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. 2025 Apr 25;11(3):e70359. doi: 10.1002/vms3.70359

Multimodal Imaging and Clinical Features of Aortic Dissection in a Cat

Yewon Ji 1, Minjoo Kim 2, Bumseok Kim 3, Sang‐Ik Oh 3, Byungkwan Oh 3, Hakyoung Yoon 1,✉
PMCID: PMC12023763  PMID: 40278543

ABSTRACT

An 11‐year‐old male castrated cat was presented for dyspnoea. Cardiomegaly and pulmonary oedema were identified radiographically. Echocardiography identified lesions of suspected aortic dissection consisting of a false lumen filled with echogenic material at the level of the aortic valve with aortic insufficiency. The cat developed pericardial effusion and chylothorax three months after the initial diagnosis. A computed tomography exam revealed a wall defect allowing connection between the true and beak‐, spiral‐shaped false lumen compressing the true lumen, which led to a diagnosis of aortic dissection. In addition, aortic wall calcification from the aortic root to the ascending aorta was identified. Ten weeks after the scan, the cat collapsed and died shortly after hospitalisation. The post‐mortem examination revealed full‐thickness aortic dissection of 2 mm and a beak‐shaped lumen surrounding the true lumen, consistent with computed tomography findings. A histopathologic exam revealed aortic dissection at the tunica media, myocyte hypertrophy and endocardial fibrosis. This case report describes clinical, multimodal imaging and histopathological features of aortic dissection in a cat and is the first to describe the corresponding computed tomography and post‐mortem findings. Aortic dissection should be considered as a differential diagnosis when true and false lumen is identified on echocardiographic and computed tomography tests.

Keywords: aortic dissecting aneurysm, computed tomography, feline, hypertrophic cardiomyopathy, systemic hypertension

Aortic dissection was diagnosed in an 11‐year‐old neutered male cat with concurrent systemic hypertension and left ventricular hypertrophy. Clinical, multimodal imaging and histopathological features of aortic dissection in a cat are described. Advanced imaging, particularly CT, revealed findings consistent with histopathologic examination, highlighting the accuracy and efficacy in diagnosing aortic dissection in veterinary patients.

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Abbreviations

AD

aortic dissection

AoI

aortic insufficiency

CT

computed tomography

HCM

hypertrophic cardiomyopathy

LV

left ventricle

LVOTO

left ventricular outflow tract obstruction

1. Introduction

Aortic dissection (AD) is characterised by separation of the aortic wall layers resulting in blood flow from the lumen into the media. In humans, AD is reported to be associated with a high mortality rate due to complications including aortic insufficiency, multi organ failure and death. (Khan and Nair 2002; Mészáros et al. 2000; Nienaber et al. 2016). In veterinary medicine, several cases of AD in small animals have been reported (Bevilacqua et al. 1981; Boulineau et al. 2005; Cohen et al. 2010; Daniel Newhard 2017; Gouni et al. 2018; Lenz et al. 2015; Lourenço et al. 2002; Oricco et al. 2019; Scollan and Sisson 2014; Waldrop et al. 2003; Wey and Atkins 2000).These include a few cases in cats with systemic hypertension and hypertrophic myocardiopathy (HCM) phenotype.

Although the complete aetiology of AD is unclear, it is thought that the fundamental component of the underlying pathology of AD is compromised aortic integrity, either due to congenital or acquired instability of the aortic wall (Oricco et al. 2019). In human medicine, systemic hypertension, genetic disorders, aortic aneurysms, atherosclerosis, previous cardiovascular surgery and inflammatory diseases are reported to be predisposing factors for AD (Gouni et al. 2018; Khan and Nair 2002; Mészáros et al. 2000; Nienaber et al. 2016). Although there is a lack of research about the specific aetiology of AD in cats, cases of AD in cats with systemic hypertension and HCM phenotype have been reported (Gouni et al. 2018; Oricco et al. 2019; Wey and Atkins 2000).

Various imaging diagnostic exams are available to detect AD, including echocardiography, computed tomography (CT), magnetic resonance imaging and aortography (Wey and Atkins 2000). Previously, a case report described CT features of AD in a cat; however, postmortem examination was not performed to compare to findings with the CT results. In this report, we describe the clinical, multimodal imaging and post‐mortem gross and histopathological features of AD in a cat.

