Acta Scientiae Veterinariae, 2020. 48(Suppl 1): 481.

CASE REPORT ISSN 1679-9216

Pub. 481

Non-Cardiogenic Thromboembolism in a
Persian Cat with Hypertrophic Cardiomyopathy

Nathália Lopes Fontoura Mateus1,2, Paula Velozo Leal3, Beatriz Candolo Marques4, Karen Fernanda da Silva2,
Douglas Rodrigo Mattei2 & Elizabeth Regina Carvalho5

ABSTRACT

Background: Hypertrophic cardiomyopathy is the most common acquired cardiovascular disease in the feline species. A
frequent complication of this cardiomyopathy is the development of cardiac congestive failure, left atrial enlargement and
subsequent development of arterial thromboembolism. In a significant percentage of affected animals there is progres-
sion to congestive heart failure, resulting in cyanosis and dyspnea, often the first clinical signs reported by owners. This
is a report of a 10-year-old Persian cat with hypertrophic cardiomyopathy and venous and arterial thromboembolism of
non-cardiogenic origin.
Case: The patient was referred for cardiac evaluation, arterial thromboembolism was the suspected cause of tetraparesis.
On clinical examination, a metacarpal pulse was present in all limbs; there was no cyanosis or peripheral hypothermia
thus, ruling out a thromboembolic event in the limbs. Changes consistent with feline asthma and pulmonary edema were
seen on radiographs, therefore hypertrophic cardiomyopathy was suspected. Treatment with enalapril (0.25 mg/kg every
12 h) for the heart condition and prednisolone (1 mg/kg every 24 h) for asthma was started. Nine days later, the patient
developed mixed dyspnea (inspiratory and expiratory) and was hospitalized with signs consistent with arterial thrombo-
embolism: paralysis and cold extremities in the right and left pelvic limbs. The patient was euthanized due to the poor
prognosis. Postmortem and histopathological findings revealed left ventricular concentric hypertrophy, with no valvular
changes; disseminated intravascular coagulation, with thrombi in the arterial (iliac arteries, pancreatic and renal vessels)
and venous (pulmonary and renal veins) beds; as well as multiple neoplastic lung masses, identified as scirrhous pulmonary
adenocarcinoma, responsible for increased interstitial radiopacity. Metastasis was also identified at the tracheal bifurcation,
causing radiographic changes similar to the alveolar pattern of pulmonary edema.
Discussion: The origin of the concentric left ventricular hypertrophy was not established. Both primary hypertrophy,
due to breed-related genetic predisposition or secondary hypertrophy, due to systemic hypertension from chronic kidney
disease are possibilities. However, despite the left ventricular concentric hypertrophy and the presence of thrombus under
the mitral valve, it was not thought that the patient had cardiogenic thromboembolism, since this would not explain the
venous thrombi. The arterial and venous thromboembolism in this case were the result of paraneoplastic syndrome due to
pulmonary adenocarcinoma, which was a triggering factor for disseminated intravascular coagulation and multiple thrombus
formation, both in arterial and venous beds. Tumor cells may promote direct and indirect modifications in the coagulation
cascade and, thus hypercoagulability. The hypercoagulatory state promoted by the tumor associated with the Virchow triad
seen in feline species, explains the occurrence of thrombosis in this case report. Sensitive imaging tests, such as computed
tomography or magnetic resonance imaging, may be required in middle-aged cats with hypertrophic cardiomyopathy and
clinical presentations of thromboembolism or respiratory signs, in order to exclude pulmonary neoplasm as a differential
diagnosis for thrombus formation and dyspnea. Furthermore, it is speculated that the antitumor effect of heparin used in
the treatment for arterial thromboembolism may delay the diagnosis of lung neoplasia in cats.
Keywords: arterial and venous thromboembolism, heparin, hypercoagulability, scirrhous pulmonary adenocarcinoma.

