Determining the Fate of Feline Aortic Thromboembolism

FATE can be the first sign of heart disease in cats- but it has also been associated with other causes, such as neoplasia, thyroid disease or endocrine disease. The major cause of FATE (about 90% of cases) is due to cardiomyopathy, and is the focus of Staff Veterinarian Jennifer Gorman’s, DVM, article.

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Feline aortic thromboembolism affects approximately 25-30 percent of cats with heart disease. Thrombus formation occurs secondary to stagnation of blood in a dilated left atrium (blood stasis), the highly reactive state of feline platelets (hypercoagulability), and endothelial lesions or damage. Clots can remain static, grow and interfere with outflow to the left ventricle, or break apart and lodge in downstream vessels. The most common location for thromboembolism is the aortic trifurcation, or terminal aorta (estimated 90 percent). Other locations include brachial, visceral (renal or mesenteric) or cerebral arteries.

Not only is the artery where the clot lodges occluded, but the collateral circulation is impaired, causing severe tissue ischemia and risk of reperfusion injury. For this reason, it is recommended to monitor renal function, serum electrolytes (especially for hyperkalemia), and lactate during the crisis stage. Additionally, elevations in creatine kinase and metabolic acidosis may be seen. Note that blood work should not be performed blood samples obtained from limb(s).


Classic presenting signs of distal aortic thromboembolism (“saddle thrombus”) are paresis or paralysis of one or both hind limbs. The right fore limb is commonly affected with brachial embolism. Femoral pulses are weak or absent with aortic thromboembolism. Rear footpads are often cool to the touch and discolored (can be described as “dusky” or pale). There is often a decreased rectal temperature and significant pain. Approximately 50 percent of cats presenting for FATE will show signs of concurrent congestive heart failure (CHF) – dyspnea, pulmonary crackles, and cyanosis. It is worth noting that not all cats with FATE or those in CHF will demonstrate cardiac murmurs or arrythmias.

Often the described clinical findings above can be evidence enough to suspect FATE. Echocardiography can confirm heart disease and the presence of a thrombus in the left atrium. Spontaneous contrast (“smoke”) in the left atrium may be observed as a precursor to clot formation. When bedside echocardiography (TFAST) is used in the ER setting, identification and visualization of heart disease, an atrial clot or thrombus in the distal aorta is directly correlated with the skill and comfort level of the clinician. While thoracic radiography may be helpful in identifying cardiomegaly (and thus suspicion for heart disease) and evidence of CHF, it cannot diagnose FATE. When imaging access is limited, measurement of glucose and lactate in the affected limb as directly compared to the central blood supply or a non-affected limb can be used to help support suspicions. Glucose will be lower, and lactate higher, in the affected limb compared to the central or unaffected supply. Thermography, where a thermal camera is used to determine difference between affected and non-affected limb temperature, is a newer, non-invasive diagnostic technique that may become more prevalent in the animal medical setting. Currently for humans, it is considered an accurate imaging technique for diagnosis of thrombosis.


Thrombolytic therapy is the standard of care for acute thromboembolism in humans with stroke or pulmonary thromboembolism, however, it is infrequently utilized in FATE. This may be due to lack of availability and expense.

The primary thrombolytic agents include streptokinase and tissue plasminogen activator (TPA). In humans, survival and functional outcome improves with intravenous TPA up to six hours after an acute ischemic stroke. Past studies in cats have suggested that TPA may shorten the time to perfusion and ambulation and improve motor function. More recent studies have not yet shown a statistical difference in survival rate or clinical improvement.

Anticoagulant therapy is recommended to decrease worsening of the thrombus. Options include unfractionated heparin (UFH), low‐molecular‐weight heparin (LMWH), aspirin, clopidogrel or warfarin. There is no veterinary specific data to support any anticoagulant over the other.