2. Case Description

An 11‐year‐old male castrated Scottish fold cat weighing 2.95 kg presented with dyspnoea and depression lasting a few days. At presentation, the cat was quiet, alert and responsive but dyspnoeic. A heart rate of 180 bpm and a systolic blood pressure of 240 mmHg were recorded. A complete blood count and serum chemistry revealed a mildly elevated blood urea nitrogen of 38.3 mg/dL (reference interval: 17.6–32.8 mg/dL) and normal creatinine of 1.6 mg/dL (reference interval: 0.8–1.8 mg/dL). Additional diagnostic results included a normal total T4 of 1.23 ug/dL (reference interval: 0.6–3.9 ug/dL) and increased feline serum amyloid A of 22.5 ug/mL (reference interval: 0–5 ug/mL). Thoracic radiographs (HF‐525 PLUS, ECORAY, Seoul, Korea) at initial presentation revealed generalised cardiomegaly with an increased vertebral heart score of 9.6 (reference interval: 6.7–8.1) and mild pulmonary infiltration at the right caudal lobe (Figures 1A and 1C).

FIGURE 1.

FIGURE 1

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Thoracic radiographs of the cat at the initial presentation and three months after diagnosis. Marked cardiomegaly with valentine heart shape and mild pulmonary infiltration at right caudal lobe was observed on the right lateral view (A) and ventrodorsal view (C). Three months after the initial presentation, marked lung retraction, an increase in pulmonary opacity in the cranioventral aspect of lung fields with border effacement of the cardiac silhouette was observed, with interlobar fissure lines evident in the dorsoventral view (D). Pleural effusion was observed on the right lateral view (B) and dorsoventral view.

An echocardiographic exam (Aplio i500, Toshiba Medical Systems, Zoetermeer and the Netherlands) revealed an AD extending from the level of the aortic valve. A false lumen with an echogenic structure surrounding the aorta appeared to compress the true lumen on a modified left parasternal apical view (Figure 2A) and right parasternal long axis view (Figure 2B). Colour flow imaging on a modified left parasternal apical view showed a jet flow from the aorta toward the anechoic portion of the false lumen (Figure 2C) and aortic insufficiency (AoI; Figure 2D). The echogenic lesion next to the false lumen was considered a haematoma resulting from dissection. A continuous wave Doppler exam revealed mild AoI; AoI velocity 5.6 m/s, incomplete envelope) and trivial tricuspid regurgitation of 2 m/s. Along with the AD, left ventricular (LV) hypertrophy; (LV end diastolic free wall thickness 0.79 cm (reference interval:0.26‐0.45 cm)(Häggström et al. 2016), intermittent systolic anterior motion (SAM) occurring mild dynamic left ventricular outflow tract obstruction (LVOTO) and left atrial enlargement; (left atrium to aortic root ratio of 2.06 (reference interval: 0.86‐1.42) (Häggström et al. 2016) were detected. Moreover, spontaneous echocardiographic contrast was noted in the left atrium (LA). After the initial presentation, the cat was hospitalised and furosemide (2mg/kg, IV bolus) was administered. After one day of hospitalisation, radiographs showed marked resolution of pulmonary oedema and the cat had a respiratory rate of 18 to 24. After two days, the cat was discharged with prescribed medications, including furosemide (1mg/kg PO q12 h) and rivaroxaban (1.25 mg PO q24 h) for two weeks. At the two‐week follow‐up, the cat showed no notable pulmonary oedema on radiographs and the owners reported that the cat was in stable condition with normal sleeping respiratory rate, vitality and appetite. However, serum chemistries revealed a markedly elevated blood urea nitrogen (BUN) of 92 mg/dL (reference interval: 17.6‐32.8 mg/dL), creatinine of 5.54 mg/dL (reference interval: 0.8‐1.8 mg/dL) and mildly elevated phosphorus of 7 mg/dL (reference interval: 2.6‐6 mg/dL). Because the cat was in relatively stable condition after discharge but had elevated BUN, creatinine and phosphorus, the dose of furosemide was decreased to 0.65 mg/kg PO q12 h for 1 week and then to 0.5 mg/kg PO q12 h. The dose of rivaroxaban was maintained.

