Abstract
Fixed subaortic stenosis as a congenital heart defect has been reported in a relatively small number of cases. The classic description of feline subaortic stenosis reflects the presence of a fibrous ring just underneath the aortic valve. The present case has a unique morphological aspect, analogous with a rare human stenosis. A 15-month-old, ESH female presented with an anamnesis consisting of respiratory distress, apathy, and anorexia. The clinical examination displayed a patient with lethargy and severe dyspnea, whilst lung auscultation identified generalized bilateral pulmonary crackles. A systolic IV/VI parasternal murmur was identified on the left thorax, while the murmur intensity on the right side was III/VI. Electrocardiogram showed a sinus rhythm interrupted by ventricular ectopic beats. Two-dimensional (2D) echocardiography revealed a concentric hypertrophy of the left ventricle, with severe left atrium enlargement and mild pleural and pericardial effusion. A subaortic, hyperechoic structure was seen from the right parasternal five-chamber view, accompanied by post-stenotic aortic dilatation. The aortic peak velocity was 5.2 m/s, a feature that characterizes the severe form of aortic stenosis. The cat died shortly after presentation and necropsy was performed. Subaortic stenosis was confirmed on gross examination. The structure that induced stenosis of the left ventricle outflow tract (LVOT) had the appearance of a rudimental valve with moderator bands attached. Microscopically, it contains fibrous and smooth muscular tissue and cardiac conduction fibers. This type of subaortic stenosis resembles the cushion-like pseudovalve type described only in human cardiology. This is the first case describing clinical signs, ECG, echocardiography, and histopathological findings in a cat with cushion-like pseudovalve subaortic stenosis. Fixed subaortic stenosis is a rare congenital disease in cats, which should be taken into consideration in young cats with dyspnea and left ventricular hypertrophy.
Introduction
Aortic stenosis (AS) is a rare congenital heart defect in cats. It is represented as a narrowing of the left ventricular outflow tract (LVOT) and/or the aorta, located below the aortic valve (subvalvular stenosis), above it (supravalvular stenosis), or at the valve level (valvular stenosis). This narrowing produces a turbulent blood flow that can be heard as a systolic murmur on the left heart base, as well as an increased blood flow velocity that can be detected and measured by Doppler echocardiography ().
In dogs, aortic stenosis is one of the most frequently diagnosed congenital heart pathology (). Based on post-mortem changes, AS is classified as a mild form, when small, whitish, slightly raised nodules are present on the endocardium of the ventricular septum, just below the aortic valve; a moderate form characterized by the presence of a ridge of fibrous tissue which extends from the base of the anterior leaflet of mitral valves across the interventricular septum to underneath the left coronary cusp; a severe stenosis characterized by the presence of a fibrous band or ridge, which completely encircles the left ventricular outflow tract below the aortic valve and forms a concentrically narrowing tunnel ().
Although no consensus, there is a generally accepted severity scale where a patient is considered to be SAS-affected with an aortic velocity greater than 2.5 m/s. Based on the aortic velocity cutoffs and pressure gradients, respectively, aortic stenosis has been graded as a. equivocal (2–2.5 m/s; 16–24 mm Hg), b. mild (2.5–3.5 m/s; 25–49 mm Hg), c. moderate (3.5–4.5 m/s; 50–79 mm Hg), and d. severe (>4.5 m/s; ≥80 mm Hg) (, ).
Based on functional characteristics of the obstruction, subvalvular aortic stenosis is further categorized as fixed (static or resting) or dynamic (labile) (, ). A dynamic form of subaortic stenosis can occur in the following events: in idiopathic hypertrophic left ventricle with the ventricular septum protrusion into the LVOT; systolic anterior motion of the mitral valve (SAM), frequent in cats, which can occur concurrently or in the absence of LVH; in cases where aortoseptal angle is smaller than 180° from various reasons (). The typically described features of feline fixed subaortic stenosis reflect the presence of a fibrous ring just underneath the aortic valve, encircling the LV outflow tract. This tissue may take the form of a discrete thin band, or as a wide plaque-like proliferation (). This can cause left ventricular outflow tract obstruction, with concomitant increased afterload and compensatory left ventricular concentric hypertrophy and left atrial enlargement ().