DOI: 10.22456/1679-9216.100519
Received: 25 September 2019 Accepted: 30 December 2019 Published: 31 January 2020
1
Setor de Clínica Médica de Pequenos Animais, Universidade da Grande Dourados (UNIGRAN), Dourados, MS, Brazil. Centro de Especialidades Médico
2

Veterinário (CEMEV), Campo Grande, MS, Brazil. 3Departamento de Anatomia, Patologia e Clínicas, Universidade Federal da Bahia (UFBA), Salvador,
BA, Brazil. 4Clínica Veterinária Mania de Gato, Campo Grande, MS, Brazil. 5Departamento de Medicina Veterinária, Universidade Federal do Espírito
Santo, UFES, Alegre, ES, Brazil. CORRESPONDENCE: N.L.F Mateus [[email protected]] & E.R. Carvalho [beth_rcarvalho@
hotmail.com]. Clínica Veterinária UNIGRAN. Rua Passo Fundo n. 55. CEP 79823-211 Dourados, MS, Brazil.

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N.L.F. Mateus, P.V. Leal, B.C. Marques, et al. 2020. Non-Cardiogenic Thromboembolism in a Persian Cat with Hypertrophic
Cardiomyopathy. Acta Scientiae Veterinariae. 48(Suppl 1): 481.

INTRODUCTION extremities or cyanotic pads were detected. In addition,

Arterial thromboembolism is usually characteri- distal pulses were detected in all limbs using the por-
zed by the formation of a clot (thrombus) inside the left table vascular Doppler method (DV 610B)1. Systolic
heart chambers and its subsequent dispersion to the arte- blood pressure, measured by the same method, was
rial system. The obstruction of an artery by the thrombus 149 mmHg. The cat was alert, with normal colored
results in clinical manifestations due to acute ischemia of ocular and oral mucosal membranes, but cyanotic pe-
the tissue supplied by the obstructed vessel [29]. nile mucosa; normal temperature and lymph node size;
Feline hypertrophic cardiomyopathy is consi- absence of ocular, nasal or penile secretions; absence
dered the main cause of arterial thromboembolism in of sensitivity during abdominal, epaxial and cervical
the species due to left atrial dilatation in advanced sta- palpation; heart rate of 204 beats per minute (bpm);
ges of the disease [29]. Hypertrophic cardiomyopathy standard heart sounds at auscultation; respiratory rate
accounts for 57.5% of the cardiomyopathies diagnosed of 24 per minute (mpm) and pulmonary auscultation
in domestic cats [7], with a predisposition in middle- revealed fine crepitation.
-age males, and a genetic predisposition in Maine Clinical examination led to investigation of
Coons, Ragdolls, and Persians. In these breeds, genetic possible bronchopathy and systemic causes of the ata-
mutations lead to functional alterations in sarcomeric xia. Therefore, blood count; search for hemoparasites
proteins, promoting concentric hypertrophy, rigidity in blood smear; serum biochemistry profile: alanine
and decreased left ventricular distensibility [22,29]. aminotransferase (ALT), gamma glutamyl transferase
