Heart disease in cats: case studies – arterial thromboembolism - Veterinary Practice
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Heart disease in cats: case studies – arterial thromboembolism

OMRI BELACHSEN presents his second in a series of case studies that follow two previous articles on the subject of managing heart disease in cats, this time focusing on the presentation, management and outcome of feline arterial thromboembolism

Heart disease in cats: case studies: 2 of 2

A FOUR-YEAR-OLD, male neutered, Siamese cat was referred to the cardiology service following an acute hind limb paresis. The owners reported a sudden weakness of the hind limbs associated with vocalisation that occurred earlier that morning while going down the stairs in the house.

Physical examination

On presentation, the patient appeared sedated but responsive
following administration of 0.2mg/kg methadone intramuscularly (IM) at the referring vet. Oral mucous membranes were pink and capillary refill time was less than two seconds. There was a bilateral hind limb paresis and reflexes were reduced (consistent with lower motor neuron signs). The limbs felt cold and the paw
pads’ colour was mildly cyanotic. Femoral and peripheral pulses were absent. The patient was tachypnoeic with a respiratory rate of 56 breaths per minute, with normal respiratory effort. Pulmonary auscultation was unremarkable. The heart rate was 220
beats per minute with regular rhythm. Cardiac auscultation revealed obvious gallop sounds but no audible murmur. Rectal temperature was 37.5°C.

Problem list and differential diagnoses

  • Hind limb paresis, pain, cold distal limbs, pale paw pads and absence of femoral pulses: although hind limb paresis can be seen with various neurological conditions and the presentation can often mimic a road traffic accident (RTA) injury, a detailed physical examination in this case revealed the “5 Ps”: paresis/ paralysis, pain, poikilothermia, pallor and pulselessness (Fuentes, 2012). Demonstration of these characteristic clinical findings is sufficient for the diagnosis of feline arterial thromboembolism (FATE) affecting the aorta (Volk, 2011). Aortic thromboembolism is predominantly secondary to feline cardiomyopathy; however, other underlying causes such as congenital heart disease, neoplastic emboli or a hypercoagulable state are also rarely reported (Laste, 1995; Smith, 2003).
  • Gallop sounds: gallop sounds are more specific for the presence of heart disease and are generally associated with diastolic dysfunction secondary to cardiomyopathy.
  • Tachypnoea: ischaemic injuries are associated with pain, especially during the initial 24 to 48 hours, and are often the cause of the tachypnoea. However, between 44% to 66% of cats presented with FATE have a concurrent congestive heart failure (CHF) (Borgeat, 2014; Smith, 2003) and it is therefore vital to assess for the presence of CHF as additional treatment may be required Pulmonary auscultation is no sensitive enough to rule out the presence of CHF and therefore thoracic radiography is indicated, even in the absence of pulmonary crackles

secondary to cardiomyopathy.

  • Tachycardia: several differentials for tachycardia exist. Physiological sinus tachycardia can occur due to pain, fear or excitement or may be related to increased sympathetic drive in cats with CHF. Concurrent hyperthyroidism is also an important differential for sinus tachycardia with suspected cardiomyopathy. Tachyarrhythmia such as paroxysmal focal atrial tachycardia, atrial fibrillation or flutter and ventricular tachycardia can also be seen in cats presented with FATE. Although atrial fibrillation is typically a chaotic rhythm on auscultation, it may occasionally be difficult to differentiate this rhythm from sinus or other forms of tachycardia on the basis of auscultation alone, as it may sound surprisingly regular at very fast heart rates.

Initial approach and further diagnostic investigations

A rapid point-of-care echocardiographic assessment was performed, demonstrating an enlarged left atrium with spontaneous echo contrast (Figure 1). This finding supported the clinical suspicion of FATE, secondary to an underlying cardiac disease. Thoracic radiographs were obtained once the patient was deemed stable enough to tolerate this procedure. Dorsoventral
and right lateral views showed an enlarged cardiac silhouette and normal to mildly enlarged pulmonary veins (Figure 2). The pulmonary pattern appeared normal, indicating a well-compensated cardiac disease. ECG paper trace was recorded and was consistent with sinus tachycardia. The tachycardia was therefore believed to be secondary to pain and an additional 0.1mg/kg of methadone was given IV. Clopidogrel 18.75mg and aspirin 18.75mg were administered orally and the patient was hospitalised in a calm and quiet environment. A comprehensive echocardiographic examination was performed later on the same day and revealed an advanced stage hypertrophic cardiomyopathy
(HCM) with a moderate degree of systolic dysfunction. A thrombus
was identified in the left auricular appendage (Figure 1). Non-invasive systolic blood pressure was measured using Doppler sphygmomanometry from the right fore leg and was 110mmHg. In light of the reduced systolic function and slightly low blood pressure, pimobendan 0.25mg/kg orally every 12 hours was added to the treatment regime. For further information regarding treatment with pimobendane, readers are referred to the first case
study published here in May 2017. Biochemistry showed a 100-fold
elevation of CK and 10-fold elevation of ALT, consistent with the ischaemic muscle injury. Renal parameters and electrolytes were within reference ranges. Thyroid function was not evaluated since hyperthyroidism is very uncommon in cats under the age of six
(Stephens, 2014).