Patient information and clinical findings
A 15-month-old female European Short Hair (ESH) cat, weighing 3 kg, was brought to the Veterinary Emergency Hospital from the Faculty of Veterinary Medicine Cluj-Napoca. The cat has been experiencing respiratory issues, worsening over the past 3 days, apathy, and anorexia for the last 48 h. Upon examination, the cat exhibited a good body condition score (5/9), mild dehydration (5%), and dyspnea. A severe respiratory distress with abdominal effort developed during the clinical examination, and pulmonary crackles were detected upon auscultation. Blood work-up was carried-out with the evidence of a mild respiratory acidosis (pH 7.2, pCO2 45.8 mmHg, HCO3 22.6 mmol/L, and lactate 3.2 mmol/L). The cat was tested for the most common viral feline infectious disease and was positive for Feline Coronavirus Antigen Test (Vet Expert rapid test). Thoracic radiography confirmed generalized lung edema and the cat was referred to the Cardiology Department for further evaluation.
On heart auscultation, left parasternal IV/VI systolic murmur was identified, while murmur intensity on the right side was III/VI. Diffuse pulmonary crackles were identified bilaterally. The femoral pulse was considered normal. ECG revealed a sinus rhythm interrupted by isolated ventricular beats with a heart rate of 120 p.m. (Figure 1).
Figure 1
Diagnostic assessment
The standard transthoracic 2D echocardiography () identified in the right-parasternal, long-axis four-chamber view, a concentric hypertrophy of the left ventricle. The interventricular septum diameter in end-diastole was 8 mm. In the right parasternal long-axis four-chamber view at end-systole, a moderate left atrium dilatation was identified, with a left atrium transversal diameter (LAD) of 20 mm, and mild pleural and pericardial effusion were observed. In the right parasternal, long-axis five-chamber view, color Doppler identified a turbulence within left ventricle outflow tract and a mitral regurgitation resembling with the classic aspect of systolic anterior motion of the septal mitral leaflet (SAM). In the same view, beneath the aortic valve, a subaortic hyperechogenic structure was noticed (Figure 2). Post-stenotic aortic dilatation was also present. On the five-chamber view from left-side, the aortic peak velocity was 5.2 m/s, which corresponds to a severe aortic stenosis ().
Figure 2
Despite specific therapy, consisting of oxygen (via box), buthorphanol (0.2 mg/kg, IV), and furosemide (2 mg/kg IV), the cat died in a short time after presentation.
During necropsy, cardiogenic severe pulmonary congestion and edema (diffuse, bilateral) was present. The gross examination of the heart showed marked concentric hypertrophy of the left ventricle, with a total cardiac mass of 28 grams, which is 0.93% of the total body weight (3 kg). This hypertrophy was accompanied by severe dilation of the left auricle. The presence of marked stenosis in the left ventricular outflow tract (LVOT), characterized by the appearance of a rudimental valve resembling the description of the cushion-like pseudovalve () with moderator bands attached (Figures 3B–D), was observed. Moderate post-stenotic dilatation was noted at the level of the aorta. Additionally, within the left auricle adjacent to the mitral valve, a well-demarcated, focal-extensive area of fibrosis measuring 1 cm × 1 cm with partial endocardial disruption was present. The heart was fixed in 10% neutral buffered formalin (Figure 3C). The routine protocol of paraffin wax embedding was followed, and the samples were sectioned at 4 μm. The slides were stained with Hematoxylin and Eosin stain (H&E stain) (Figures 3E–G) and Masson’s trichrome stain (Figure 3H) (). The myocardium showed concentric hypertrophy without myofiber disarray or diffuse interstitial fibrosis, features required for the diagnosis of primary HCM. The changes were consistent with pressure-overload hypertrophy secondary to a fixed subaortic obstruction. Microscopically, the cushion-like pseudovalve (Figure 3E) was composed of irregularly arranged bundles of cardiomyocytes interspersed with edematous fibrous connective tissue, foci of the metaplastic cartilage (Figure 3F), and glycogen-rich cardiomyocytes, resembling cells of the conduction system (Figure 3G) (, ). The predominance of the fibrous connective tissue within the composition of the pseudovalve was confirmed with Masson’s trichrome staining (Figure 3H).
Figure 3
Table 1 summarizes the progression of clinical signs, diagnostic evaluations, therapeutic interventions, and outcome.