FIGURE 2.

FIGURE 2

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Transthoracic echocardiographic images from modified left apical long axis view (A, C, D) and right parasternal long axis view (B). An intimal flap separating the false lumen (FL) and true lumen (TL) was observed. A defect (white arrow) between FL and TL is shown (A). FL filled with echogenic material suspected to be a hematoma coursing next to TL, separated by an intimal flap is shown (B). At the level of the defect, a jet flow from the true lumen to the false lumen right distal to the aortic valve (arrowhead) during systole, indicating a connection between two lumens (C), was identified on the colour Doppler exam. Aortic insufficiency during diastole was identified (D). However, no remarkable flow was observed at the level of the echogenic lesion. FL, false lumen; TL, true lumen.

The cat had regular follow‐up appointments every month. At the one‐month and two‐month follow‐ups, the cat remained asymptomatic under the medical therapy. However, a week before the three‐month follow‐up, the cat was presented for dyspnoea and lethargy. Pleural effusion was suspected based on the radiographic exam (Figures 1B and 1D) and thoracocentesis revealed chylothorax. CT was performed using a Revolution ACT scanner (GE Healthcare, Milwaukee, WI, USA) and the following parameters: 1.25 mm slice thickness, 120 kVp, 84 mAs, 512 × 512 matrix and 1 rotation time. On the pre‐contrast scans, aortic wall calcification from the aortic root to the descending aorta was identified (Figure 3C). A single post‐contrast CT scan was performed at 60 s after a 700 mg/kg injection of Iohexol (Omnipaque 300, GE Healthcare, Shanghai, China). The exam revealed that the AD originated at the level of the aortic valve, extending 1.9 cm cranial toward the ascending aorta (Figure 3D). Multi‐plane reconstruction showed both contrast‐enhanced true and false lumens (Figures 3A, 3B and 3D). A beak‐shaped dissection composed of a false lumen and a non‐enhanced lesion (suspected to be a haematoma) that appeared to compress the aorta from the level of the aortic root to the proximal ascending aorta was observed (Figure 3B). The contrast‐enhanced false lumen appeared to have a spiral course, surrounding the aortic root and a wall defect of 2.7 mm at the aortic valve level through which both lumens communicated was identified (Figures 3E and 3F). Due to the deteriorated clinical symptoms of the patients, including the development of chylothorax, recurrent dyspnoea and lethargy, furosemide (1.5 mg/kg PO, q12 h), hydralazine (2.5 mg PO, q12 h) and rivaroxaban (1.25 mg PO, q24 h) were prescribed.

FIGURE 3.

FIGURE 3

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Axial (A, B) and multi‐plane reconstructed CT images (C‐E) of the aortic dissection. The true lumen (black asterisk) and false lumen (black arrowhead) of the aorta connected through a defect suspected as a dissection (black arrow) was identified (A). The false lumen of the aorta (black arrowhead) and non‐contrast enhanced lesion (white arrowhead) composing a beak‐shaped lesion (B), which compresses the true lumen of the aorta from the axial and reconstructed images are shown (A, B, D, E). A pre‐contrast reconstructed image shows aortic wall calcification (white arrow) from the aortic root to the ascending aorta (C). Note that the calcification is most prominent at the level of dissection. Panel D shows dissection compressing the true lumen of the aorta at the level of the aortic root. The connection between the true lumen and false lumen (asterisk) through a defect (black arrow) (E) on the dorsal image is shown. Marked pleural effusion is observed throughout the CT images. CT, computed tomography.