Feline hypertrophic cardiomyopathy structural (GGT), albumin, globulins, urea, creatinine, urinalysis
changes result in hemodynamic modifications, such and urine protein creatinine ratio (UPC) were assessed.
as systolic and diastolic dysfunction and consequent Abdominal ultrasonography; plain chest radiographs
reduction of cardiac output and activation of the and contrast-enhanced radiography of the esophageal
compensatory mechanisms of congestive heart failure pathway (cervical and thoracic); echocardiogram and
[1,9,25,32]. Atrial congestion and remodeling due electrocardiogram were performed. A new immuno-
to low left ventricular compliance, associated with chromatographic test (FIV Ac / FeLV Ag Test Kit)2 for
Virchow triad factors (hypercoagulability, endothelial feline immunodeficiency and feline leukemia virus had
lesion, and blood stasis) result in an increased risk of negative result; glycemia was measured with a portable
hypertrophic cardiomyopathy-affected cats developing glucometer (Accu-Chek Active)3 and total thyroxine
arterial thromboembolism [29]. (T4) by chemiluminescence.
This report describes the case of a Persian cat, The laboratory abnormalities observed were:
diagnosed with hypertrophic cardiomyopathy with hemoconcentration (hematocrit 48% and 11.9 million
non-cardiogenic arterial and venous thromboembolism. red blood cells/mm3); azotemia (creatinine 1.8 mg/dL
and urea 66 mg/dL); increased GGT (17 IU/L) and
CASE
presence of red cells (+++), leucocytes (+++), bacteria
A 10-year-old male Persian cat, weighing 4.8 (+), protein (+; UPC: 0.32) and glucose (+) in the urine
kg, was referred for cardiac evaluation due to suspected sample collected through cystocentesis, even though
arterial thromboembolism. Owners reported lethargy, the patient was normoglycemic (113 mg/dL).
less interaction with the environment and people, spo- No abnormalities were seen on abdominal
radic cough and difficulty walking and swallowing. ultrasonography, but thoracic radiographs (Figure 1)
The patient had been previously treated for hemopa- revealed increased radiopacity in caudal (near dia-
rasitosis using doxycycline (10 mg/kg, once a day, phragmatic recess/pillars) and cranial pulmonary fiel-
orally). Vaccines were up to date (anti-rabies vaccine ds, with a focal alveolar pattern, suggestive of localized
and tetravalent vaccine) and immunochromatographic pulmonary edema. There was increased radiopacity
tests for feline immunodeficiency and feline leukemia (interstitial pattern) and bronchial mineralization in
virus had been negative as a kitten. other lung fields, compatible with aging changes and/
During the cardiologic evaluation, the patient or moderate chronic bronchopathy. In addition, ventral
had no hind limb paralysis, however, motor incoor- spondylosis was observed between thoracic vertebrae
dination due to tetraparesis was observed. No cold 11-12 and 12-13.