Table 1
| Time Point | Findings | Diagnostics | Interventions |
|---|---|---|---|
| Day −3 | Respiratory distress | – | – |
| Day −2 to 0 | Apathy, anorexia | – | – |
| Day 0 (admission) | Dyspnea, 5% dehydration, pulmonary crackles | Blood gas: pH 7.2, pCO₂ 45.8; FCoV + | O₂, butorphanol, furosemide |
| Day 0 (imaging) | Pulmonary edema | Thoracic radiographs | – |
| Day 0 (cardiology) | Murmur (IV/VI), arrhythmia | Echo: LV hypertrophy, LA dilation, LVOT obstruction, AV 5.2 m/s | – |
| After echo | Respiratory worsening | – | O₂, diuretic |
| Same day | Death | – | – |
| Post-mortem | Severe pulmonary edema, LV hypertrophy, LVOT stenosis | Histology: fibrous tissue, cartilage in pseudovalve | – |
Timeline of clinical events, diagnostic findings, and interventions.
Discussion
Subaortic stenosis is a rare congenital disease in cats (, , , , ), and although the numbers are sparse, subvalvular AS appears to be the most common form (, ). However, the scarcity of recent descriptions of this congenital heart disease makes it questionable nowadays if it is indeed a common disease (). With only a few cases published recently (, , , ), SAS remains on top of congenital pathology in cats, being the second, after ventricular septal defect (), and the sixth according to Tidholm (). It is encountered in 7%–17% of all congenital cardiac defects in this species ().
In humans, subaortic stenosis is divided in four categories: type I, a thin membranous diaphragm at the cranial portion of the left ventricular outflow tract; type II, a thick fibrotic ring, few centimeters below the aortic valve; type III, irregular fibromuscular additional tissue just below the aortic valve; and type IV, tunnel-like obstruction of the left ventricular outflow tract (, ). In only two cases, postmortem necropsy revealed a membranous or cushion-like pseudovalve that produced the obstructions of the left ventricular outflow tract (). In our case, subaortic obstruction does not resemble the classical forms described in dogs and human (), yet more with the cushion-like pseudovalve type.
Currently, diagnosis of stenosis is based on echocardiographic evaluation of the left ventricular outflow tract morphology and the measurement of LVOT/aorta peak velocity with continuous wave (CW) Doppler (). In a study describing six cats with SAS (), the diagnosis was confirmed by different methods: angiography, echocardiography, or necropsy. Only four out of six cats were further sent for a complete necropsy examination, and each of them had classic fibrous-appearing subaortic bands encircling and obstructing the left ventricular outflow tract.
The clinical signs reported in our case, especially dyspnea and pulmonary crackles, and systolic murmur with the point of maximum intensity on the left cardiac base, along with the echocardiography findings, such as LVH, LA dilation, turbulent jet on LVOT, elevated transvalvular pressure gradient at the level of the aortic artery, and post stenotic dilatation, are consistent findings found in all previously described feline subaortic stenosis (SAS) cases (, , , , ). The novelty of our case represents the ECG examination with abnormalities identified, consisting of ventricular premature contraction (VPC’s). Usually, on ECG, depression of the ST segment may appear due to a hypoxic, hypertrophied left ventricle, suggesting myocardial ischemia or secondary repolarization changes (). However, in most cases, the ECG reveals a normal sinus rhythm (, ). A particular change identified in this case is the macroscopic appearance of the subaortic stenosis structure, a rudimental valve with a moderator bands attached, or a cushion-like pseudovalve, as described in human cardiology (). This type of structure was described in two cases, and in only one, the histopathology was available, which confirmed the stenosis as being a fibrous pseudovalve. There are no other specifications, as in our case, there were also moderator bands attached or other tissues involved beside the fibrous one. Therefore, a clear definition or set of standard diagnostic criteria for this subtype of subaortic stenosis is lacking. However, it can be noted that this type of stenosis is distinguished by its macroscopic appearance, resembling a pseudovalve. The moderator bands are considered to be a congenital malformation (), which appear as muscular tendons bundles, with the role of creating a connection between the ventricular septum and the free ventricular wall (), and with a potential role to prevent excessive straining in ventricular diastole (). Moderator bands are a common finding in mammals within the structure of the right ventricle, but they are considered rather rare in the left ventricle (, ).
SAS have hypertrophic cardiomyopathy as the primary differential diagnosis followed by secondary LVH, caused by systemic hypertension, acromegaly, myocardial infiltrative disease (e.g., lymphoma), hyperthyroidism, dystrophin-deficient hypertrophic feline muscular dystrophy, or administration of steroids (, ). The difficulty in confirming feline aortic stenosis lies in the high prevalence of HCM (, , ) with systolic anterior motion of the mitral valve. The mitral regurgitation noticed in some cases of subaortic stenosis may develop as the anterior mitral leaflet is drawn into the left ventricular outflow tract during the systole by the high velocity flow (), which makes the diagnosis even more difficult. In cats with longstanding SAM or focal basilar septal hypertrophy, it may be impossible to be confident in a diagnosis of subaortic stenosis when high LVOT velocities are also visualized (). AS shares many clinical and diagnostic features with idiopathic HCM, including left ventricular hypertrophy, mitral regurgitation, left atrial dilation, varying degrees of left ventricular outflow obstruction, high aortic blood flow velocity, and left-sided congestive heart failure (, , , , ).