After the CT scan, the cat was hospitalised for two days and discharged with prescribed drugs of furosemide 1 mg/kg PO q12 h, mirtazapine 1.88 mg/cat PO and rivaroxaban 1.25 mg/cat PO. At two‐week follow‐up, chylothorax was identified and thoracocentesis was performed. Afterwards, the dose of furosemide was increased to 1.5 mg/kg PO q12h. The cat was presented for an emergency check‐up after four weeks and re‐hospitalised for two days. By the request of the owners, the cat was discharged; however, it presented with collapse at 10 weeks after the CT scan. Shortly after hospitalisation the cat died. Gross post‐mortem examination revealed a full‐thickness fissure of 2 mm in the aortic wall at the level of the aortic valve and a beak‐shaped lumen surrounding the aorta, which was larger than the true lumen (Figures 4A and 4B), which was consistent with the CT and echocardiographic findings. There was no evidence of any additional dissections or suspected tears in addition to the previously observed dissections. Histopathological examination of the aorta confirmed the presence of dissection into the tunica media with fibrotic change (Figures 4C–E) and calcification at the surface of the dissection. Cardiomyocyte hypertrophy within the myocardial tissue was observed in the LV, particularly in the slightly upper part of the apex (Figure 4F). In addition, fibrotic lesions were observed in the myocardium and endocardium of the LV (Figures 4G and 4H). Although myofiber disarray was not observed in this case, the histopathologic findings, including cardiomyocyte hypertrophy and interstitial fibrosis of the myocardium and the endocardium of the LV, indicated a strong association with the HCM phenotype. Lastly, PAS‐stained tissue showed no remarkable polysaccharide abnormality.

FIGURE 4.

FIGURE 4

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Gross and histopathological findings. Bulging of the aortic root (black arrow) at the level of dissection was identified on gross post‐mortem examination (A). A full‐thickness fissure of 2 mm (arrowhead) in the aorta at the level of the aortic valve and dissecting hematoma (*;asterisk) larger than the true lumen were identified. Note that the aortic valve (white arrow) is observed on the right proximal to the fissure (B). The histopathological examination shows a dissection at the tunica media. H and E staining (C) and presence of a thrombus in the false lumen (D). Fibrous change was identified in the dissected aorta. Masson's trichrome staining (E), corresponding to the black rectangular area from (D). Cardiomyocyte hypertrophy (yellow arrows) in myocardium (F). Myocardial fibrosis green arrow) in the left ventricle. Masson's trichrome staining (G). Endocardial fibrosis (#;hash) within the left ventricles. H and E staining (H).

3. Discussion

AD is a rare and fatal condition in humans and small animals (Bevilacqua et al. 1981; Boulineau et al. 2005; Cohen et al. 2010; Daniel Newhard 2017; Gouni et al. 2018; Khan and Nair 2002; Lenz et al. 2015; Lourenço et al. 2002; Mészáros et al. 2000; Nienaber et al. 2016; Oricco et al. 2019; Scollan and Sisson 2014; Waldrop et al. 2003; Wey and Atkins 2000). In humans, the incidence of AD is reported to be approximately 2.9 cases per 100,000 people per year (Khan and Nair 2002) and it goes up to 35 cases per 100,000 people per year in the 65–75 years age range (Howard et al. 2013). Although cases of AD in dogs and cats have been reported, its incidence in small animals remains unknown. Impaired aortic integrity is considered a critical component in the aetiology of AD and various factors have been associated with the instability by increasing the stress on the walls, including systemic hypertension, aortic dilation, aortic coarctation and aortic arch hypoplasia (Gouni et al. 2018). Among these, chronic systemic hypertension is the most common factor predisposing humans to AD.

In veterinary medicine, few cases of AD in cats with systemic hypertension have been reported (Daniel Newhard 2017; Gouni et al. 2018; Lourenço et al. 2002; Oricco et al. 2019; Scollan and Sisson 2014; Wey and Atkins 2000). However, more than half of reported cases of cats with AD were normotensive (Bevilacqua et al. 1981; Scollan and Sisson 2014). Although systemic hypertension is a common finding in geriatric cats, AD is rare (Wey and Atkins 2000). Therefore, additional pathological changes, including degeneration and damage of the aortic wall, may be additional predisposing factors for AD occurrence in this species. Congenital anomalies such as Marfan syndrome and congenital connective tissue disorders were reported to be associated with AD in humans (de Beaufort et al. 2017). Similarly, a few cases of AD with Marfan or Marfan‐like syndrome in cattle (Potter and Besser 1994) and dogs (Howard et al. 2013) have been reported. However, the present case did not show polysaccharide abnormalities on histopathological examination. In addition, vasa vasorum lesions secondary to systemic arterial hypertension in cats could be a predisposing factor for damage of the great vessel wall (Kohnken et al. 2017).