The patient remained in hospital for 72 hours. Analgesia was adjusted based on serial pain assessments, commencing with methadone 0.1-0.3mg/kg every four to six hours for the first 24 hours and later substituted for buprenorphine 0.01-0.02mg/kg every six to eight hours. By the time of discharge, the patient was comfortable and no longer required analgesia. During the time in hospital, renal parameters, electrolytes, serum calcium and acid-base status were closely monitored with repeated blood samples every eight to 12 hours in order to identify potential signs of
reperfusion injury. No significant abnormalities were noted. Early signs of improved perfusion were noted on day two, as indicated by
improved (pinker) colour of hind limb paw pads, increased warmth of distal limbs and evidence of arterial flow in the lateral plantar artery on Doppler interrogation. Improvement in motor function was seen on day three. Following discussion with the cat’s owners, he was subsequently discharged despite having only regained a very limited use of the hind limbs, as the home was considered to
provide a less stressful environment. Outpatient treatment was prescribed with clopidogrel 18.75mg once-daily and aspirin 18.75mg every third day. Pimobendan was given as outlined above. The owners were asked to monitor the patient’s resting respiratory
rates, and to assess hind limbs’ temperature and function. It was made clear that the patient is dependent and would require nursing and help with toileting. Physiotherapy was recommended
and passive movement exercises were demonstrated. A re-assessment appointment was scheduled for four days’ time.


The patient regained motor function within seven days of presentation, although reduced hind limb reflexes were present at the re-assessment appointment, consistent with ischaemic nerve damage. No signs of reperfusion injury were noted at any point.
After initial re-assessment, the patient remained asymptomatic
for a period of four months but subsequently developed signs of CHF, which was medically managed with diuretic therapy (the reader is referred to part 1 of this case series, published here in May 2017, for a more detailed description of management of acute CHF). Unfortunately, the patient was later euthanased following a recurrence of FATE six months after the initial presentation.


The diagnosis in this case was relatively straightforward as the lower motor neuron signs in the hind limbs, cold extremities and absence of femoral pulses are pathognomonic for “saddle lesion” aortic thromboembolism; however, other presentations of FATE may prove more challenging to diagnose. Although “saddle lesions” are seen in 60% to 78% of cases (Smith, 2003; Borgeat, 2014; Hogan, 2015), any single or a combination of limbs, or other organs, can be affected. As some cats with cardiomyopathy do not have a heart murmur (Payne, 2015a), signs as subtle as a forelimb lameness/paresis may be the only clue of an underlying cardiomyopathy. Unfortunately, FATE is associated with a poor prognosis with only around 35% of cats surviving to discharge in a referral setting (Smith, 2003) and maybe fewer in general
practice (Borgeat, 2014). Several factors are likely to be responsible for this discrepancy, including financial constraints, practice facilities and the attending vet’s attitude towards treatment of FATE. In one retrospective study (Smith, 2003), for cats in which treatment was attempted, 45% survived to discharge,
with numbers increasing to over 70% in the later years of the study.
The decision as to whether treatment should be attempted is not always an easy task and the welfare of the patient should always be kept in mind. Several factors such as low rectal temperature
(< 37.2°C), absence of motor function, number of limbs affected (≥ 2) and presence of CHF have been associated with worse outcomes (Smith, 2003; Borgeat, 2014). In cases where treatment is attempted, it should initially focus on providing adequate analgesia. Attempts to lyse the thrombus using an agent
such as tissue-type plasminogen activator (tPA) or streptokinase are currently not recommended as the reports describing the use of thrombolytic treatment have documented major complications,
particularly relating to rapidly occurring reperfusion injury, and a poor outcome (Welch, 2010; Moore, 2000). The aim of treatment is therefore to prevent further development of the existing thrombus and to reduce the probability of the formation of a new thrombus.