In our case, the age of the patient and the appearance of a hyperechogenic structure just below the aortic valve, accompanied by a post-stenotic aortic dilatation, helped in certifying SAS as the diagnosis. Usually in ESH cats, HCM appears in middle-aged to older cats (), and our patient was young, therefore the diagnosis was oriented toward a congenital pathology. In neither of the literature consulted was it specified that HCM can induce aortic dilatation and the hyperechogenic appearance below the aortic valve was the key element. Based on both the echocardiographic and histopathological findings, the possibility of concomitant hypertrophic cardiomyopathy in this case can be considered extremely unlikely.
As a clinical sign, dyspnea is the most common finding in cats with SAS or other types of AS (, , , , ). Dyspnea appears due to pulmonary edema and/or pleural effusion. Pulmonary edema develops from increased left ventricular filling pressures, secondary to left ventricular diastolic dysfunction and mitral regurgitation, which is the most frequent and pernicious complication of cardiomyopathies.
Pericardial effusion in cats is relatively rare, and the most common underlying cause of pericardial effusion is congestive heart failure (induced by cardiomyopathies, mitral valve disease, or pulmonic and aortic stenosis) and feline infectious peritonitis (, ), followed by neoplasia, pericardial–peritoneal diaphragmatic hernia, systemic infections, and uremia (, , ). Pleural effusion in cases of HCM indicates a biventricular failure (41). Right ventricular failure in the setting of AS may be secondary to pulmonary venous and arterial hypertension, caused by elevated left atrial pressures (). Therefore the pleural effusion presented here most probably was related with the congestive heart failure caused by the myocardial hypertrophy rather than coronavirus (feline infectious peritonitis). One cat had pericardial effusion, diagnosed postmortem with SAS (), with no evidence of feline coronavirus infection.
Another possible complication of SAS is thromboembolism. There is only one case that developed it (), and it had specific clinical signs: hindlimbs paralysis with no palpable femoral pulses, cyanosis of the footpads, and excessive vocalization. Even though our cat presented a severely enlarged LA, on echocardiography and necropsy, there were no thrombus identified.
Stepien and Bonagura () consider a high risk of bacterial endocarditis in SAS and recommend antibiotic therapy, although this complication has not been reported so far in feline fixed SAS. On histopathological examination of the endocardium and the structure that produced the stenosis, there was no evidence of bacteria involvement.
To the author’s best knowledge, this is the first case describing clinical signs, ECG, echocardiography, and histopathological findings in a cat with cushion-like pseudovalve subaortic stenosis.
Statements
Data availability statement
The raw data supporting the conclusions of this article will be made available by the authors upon request. Requests to access the datasets should be directed to constantin.cerbu@usamvcluj.ro.
Ethics statement
Ethics review and approval and written informed consent were not required as per local legislation and institutional requirements. Written informed consent was obtained from the participants for the publication of this case report.
Author contributions
MC: Writing – original draft, Writing – review & editing, Investigation. IC: Writing – review & editing, Investigation. I-CS: Writing – original draft, Formal analysis, Investigation. CC: Writing – review & editing, Methodology. A-FT: Writing – review & editing, Investigation.
Funding
The author(s) declare that financial support was received for the research and/or publication of this article. The article processing charge was supported by a grant from the Ministry of Education and Research, project number CNFIS-FDI-2025-F-0115.
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References
1.
PetričADPerovičAŠvaraTDovčP. Aortic stenosis in dogs and cats: past, present and future In: MagnussonP, editor. Aortic stenosis-current perspectives. London, UK: IntechOpen (2019). 1–20.
2.
SchropeDP. Prevalence of congenital heart disease in 76,301 mixed-breed dogs and 57,025 mixed-breed cats. J Vet Cardiol. (2015) 17:192–202. doi: 10.1016/j.jvc.2015.06.001
3.
BussadoriCAmbergerCLe BobinnecGLombardCW. Guidelines for the echocardiographic studies of suspected subaortic and pulmonic stenosis. J Vet Cardiol. (2000) 2:15–22. doi: 10.1016/S1760-2734(06)70007-8
4.