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N.L.F. Mateus, P.V. Leal, B.C. Marques, et al. 2020. Non-Cardiogenic Thromboembolism in a Persian Cat with Hypertrophic
Cardiomyopathy. Acta Scientiae Veterinariae. 48(Suppl 1): 481.

Contrast-enhanced (100% barium sulphate, lameness and a plantigrade gait. Therefore, methadone
oral) radiography showed contrast uptake at oropha- was included in therapy (0.2 mg/kg, h, intravenous).
ryngeal and esophageal mucosa, compatible with On the night of D4, the cat developed signs of
stomatitis and esophagitis. arterial thromboembolism in the right hindlimb, with
Echocardiography was inconclusive due to in- cyanosis of pads, peripheral hypothermia and absence
tense agitation during the exam; while the electrocardio- of pulse in the affected limb. Tachycardia and hyper-
gram (Figure 2) suggested left atrioventricular overload tension (190 mmHg) developed, hence, antiplatelet
with increased duration of P waves and QRS complexes; therapy was started: acetyl salicylic acid (5 mg/kg,
no extra-systolic events were observed, and sinus rhythm every 72 h, orally) and clopidogrel (1/4 of a 75mg tablet
was predominant, with sinus tachycardia episodes. every 24 h, orally). Anticoagulant therapy was also
Based on the findings, an allergic cough due to initiated with a single dose of sodium heparin (200 IU/
feline asthma was suspected, and treatment was initia- kg, intravenously), subsequently replaced by sodium
ted with prednisolone (1 mg/kg once daily orally for 10 enoxaparin (1.5 mg/kg, every 6 h, subcutaneously).
days). In addition, possible drug-induced esophagitis Despite the use of tramadol, methadone and
due to oral doxycycline was treated with omeprazole warm compresses on the right hindlimb for analgesia,
(0.5 mg/kg, every 24 h, orally, for 10 days) and sucral- the cat remained tachycardic (280 bpm) and a reduction
fate (250 mg every 8 h, for 10 days, orally). in systemic arterial pressure was observed (100 mmHg).
Although the echocardiographic examination On D6 morning, the patient was hypotensive
was inconclusive, enalapril (0.25 mg/kg, every 12 h, and tachycardic (280 bpm). Volume loading test
orally, until further recommendations) was prescribed, (10 mL/kg of Ringer’s Lactate intravenously over
due to a medical history suggestive of symptomatic 3 minutes) was performed, but the animal remained
feline hypertrophic cardiomyopathy (lethargy, depres- hypotensive. Therefore, a continuous infusion of
sion), and an alveolar/interstitial pattern observed on dobutamine (5 μg/kg/min) was given, however, no
thoracic radiography. No diuretic therapy was initiated increase in systemic pressure was observed. In the late
due to azotemia and proteinuria, and serial clinical and afternoon of D6, the cat developed dyspnea, sialorrhea,
radiographic follow-ups were scheduled to monitor the prostration, oral mucosal cyanosis, intense pain and
alveolar pattern observed initially. paralysis of right hindlimb. On the same day (D6),
The patient was hospitalized five days after signs of arterial thromboembolism were also observed
initial discharge to allow treatment during the owners’ in the left hindlimb, and euthanasia was requested, with
scheduled vacation. During hospital care, benazepril subsequent cosmetic necropsy and histopathologic
(0.5 mg/kg, every 24 h, orally) was prescribed instead examination the same night (D6).
of enalapril due to drug availability, omeprazole (1 mg/ The cause of death according to necropsy and
kg, every 24 h, intravenously) and prednisolone (1 mg/ histopathology was disseminated intravascular co-
kg, every 24 h, orally) were continued. agulation, possibly due to a paraneoplastic syndrome
On the second day of hospitalization (D2), due related to scirrhous pulmonary adenocarcinoma. Pa-
to the patient’s difficulty swallowing on account of ralysis of the hind limbs occurred due to the presence
esophagitis, tramadol hydrochloride (2 mg/kg, every 12 of a saddle thrombus (Figure 3), that had partially
h) was added for analgesia. On the same day (D2), the occluded the left iliac artery and totally obstructed the
animal had a short episode of mixed (inspiratory and right iliac artery. In addition, multiple thrombi were
expiratory) dyspnea of approximately 60 s, unrelated observed occluding the lumen of pancreatic vessels,
to any event (manipulation or drug administration), resulting in coagulative necrosis and steatonecrosis.
without the concomitant or subsequent occurrence of Arterial and venous thrombosis were observed in both
cyanosis, tachypnea or panting. kidneys, which had coalescing multifocal infarcts.
Thoracic radiography was repeated on D2 and The clinical suspicion of feline hypertrophic
the alveolar radiopacity was unchanged. Furosemide cardiomyopathy was confirmed by the finding of
(1 mg/kg, intravenously, every 24 h) was then added myocardial hypertrophy in the left ventricle with lumen
to prescription due to the dyspnea and radiographic reduction of the chamber (Figure 4) and thickening of
findings. Later, on D4, the cat developed right hindlimb left ventricular free wall, measuring approximately

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N.L.F. Mateus, P.V. Leal, B.C. Marques, et al. 2020. Non-Cardiogenic Thromboembolism in a Persian Cat with Hypertrophic
Cardiomyopathy. Acta Scientiae Veterinariae. 48(Suppl 1): 481.

