatic cat with HCM. (E) Pulsed Doppler tracing from a cat without heart disease. Normal left auricular flow velocities showing mean emptying flow velocity of 0.8 m/s (arrow). The filling flow velocity is shown as an arrowhead. (F) Recorded pulsed Doppler tracing from a cat with HCM and left atrial enlargement showing low mean flow velocity (arrow).