TidholmA. Retrospective study of congenital heart defects in 151 dogs. J Small Anim Pract. (1997) 38:94–8. doi: 10.1111/j.1748-5827.1997.tb03326.x
5.
OliveiraPDomenechOSilvaJVanniniSBussadoriRBussadoriC. Retrospective review of congenital heart disease in 976 dogs. J Vet Intern Med. (2011) 25:477–83. doi: 10.1111/j.1939-1676.2011.0711.x
6.
PyleRLPattersonDFChackoS. The genetics and pathology of discrete subaortic stenosis in the Newfoundland dog. Am Heart J. (1976) 92:324–34. doi: 10.1016/S0002-8703(76)80113-5
7.
CroftonAEKovacsSLSternJA. Subvalvular aortic stenosis: learning from human and canine clinical research. Cardiol Res. (2023) 14:319–33. doi: 10.14740/cr1547
8.
KittlesonMDKienleRD. Small animal cardiovascular medicine. St. Louis, MO: Mosby (1998). 603 p.
9.
ZuluagaSAAldanaSNGutiérrezMCBustamanteZSMuñozCGPZuluagaMN. Left ventricular outflow tract obstruction. Rev Colomb Radiol. (2017) 28:4609–15.
10.
ScansenBASchneiderMBonaguraJD. Sequential segmental classification of feline congenital heart disease. J Vet Cardiol. (2015) 17, 10–52. doi: 10.1016/j.jvc.2015.04.005
11.
MargioccoMLZiniE. Fixed subaortic stenosis in a cat. Vet Rec. (2005) 156:712–4. doi: 10.1136/vr.156.22.712
12.
ThomasWPGaberCEJacobsGJKaplanPMLombardCWMoiseNSet al. Recommendations for standards in transthoracic two-dimensional echocardiography in the dog and cat. Echocardiography committee of the specialty of cardiology, American College of Veterinary Internal Medicine. J Vet Intern Med. (1993) 7:247–52. doi: 10.1111/j.1939-1676.1993.tb01015.x
13.
SlezakPSteinhartLProchazkaJEndrysJJurinI. The angiographic appearances of subvalvar aortic stenosis. Br J Radiol. (1965) 38:350–5. doi: 10.1259/0007-1285-38-449-350
14.
ProphetEBMillsBArringtonJBSobinLH. (1992). Laboratory methods in Histotechnology. Washington, DC: Armed Forces Institute of Pathology-American Registry of Pathology; 29–58, 132-133.
15.
MaxieMG. Jubb, Kennedy, and palmer's pathology of domestic animals, vol. 3. 6th ed. St. Louis, Missouri: Elsevier (2016).
16.
StepienRLBonaguraJD. Aortic stenosis: clinical findings in six cats. J Small Anim Pract. (1991) 32:341–50. doi: 10.1111/j.1748-5827.1991.tb00945.x
17.
WatsonCEPayneJRBorgeatK. Valvular aortic stenosis in three cats. J Vet Cardiol. (2019) 25:1–6. doi: 10.1016/j.jvc.2019.06.005
18.
LiuSK. Pathology of feline heart diseases. Vet Clin North Am. (1977) 7:323–39. doi: 10.1016/s0091-0279(77)50033-0
19.
SeverinGA. Congenital and acquired heart disease. J Am Vet Med Assoc. (1967) 151:1733–6.
20.
BoltonGRLiuSK. Congenital heart diseases of the cat. Vet Clin North Am. (1977) 7:341–53. doi: 10.1016/S0091-0279(77)50034-2
21.
SapersteinGHarrisSLeipoldHW. Congenital defects in domestic cats. Feline Pract. (1976) 6:18–43.
22.
SousaMGPasconJPESantosPACCamachoAA. WSAVA- Worls small animal veterinary assoc. editor severe aortic stenosis in a Persian kitten In: World small animal veterinary association world congress proceedings. São Paulo State University, Brazil: (2008)
23.
FerreiraAMStedileST d OSilvaVBCSouzaMG. Arterial thromboembolism secondary to subaortic stenosis in a Persian kitten. Acta Sci Vet. (2018) 46:5. doi: 10.22456/1679-9216.86826
24.
TidholmALjungvallIMichalJHaggstromJHoglundK. Congenital heart defects in cats: a retrospective study of 162 cats (1996-2013). J Vet Cardiol. (2015) 17:S215–9. doi: 10.1016/j.jvc.2014.09.004
25.
