
Feline Aortic Thromboembolism
🐾 Comprehensive Information on Feline Aortic Thromboembolism (FATE / CATE) for NAVLE Preparation 🐾 Feline Aortic Thromboembolism (FATE), also known as Cardiogenic Arterial Thromboembolism (CATE) or “saddle thrombus,” is a life-threatening condition in cats characterized by the embolization of a cardiac thrombus—most often originating in a dilated left atrium—into systemic arteries, especially the terminal aorta. It is most commonly associated with underlying cardiomyopathies, particularly Hypertrophic Cardiomyopathy (HCM). Affected cats present acutely with hindlimb paralysis, pain, absent pulses, and hypothermia due to ischemic neuromyopathy. This condition is a true emergency requiring rapid diagnosis, stabilization, and aggressive multimodal treatment to reduce morbidity and mortality. This note provides a detailed and clinically focused overview of the etiology, pathophysiology, clinical signs, diagnostic approach, treatment options (including anticoagulation and thrombolysis), prognosis, and preventive strategies. It is intended to prepare veterinary professionals for recognizing and managing FATE with confidence during the NAVLE and in clinical practice.
🐱 Comprehensive Information on Feline Aortic Thromboembolism (FATE / CATE) for NAVLE Preparation
🔍 Definition and Overview
Feline Aortic Thromboembolism (FATE), also referred to as Cardiogenic Arterial Thromboembolism (CATE) or "saddle thrombus," is a life-threatening condition characterized by the embolization of a cardiac thrombus—most commonly from the left atrium—to the distal aortic trifurcation. It results in acute ischemia of the pelvic limbs and, less commonly, other systemic arteries.
Prevalence:
~1 in 175 cases in US tertiary centers
~1 in 379 in UK general practices
Primary cause: Cardiomyopathy in ~90% of cases
Most common: Hypertrophic Cardiomyopathy (HCM)
Others: Dilated Cardiomyopathy (DCM), Restrictive Cardiomyopathy (RCM), Unclassified Cardiomyopathies
⚙️ Pathophysiology
FATE results from Virchow’s triad:
Blood stasis: Due to poor left ventricular filling, leading to left atrial dilation and stagnation.
Endothelial injury: Damage to atrial endocardium promotes platelet activation and adhesion.
Hypercoagulable state: Includes:
↑ Platelet hypersensitivity
↓ Antithrombin and Protein C
↑ Factor VIII and fibrinogen
🧬 Thrombus Formation:
Platelet-rich → fibrin-rich thrombus within left atrium
Embolizes to:
Aortic trifurcation (70–75%) → Bilateral hindlimb infarction
Unilateral pelvic limb (10–15%)
Brachial arteries (~10%)
Less common: renal, cerebral, mesenteric arteries
🚨 Clinical Signs
Classic “5 Ps” of acute limb ischemia:
Paresis/paralysis
Pulselessness
Pallor (cyanotic nail beds)
Pain
Polar (cold limbs)
🩺 Other signs:
Hindlimb rigidity, absent reflexes, firm painful musculature
Hypothermia
Respiratory distress (from CHF or cardiomyopathy)
Signs of underlying heart disease (dyspnea, gallop rhythm, murmurs)
Neurologic deficits (if emboli affect CNS)
Acute renal failure (renal infarction)
🧪 Diagnostics
Clinical Examination:
Sudden onset of hindlimb paresis/paralysis
Cyanotic, cold limbs
Absent femoral pulses
Pain response in affected limb
Point-of-Care Ultrasound (C-POCUS):
Enlarged left atrium
Visualization of intra-atrial thrombi
Identification of underlying cardiomyopathy
Imaging:
Thoracic radiographs: Evaluate pulmonary edema or CHF
Echocardiography: Assess atrial size, myocardial structure
Laboratory Findings:
↑ CK, AST, ALT (muscle enzymes)
Azotemia (pre-renal or renal)
Hyperkalemia, hyperglycemia, metabolic acidosis
Elevated lactate in affected limbs (especially >11.5 mmol/L = poor prognosis)
Hypocalcemia, hypercholesterolemia
💊 Treatment
1. Acute Emergency Management
Analgesia:
Methadone, fentanyl CRI, buprenorphine, oxymorphone
Cardiopulmonary Stabilization:
Oxygen supplementation
Furosemide if pulmonary edema is present
Thromboprophylaxis:
Anticoagulants:
Unfractionated Heparin (UFH):
250–375 IU/kg IV loading dose
150–250 IU/kg SC q6–8h
Low Molecular Weight Heparins (LMWH):
Dalteparin: 100 IU/kg SC q12h
Enoxaparin: 1.0–1.5 mg/kg SC q12h
Thrombolytics (controversial):
Tissue Plasminogen Activator (t-PA):
0.25–1 mg/kg/hr IV infusion
Total dose 1–10 mg/kg
High risk of bleeding; no definitive survival benefit
Reperfusion Injury Monitoring:
Hyperkalemia
Acidosis
Bradyarrhythmias → ECG monitoring critical
2. Chronic Management & Prevention of Recurrence
Antiplatelet Therapy:
Clopidogrel: 18.75 mg PO q24h (first-line)
Aspirin: 5 mg/cat PO q48h (less effective)
Oral Anticoagulants:
Rivaroxaban: 0.5–1 mg/kg PO q24h
Apixaban: Alternative, dose varies
Dual Therapy:
Clopidogrel + Rivaroxaban offers best protection against recurrence
Warfarin:
0.06–0.09 mg/kg PO q24h
Requires close INR monitoring (target: 2–3)
Supportive Care:
Nutritional support
Passive range-of-motion physiotherapy
Management of concurrent CHF or cardiomyopathy
📊 Prognosis
Variable; depends on:
Number of limbs affected
Initial motor function
Rectal temp <37°C = poor outcome
Limb lactate >11.5 mmol/L = grave prognosis
Survival to discharge (bilateral): ~37.5%
Median survival post-discharge: 350–500 days
⚠️ Complications
Reperfusion injury: Hyperkalemia, acidosis, arrhythmias
Chronic ischemia: Risk of muscle necrosis, contracture, limb amputation
Acute kidney injury (from myoglobinuria or hypotension)
✅ Key Takeaways for NAVLE
FATE is often the first clinical manifestation of cardiomyopathy in cats.
Left atrial thrombus is the origin in >90% of cases.
Classic “5 Ps” help identify ischemic neuromyopathy.
First-line treatment includes clopidogrel; dual therapy is best for recurrence prevention.
Acute management must include analgesia, anticoagulation, and CHF stabilization.
Prognosis is guarded to poor, especially with bilateral involvement and hypothermia.
📚 References
Guillaumin, Julien. Feline aortic thromboembolism: recent advances and future prospects. Journal of Feline Medicine and Surgery. 2024.
Kittleson, M. D., & Côté, E. (2021). The feline cardiomyopathies II: Hypertrophic cardiomyopathy. Journal of Veterinary Cardiology.
Merck Veterinary Manual. Heart Disease and Thromboembolism in Cats.

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