1.5 cm in the central portion. Moderate dilation of the crinopathy, such as: polyphagia, hyperthermia, polyu-
right ventricle was also observed, with a flaccid free ria, polydipsia, intense vocalization and agitation [6].
wall measuring approximately 0.6 cm. A thrombus was About 61-65% of cats with chronic kidney
found under the mitral valve (Figure 5) and, when the disease have secondary systemic arterial hyperten-
route of the retrograde blood flow to the left atrium sion [33]. The exact pathophysiologic mechanism of
was opened, almost total occlusion of the pulmonary hypertension in chronic kidney disease has not yet been
vein by thrombi was noted. fully elucidated; however, activation of the renin-an-
In the lungs, multiple infiltrating, multifocal to giotensin-aldosterone system and its secretory effects
coalescing, neoplastic masses were observed, ranging of epinephrine, norepinephrine, and vasopressin, as
from 0.3 to 1.5 cm, confirmed on histopathological well as the vasoconstrictive reaction and increased
examination to be scirrhous pattern pulmonary adeno- peripheral vascular resistance in response to these
carcinoma (Figure 6). These tumors were responsible mechanisms may play a part [26].
for increased interstitial radiopacity. In addition, the On presentation the patient was azotemic and
radiopaque area observed in the cranial lung field of the showed glycosuria despite being normoglycemic.
patient’s thoracic radiograph, which was suggestive of These laboratory alterations classify the animal as a
pulmonary edema, turned out to be a firm mass 3.4 cm stage II renal patient, with borderline proteinuria and
in diameter, located at the bifurcation of the trachea, prehypertensive, according to the International Society
causing partial compression of the vena cava (Figure of Renal Interest (IRIS) [14].
An ischemic etiology was suggested for the
7). This mass was identified on histopathological exa-
patient’s renal disease, on account of the histologic
mination as a metastatic lung neoplasia.
evidence of multifocal thrombosis, associated with
Congestive liver disease with diffuse centrilo-
multiple areas of coagulative necrosis, and infarcted
bular necrosis was observed, and the spleen had diffuse
areas already replaced by fibrous connective tissue,
pronounced congestion. It was not possible to verify
in which thrombi were already organized and often
changes in the central nervous system since the owner
recanalized. Thus, it was confirmed by histopatholo-
demanded the preservation of the cat’s skull for burial.
gic examination that the patient had both chronic and
DISCUSSION acute renal injuries, and these could be the cause of
hypertension and left ventricular hypertrophy.
Feline hypertrophic cardiomyopathy is cha-
Other less frequent causes of hypertension
racterized by concentric left ventricular hypertrophy,
such as acromegaly and aortic stenosis were also ruled
in the absence of metabolic causes or hemodynamic out. Congenital heart disease was excluded because
overload, capable of producing left ventricular wall no post-mortem narrowing, or obstruction of aortic
thickening (> 6 mm diameter in diastole), without flow was found [30]. Some clinical signs frequently
dilation [24,31]. observed in acromegaly such as the presence of dia-
Systemic arterial hypertension can be consi- betes mellitus, organomegaly and prognathism were
dered a metabolic cause of left ventricular concentric not observed in this patient [13].
hypertrophy. An increase in vascular resistance of The possibility of feline hypertrophic cardio-
the left ventricular outflow tract promotes pressure myopathy could not be excluded in this case, since
overload in this chamber and, consequently, increases echocardiographic and histopathological findings are
afterload and promotes cardiac remodeling [10]. Our indistinguishable between this cardiomyopathy and se-
patient had a discrete increase in arterial blood pressure condary concentric left ventricle hypertrophy [2,8,17,27].
and was classified as a prehypertensive patient [2]. The patient was from a breed predisposed to the deve-
The causes of systemic arterial hypertension in lopment of hypertrophic cardiomyopathy [21]. Thus, to
cats include chronic kidney disease and hyperthyroi- exclude this diagnosis, specific genetic tests would be
dism [2]. Feline hyperthyroidism was ruled out in this necessary to identify mutations in genes encoding ele-
patient by a normal serum T4 value and no alterations in ments involved in cardiac contraction [1]. It is important
the thyroid gland on the histopathological evaluation. In to emphasize that there are no commercial tests available
addition, the patient had no clinical signs of this endo- to detect these abnormalities in the Persian breed.

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N.L.F. Mateus, P.V. Leal, B.C. Marques, et al. 2020. Non-Cardiogenic Thromboembolism in a Persian Cat with Hypertrophic
Cardiomyopathy. Acta Scientiae Veterinariae. 48(Suppl 1): 481.

Figure 1. Right lateral-lateral thoracic radiograph of a 10-year-old Persian cat with hypertrophic cardiomyopathy and arterial and venous thromboembo-
lism due to paraneoplastic syndrome. Radiopacity in caudal (yellow arrow) and perihilar (black arrow) lung fields are shown. A discrete alveolar pattern
and pulmonary fields with increased interstitial radiopacity with bronchial mineralization can also be seen.

Figure 2. Electrocardiogram of a 10-year-old Persian cat with hypertrophic cardiomyopathy and arterial and venous thromboembolism due to para-
neoplastic syndrome. Note the sinus rhythm and increased duration of P waves (40 ms) and QRS complex (50 ms), suggestive of left atrioventricular
overload. Mean heart rate of 207 beats per minute, velocity of 50 mm/s, normal amplitude (N).