Thromboprophylactic therapy with aspirin is well-studied in human medicine; however, data are limited in veterinary medicine. The most robust evidence for choice of thromboprophylaxic agent comes from the recently published “FATCAT” study (Hogan, 2015). In this multicentre study, chronic administration of clopidogrel was superior to aspirin to reduce the risk of recurrent FATE. Although scientific evidence is lacking, the author uses both clopidogrel and aspirin in the acute setting, and long-term when possible.
With that said, the benefits of using both medications for longterm treatment need to be carefully considered as polypharmacy may discourage owners and result in poor compliance. In human medicine, anticoagulants (warfarin, heparin) are the preferred treatment for primary and secondary prevention of thromboembolic disease. The discussion of the use of this class of drugs in FATE is beyond the scope of this article, but it can be noted that the potential bleeding complications and lack of published evidence are the main reasons for the limited use of these drugs in cats. Specific recommendations are lacking regarding the most effective thromboprophylactic treatment in cats that have not yet experienced a thromboembolic event.

Extrapolating from the “FATCAT” study, clopidogrel is generally considered to be the best first-line approach for cats considered to be at risk of thromboembolic complications, although aspirin, as
above, may also be added to therapy. The optimal timing at which to introduce therapy is also unknown; however, cats that have echocardiographic evidence of atrial thrombus, spontaneous echo contrast, left atrial enlargement and systolic dysfunction of the left atrium and/ or ventricle, have an increased risk of developing FATE (Fuentes, 2012; Payne, 2015b) and should therefore be treated.


FATE is a devastating complication seen almost exclusively in relation to feline cardiomyopathy. The provision of adequate analgesia with opioids is a priority, especially during the initial 48 hours. Treatment is encouraged where animal welfare can be preserved and should be based on antiplatelet medications together with treatment for CHF when indicated. Major complications may occur due to reperfusion injury and thus close monitoring is indicated for the initial couple of weeks. Clopidogrel is superior to aspirin in prevention of secondary thromboembolic disease. However, some cardiologists use both drugs when possible. Long-term prognosis is typically poor due to early recurrence of thromboembolic events or congestive heart failure, but cats treated with clopidogrel following an event had a median time to a second event of 443 days (Hogan, 2015), suggesting that a proportion of cats can do very well for a significant period of time.


Borgeat, K., Wright, J., Garrod, O., Payne, J. R. and Fuentes, V. L. (2014) Arterial thromboembolism in 250 cats in general practice: 2004-2012. Journal of Veterinary Internal Medicine 28 (1): 102-108.

Fuentes, V. L. (2012) Arterial Thromboembolism Risks, realities and a rational first-line approach. Journal of Feline Medicine and Surgery 14 (7): 459-470.

Hogan, D. F., Fox, P. R., Jacob, K., Keene, B., Laste, N. J., Rosenthal, S., Sederquist, K. and Weng, H. Y. (2015) Secondary prevention of cardiogenic arterial thromboembolism in the cat: the double-blind, randomized, positivecontrolled feline arterial thromboembolism; clopidogrel vs. aspirin trial (FAT CAT). Journal of Veterinary Cardiology 17: S306-S317.

Laste, N. J. and Harpster, N. K. (1995) A retrospective study of 100 cases of feline distal aortic thromboembolism: 1977-1993. J Am Anim Hosp Assoc 31: 492-500.

Moore, K., Morris, N., Dhupa, N., Murtaugh, R. and Rush, J. (2000) Retrospective study of streptokinase administration in 46 cats with arterial thromboembolism. Journal of Veterinary Emergency and Critical Care 10 (4): 245-257.

Payne, J. R., Brodbelt, D. C. and Fuentes, V. L. (2015) Cardiomyopathy prevalence in 780 apparently healthy cats in rehoming centres (the CatScan study). Journal of Veterinary Cardiology 17: S244-S257.

Payne, J. R., Borgeat, K., Brodbelt, D. C., Connolly, D. J. and Fuentes, V. L. (2015) Risk factors associated with sudden death vs. congestive heart failure or arterial thromboembolism in cats with hypertrophic cardiomyopathy. Journal of Veterinary Cardiology 17: S318-S328.

Smith, S. A., Tobias, A. H., Jacob, K. A., Fine, D. M. and Grumbles, P. L. (2003) Arterial thromboembolism in cats: Acute crisis in 127 cases (1992–2001) and longterm management with low-dose aspirin in 24 cases. Journal of Veterinary Internal Medicine 17 (1): 73-83.

Stephens, M., O’Neill, D., Church, D., McGreevy, P., Thomson, P. and Brodbelt, D. (2014) Feline hyperthyroidism reported in primary care veterinary practices in England: prevalence, associated factors and spatial distribution. Veterinary Record 175 (18): 458-462.

Volk, H. A., Shihab, N. and Matiasek, K. (2011) Neuromuscular disorders in the cat: Clinical approach to weakness. Journal of Feline Medicine and Surgery 13 (11): 837-849.

Welch, K. M., Rozanski, E. A., Freeman, L. M. and Rush, J. E. (2010) Prospective evaluation of tissue plasminogen activator in 11 cats with arterial thromboembolism. Journal of Feline Medicine and Surgery 12 (2): 122-128. Cardiology webinars available on demand

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