SzatmáriV. Congenital supravalvular aortic stenosis in a kitten. J Vet Cardiol. (2022) 41:227–30. doi: 10.1016/j.jvc.2022.04.001
26.
DeutschVShem-TovAYahiniJHNeufeldHN. Subaortic stenosis (discrete form). Classification and angiocardiographic features. Radiology. (1971) 101:275–86. doi: 10.1148/101.2.275
27.
VogtJDischeRRupprathGde VivieERKotthoffSKececiogluD. Fixed subaortic stenosis: an acquired secondary obstruction? A twenty-seven year experience with 168 patients. Thorac Cardiovasc Surg. (1989) 37:199–206. doi: 10.1055/s-2007-1020318
28.
FerasinL. Feline myocardial disease. 1: classification, pathophysiology and clinical presentation. J Feline Med Surg. (2009) 11:3–13. doi: 10.1016/j.jfms.2008.11.008
29.
FujiiYMasudaYTakashimaKOgasawaraJMachidaNYamaneYet al. Hypertrophic cardiomyopathy in two kittens. J Vet Med Sci. (2001) 63:583–5. doi: 10.1292/jvms.63.583
30.
FuentesVLJohnsonLDennisS. BSAVA manual of canine and feline cardiorespiratory medicine. 2nd ed. Quedgeley, Gloucestershire, United Kingdom: BSAVA (2010).
31.
PartoPTadjalliMGhaziSR. Macroscopic and microscopic studies on moderator bands in the heart of ostrich (Stuthio camelus). Global Veterinária. (2010) 4:374–9.
32.
WrayJDGajanayakeISmithSH. Congestive heart failure associated with a large transverse left ventricular moderator band in a cat. J Feline Med Surg. (2007) 9:56–60. doi: 10.1016/j.jfms.2006.03.006
33.
FoxPR. Textbook of canine and feline cardiology, principle and clinical practice. Philadelphia, USA: WB Saunders (1999).
34.
FerasinL. Feline cardiomyopathy. In Pract. (2012) 34:204–13. doi: 10.1136/inp.e2271
35.
PayneJRBrodbeltDCLuisFV. Cardiomyopathy prevalence in 780 apparently healthy cats in rehoming centres (the CatScan study). J Vet Cardiol. (2015) 17:S244–57. doi: 10.1016/j.jvc.2015.03.008
36.
CôtéEMacDonaldKAMeursKMSleeperMM. Feline Cardiology. Chichester, West Sussex, United Kingdom: Wiley-Blackwell (2011).
37.
DavidsonBJPalingACLahmersSLNelsonOL. Disease association and clinical assessment of feline pericardial effusion. J Am Anim Hosp Assoc. (2008) 44:5–9. doi: 10.5326/0440005
38.
RushJEKeeneBWFoxPR. Pericardial disease in the cat: a retrospective evaluation of 66 cases. J Am Anim Hosp Assoc. (1990) 26:39–46.
39.
BoonJA. Veterinary echocardiography. 2nd ed. Chichester, West Sussex, United Kingdom: Wiley-Blackwell (2010).
40.
HallDJShoferFMeierCKSleeperMM. Pericardial effusion in cats: a retrospective study of clinical findings and outcome in 146 cats. J Vet Intern Med. (2007) 21:1002–7. doi: 10.1111/j.1939-1676.2007.tb03056.x
41.
FoxPR. Canine and feline cardiology. New York: Churchill Livingstone (1988). 676 p.
Summary
Keywords
fixed subaortic stenosis, cushion-like pseudovalve, rare, feline, case report
Citation
Cerbu M, Constantin I, Scurtu I-C, Cerbu C and Tăbăran A-F (2025) Case Report: a newly described form of fixed subaortic stenosis in a feline patient. Front. Vet. Sci. 12:1672336. doi: 10.3389/fvets.2025.1672336
Received
24 July 2025
Accepted
15 October 2025
Published
02 December 2025
Volume
12 - 2025
Edited by
Ryohei Suzuki, Nippon Veterinary and Life Science University, Japan
Reviewed by
Yohei Mochizuki, Okayama University of Science, Japan
Karlapudi Satish Kumar, P.V. Narsimha Rao Telangana Veterinary University, India
Updates
Copyright
© 2025 Cerbu, Constantin, Scurtu, Cerbu and Tăbăran.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Constantin Cerbu, constantin.cerbu@usamvcluj.ro
† These authors have contributed equally to this work
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.