5
N.L.F. Mateus, P.V. Leal, B.C. Marques, et al. 2020. Non-Cardiogenic Thromboembolism in a Persian Cat with Hypertrophic
Cardiomyopathy. Acta Scientiae Veterinariae. 48(Suppl 1): 481.

Figure 3. Abdominal cavity of a 10-year-old Persian cat with hypertrophic Figure 4. Transverse section of the heart of a 10-year-old Persian cat with
cardiomyopathy and arterial and venous thromboembolism due to para- hypertrophic cardiomyopathy and arterial and venous thromboembolism
neoplastic syndrome. The lumen of the abdominal aorta is observed in the due to paraneoplastic syndrome. There is marked thickening of the left
bifurcation region, with the presence of a saddle thrombus (arrow), partially ventricular wall and consequent marked narrowing of the cardiac lumen.
occluding the left iliac artery and totally obstructing the right iliac artery.
and predisposition for thrombi formation due to blood
stasis in this compartment [1,24].
The prognosis in cardiogenic arterial throm-
boembolism is poor, with survival rates around 35%
[28]. Euthanasia is frequently recommended by
veterinarians and represented the outcome of 91.6%
of cases in a study evaluating 250 feline patients [5].
Despite administration of antithrombotic therapy with
antiplatelet agents and anticoagulants [12] in this case,
euthanasia was ultimately recommended due to the
deterioration of the patient, with thrombotic clinical
manifestations in both hind limbs, since it is known that
cats with two or more limbs affected have a mortality
Figure 5. Presence of thrombus (arrow) above the mitral valve of a 10-year-
rate of 73.6% over a period greater than 24 hours, but
old Persian cat with hypertrophic cardiomyopathy and arterial and venous less than 7 days [5].
thromboembolism due to paraneoplastic syndrome.
It should be noted that in the case described,
despite the presence of emboli under the mitral valve
Other facts supported the post-mortem diag- and in the branch of the abdominal aorta, no dilation of
nosis of hypertrophic cardiomyopathy in this case, the left atrium was observed, which would be essential
such as symmetric hypertrophy (1.3 cm) of the left to establish the diagnosis of arterial thromboembolism
ventricular free wall, which was greater than the mean secondary to feline hypertrophic cardiomyopathy. There-
values (​ 0.7-0.8 cm) reported in other histopathologic fore, thrombi formation was not due to blood stasis in the
studies [4,18] and the derangement between myofibrils left atrium, a fact supported by the presence of thrombi
observed in the hypertrophied tissue. Advanced cases inside pulmonary veins, which could not be explained
of feline hypertrophic cardiomyopathy culminate in by the pathophysiology of hypertrophic cardiomyopathy.
left heart failure due to diastolic dysfunction and mitral Other causes of blood hypercoagulability such
valve regurgitation because of structural changes in the as hyperadrenocorticism, immune-mediated hemolytic
left ventricle and its papillary muscles, or due to the anemia, pancreatitis, hyperthyroidism, diabetes melli-
anterior systolic movement of this valve [24]. These tus; as well as causes of hypoalbuminemia, represented
factors may lead to non-coaptation of the left atrio- by enteropathy, sepsis, and nephropathy were ruled out
ventricular valve and blood regurgitation towards the based on laboratory and histopathological findings.
left atrium, with consequent dilation of this chamber Nephropathic animals with severe protein loss may

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N.L.F. Mateus, P.V. Leal, B.C. Marques, et al. 2020. Non-Cardiogenic Thromboembolism in a Persian Cat with Hypertrophic
Cardiomyopathy. Acta Scientiae Veterinariae. 48(Suppl 1): 481.

Figure 6. Histological section of the lung of a 10-year-old Persian cat with hypertrophic cardiomyopathy and arterial and venous thromboembolism
due to paraneoplastic syndrome. A- Pulmonary adenocarcinoma, characterized by neoplastic masses with coalescent, multiple, well-demarcated lesions
composed of epithelial cells arranged in predominantly acinar or papillary structures [HE; 10x]. B- Scirrhous areas where marked amounts of collagenous
stroma are found to be slightly to moderately cellular, however abundantly collagenous [HE; 10x].