Platelet inhibitors include aspirin which has variable dosing recommendations. The FATCAT study investigated an aspirin dose of 25 mg/kg (or 81 mg per cat) every three days, versus clopidogrel dosed at 18.75 mg/cat PO q 24 hours on the recurrence rate of ATE in cats

Cats with FATE have been shown to have a worse prognosis where aspirin or clopidogrel was not part of their maintainence therapy. In the prospective clinical trial evaluating secondary prevention of FATE in cats, Feline Arterial Thromboembolism: Clopidogrel vs. Aspirin Trial, clopidogrel was shown to be superior to aspirin with an ATE recurrence rate of 49 percent (versus 75 percent) and a one‐year recurrence rate of 36 percent (versus 64 percent). Clopidogrel was also associated with longer median time to ATE event (443 days) compared with aspirin (192 days).

Surgical treatment (embolectomy) is not recommended due to high risk of death during the procedure and potential re-embolization post procedure.

Ancillary treatments include those for pain relief (recommend full mu opioids in the acute setting and buprenorphine on discharge), cardiac disease and congestive heart failure (oxygen supplementation, furosemide and others), and reperfusion injury (treatment of hyperkalemia when indicated).


Prognosis is variable based on patient baseline characteristics, available treatment options and clinician experience. Survival to hospital discharge is approximately 50 percent. This may be biphasic in distribution where patients with no motor, no pulses, and two or more affected limbs have a 20 to 30 percent survival rate, and patients with motor, pulses and/or only one limb affected have a 60 to 70 percent survival to discharge rate. Cats with lower body temperature, decreased heart rate and concurrent CHF are also considered to have a lower prognosis. Those that develop life-threatening hyperkalemia and acute kidney injury are considered to have a lower prognosis.

The chance of re-embolization is approximately 50 percent and average time for re-embolization is roughly six months. Half of the cats will die within three to six months and mean survival time can be up to one year with therapy. Once beyond the acute crisis phase, with no life-threatening reperfusion injury in the following two to three weeks (distal extremity necrosis, dry gangrene or muscle retraction requiring amputation, which occurs in about five percent of cases), survival is considered similar to those cats with congestive heart failure, six to 12 months.

Pulses have been reported to return within three to five days, but may take up to two to three weeks to return. Neuromuscular function and ambulatory abilities may take weeks to months to resolve.

Euthanasia should be considered in patients with extreme or uncontrolled pain, and combination of complete paralysis and severe congestive heart failure, as prognosis is considered poor.


FATE is one of the more common devastating conditions in cats that an emergency clinician willevaluate. DoveLewis Veterinary Emergency and Specialty Hospital has reported 48 of these cases in the last year (2017).The following is a case description of a recent patient who was presented to the emergency room at DoveLewis. Duke is an 11-year-old male domestic long-haired cat. Owners reported an acute onset vocalization and inability to use either of his hind legs. Duke is an indoor only cat with no history of trauma or previous pertinent medical history.


Presenting examination:

Hypothermia with temperature of 97.9, normal HR of 180 bpm, and moderate tachypnea of RR 68 bpm with mild increased respiratory effort. On auscultation, lung sounds are mildly increased with no crackles. No audible heart murmur or arrythmia is present. Initial blood pressures obtained revealed doppler 42 mmHg measured on the tail, and doppler 120 mmhg measured in a fore limb. Resting in lateral recumbency, and when lifted upright, able to ambulate with moderate weakness/dropped hock gait in the pelvic limbs, and a pronounced (estimated grade 2-3/4) lameness in the left pelvic limb. Femoral pulses are absent bilaterally, and pelvic limb paw pads are symmetrically cool to the touch (paw pads are pigmented, so color change was not evaluated). Duke became fractious and resistant to handling following his initial evaluation.


Initial therapy:

Methadone 0.2 mg/kg IV

Supplemental oxygen at 40 percent

Following radiograph review, Furosemide ~1 mg/kg IM

Butorphanol 0.25 mg/kg IM and Acepromazine 0.02 mg/kg IM administered to facilitate IV catheter placement

Methadone 0.3 mg/kg IV and Midazolam 0.2 mg/kg IV to facilitate cardiology consult with echocardiogram


Initial diagnostics:

Two-view thoracic radiographs: Moderate to severe cardiomegaly with moderate unstructured interstitial infiltrate bilaterally, consistent with cardiogenic pulmonary edema. Figure 1: Lateral thoracic radiograph

Echocardiogram: Moderate concentric left ventricular hypertrophy, marked dilation of the left atrium, and severe spontaneous echo contrast in the left atrial appendage (highly suspect thrombus) Figure 2

CBC: unremarkable

PCV/TS: 40/7.5, clear serum

Chemistry: Stress hyperglycemia of 226 mg/dL (74-159), CK elevation of 1115 mg/dL (0-314), otherwise unremarkable



Hypertrophic cardiomyopathy with likely distal aortic thromboembolism


Therapy in the ICU:

Oxygen supplementation at 40%

Furosemide 1 mg/kg IV q8hr while in hospital

Clopidogrel 18.75 mg PO q24hr

Enoxaparin 1 mg/kg SC q8hr while in hospital

Methadone 0.2 mg/kg IV q4hr for the first 24 hours, then transitioned to Buprenorphine 0.012 mg/kg IV/PO q8hr


Diagnostic monitoring:

Electrolytes q8hr

Partial chemistry (BUN, Cre, electrolytes, PCV/ts) rechecked 24 hours after presentation


Figure 1. Lateral Thoracic Radiograph


Figure 2.Echocardiogram image with thrombous in left atrial appendage

While owners were committed to diagnosing and treating Duke’s condition, finances dictated that Duke was discharged as soon as he was no longer oxygen dependent. Duke spent 29 hours in the hospital prior to discharge. By the time of discharge, he was eupneic on room air, was comfortable on buprenorphine analgesia, and was eating readily. His bilateral hind limb weakness was persistent but improving, and his left rear lameness had improved to grade 1-2/4. His mobility was good, and he was able to move around his kennel and use his litter box consistently. His femoral pulses were bilaterally faint but present. Both rear paw pads were warm to the touch; however, the right was notably warmer than the left. No hyperkalemia was noted on recheck of potassium levels while in hospital. BUN and Cre both increased to high end of normal range on recheck 24 hours from admit labwork, consistent with furosemide administration.


Duke was discharged home with clopidogrel 18.75 mg PO SID, furosemide 1.2 mg/kg PO BID, and buprenorphine 0.012 mg/kg transmucosally TID for three to four days. An echocardiogram follow up (or a recheck with their general practice veterinarian) was recommended five to seven days later to reassess clot formation. At the time of writing, Duke is reported to be doing well and has continued improvement at home.

While Duke’s case may be on the lower end of the severity spectrum, it remains encouraging that he has been given additional quality time at home with his family. He is also a good reminder that these cases can have a positive outcome, and may deserve more enthusiasm for treatment than they may have previously received.


Resources/Suggested Readings

Borgeat K, Wright J, Garrod O, et al. Arterial thromboembolism in 250 cats in general practice: 2004‐2012. J Vet Intern Med 2014 Jan‐Feb;28(1):102‐8.

Guillaumin J. Recent advancements in thrombolysis in feline aortic thromboembolism. In: Proceedings of the 23rd annual IVECCS; 2017 Sept 13-17; Nashville, TN; pp 153-156.

Hogan DF. Feline Cardiogenic Arterial Thromboembolism: Prevention and Therapy. Vet Clin North Am Small Anim Pract 2017 Jun 27.

Hogan D, Fox P, Jacob K, et al. Secondary prevention of cardiogenic arterial thromboembolism in the cat: The double‐blind, randomized, positive‐controlled feline arterial thromboembolism; clopidogrel vs. aspirin trial (FAT CAT). J Vet Cardiol 2015 Dec;17 Suppl 1:S306‐17.

Kirby R, Linklater A. Coagulation. In: Monitoring and intervention for the critically ill small animal: The rule of 20. 1st ed. Ames, Iowa: John Wiley & Sons, Inc; 2017: 138, 152.

Klainbart S, Kelmer E, Vidmayer B, et al. Peripheral and central venous blood glucose concentrations in dogs and cats with acute arterial thromboembolism. J Vet Intern Med 2014;28:1513‐1519.

Macintire DK. Cardiac emergencies. In: Small animal emergency and critical care medicine. 2nd ed. West Sussex, UK: John Wiley & Sons, Inc; 2012: 214-216.

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