Cancer patients have high levels of fibrinopep-

tide A, thrombin fragments and thrombin-anti-thrombin
complex, and also produce oncological pro-coagulant
factor and inhibitory factors of fibrinolysis. This set
of elements plays a key role in the hypercoagulability
observed in lung neoplasms, besides contributing to
tumor angiogenesis and subsequent neoplastic growth
and dissemination [20]. In dogs and cats, neoplasms also
play an important role as the cause of thrombosis [3,34].
In the study performed by Smith et al. [28], 5% of the
cats with arterial thromboembolism had a neoplasm as
the underlying cause of thromboembolism; other authors
have specifically identified the presence of lung tumors in
Figure 7. Firm, whitish mass at tracheal bifurcation region of a 10-year- feline patients with arterial thromboembolism [11,16,23].
old Persian cat with hypertrophic cardiomyopathy and arterial and venous It is assumed that the concomitant occurrence
thromboembolism due to paraneoplastic syndrome. The mass was 3.4 cm
diameter, did not invade the tracheal lumen, however it partially com- of feline hypertrophic cardiomyopathy and lung can-
pressed vena cava (arrows). Multiple foci of pulmonary infarction (*) due cer may be underdiagnosed, since both diseases may
to neoplastic emboli.
cause similar clinical signs, such as cyanosis, lethargy,
present with coagulation disorders, but the cat had and dyspnea; and may both progress to thrombosis. In
mild proteinuria and no glomerular lesions on the addition, anticoagulants such as heparin, frequently
histopathological analysis. used in the treatment of arterial thromboembolism,
Hence, the thromboembolism in this patient also exhibit antitumor effect, preventing the binding of
could only be explained by the presence of pulmonary neoplastic cells to platelets and endothelium; inhibiting
adenocarcinoma, which was a triggering factor for disse- tumor angiogenesis; and also regulating the immune
minated intravascular coagulation and multiple thrombus system function, modulating cytokines and migration
formation, both in arterial and venous beds. It is known of leukocytes that aid in malignant cells destruction
that tumor cells can have paraneoplastic effects, such as [15,19,20]. Therefore, the therapy used for arterial
direct and indirect activation of the coagulation cascade, thromboembolism benefits human patients with pul-
and more than 90% of human patients with metastasis monary malignant tumor [15] and could conceal clini-
may present with coagulative disorders [20]. cal signs and delay suspicion of feline lung neoplasia.

7
N.L.F. Mateus, P.V. Leal, B.C. Marques, et al. 2020. Non-Cardiogenic Thromboembolism in a Persian Cat with Hypertrophic
Cardiomyopathy. Acta Scientiae Veterinariae. 48(Suppl 1): 481.

Hence, feline hypertrophic cardiomyopathy Alere (Abbot). São Paulo, SP, Brazil.
2

should be suspected in cats with thromboembolism, ho- Roche Diabetes Care Brasil Ltda. Jaguaré, SP, Brazil.
3

wever we suggest that a thorough screening (including Acknowledgements. We are thankful for the veterinarians from
sensitive imaging exams, such as radiography, computed Mania de Gato Veterinary Clinic, veterinarians of the Intensive
tomography or magnetic resonance) should be performed Care Unit (ICU) and Imaging sector from Centro de Especiali-
in older cats to rule out respiratory conditions; based on the dades Médico Veterinário (CEMEV); Teacher Veronica Jorge
fact that radiographic findings of lung neoplasia may mimic Babo Terra from Federal University of Mato Grosso do Sul and
pulmonary edema or resemble chronic bronchopathy, a the tutor Priscila for kindly have authorized the report of the
case of her beloved feline.
respiratory disease frequently seen in cats in this age group.
Declaration of interest. The authors report no conflicts of
MANUFACTURERS
interest. The authors alone are responsible for the content and
Medmega Indústria e Equipamentos Médicos Ltda. Franca, SP, Brazil.
1
writing of the paper.

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