In addition to systemic hypertension, a few reported cases of cats with AD had a concurrent HCM phenotype (Oricco et al. 2019; Scollan and Sisson 2014; Wey and Atkins 2000). In this case, the cat had both the HCM phenotype, mild dynamic LVOTO and systemic hypertension. Although myofiber disarray, a hallmark of the HCM phenotype, was not observed, thus HCM phenotype was not definitively diagnosed in this case, the observed myocardial changes suggested an association with AD and the HCM phenotype. The possibility of shear stress from LVOTO in cats with an HCM phenotype as a contributing factor to the clinical signs and subsequent AD was considered. However, as the condition of the cat prior to the AD was unknown, the possibility of a pre‐existing HCM phenotype being the cause of the clinical signs and AD remains unproven. In addition to HCM phenotype, diffuse or segmental LV hypertrophy is commonly observed in cats with systemic hypertension without concurrent HCM phenotype (Luis Fuentes V. et al. 2020) and AD can be associated with systemic hypertension. HCM phenotype with LVOTO could also function as a predisposing factor by increasing shear stress, becoming a potential trigger for AD (Scollan and Sisson 2014) along with systemic hypertension. This can be one of the main complications of AD, leading to heart failure when severe (Patel et al. 2018; Patel and Arora 2008). Thus, we considered that HCM phenotype and systemic hypertension may both be suspected as possible contributing factors to the AD in this cat.

Previously, pulmonary oedema, pleural effusion and pericardial effusion have been reported in cats with AD (Daniel Newhard 2017; Gouni et al. 2018; Scollan and Sisson 2014; Wey and Atkins 2000). In our case, the cat had presumed pulmonary oedema at the initial presentation and follow‐up exams at three months revealed pericardial effusion and chylothorax. Chylothorax can develop due to various causes in cats (Fossum et al. 1991; Gould 2004; Reeves et al. 2020), yet this is the first reported case of a cat with chylothorax following AD. However, any disease that results in high venous pressure, such as cardiomyopathy, pericardial effusion and other cardiac abnormalities, can cause chylothorax (Fossum 2001); thus, the development of chylothorax could have been the result of a combination of secondary complications of AD, HCM phenotype and AoI leading to an increase in LA pressure. Since chylothorax was absent at the initial diagnosis, the possibility of thoracic duct rupture due to a potential event associated with AD was considered low. All reported feline cases with acute AD had pericardial effusion with cardiac tamponade, while one reported case of a cat with chronic AD did not (Scollan and Sisson 2014). However, pericardial effusion developed at the chronic AD stage in this case, suggesting that it is not only associated with acute AD but also with other factors, including severity, underlying diseases and other complications. Thus, further studies are needed to evaluate the association between pericardial effusion and AD.

The present case showed aortic wall calcification from the aortic root to the proximal descending aorta. Vascular calcification is the pathological deposition of mineral in the vascular system, which is associated with various diseases such as atherosclerosis, hypertension, genetic factors and diabetes in humans (Demer and Tintut 2014; Iribarren et al. 2000; Wu et al. 2013). Aortic and cardiac mineralisation has been reported in cats with severe chronic renal failure, systemic hypertension and chronic aortic and mitral valvular endocarditis (Lamb et al. 1991; Keppie et al. 2006; Lefbom et al. 1996; Malik et al. 1999). Despite its complex aetiology, it is possible that underlying predisposing factors such as systemic hypertension (which can lead to aortic degeneration) or the aortic calcification itself may have resulted in adverse effects on vascular compliance, aortic stiffness, vasomotion and plaque stability, leading to AD (Patel and Arora 2008). Moreover, CT scans were performed three months after the initial diagnosis; thus, it can be a subsequent change after dissection. Although controversial studies in humans reported that type A AD is associated with a lower prevalence of atherosclerosis, there is a lack of literature investigating this relationship in cats. (Achneck et al. 2005; Grewal et al. 2023).

In human medicine, the Stanford and DeBakey classifications are used based on the location of the dissection (Czerny et al. 2019; Hebballi and Swanevelder 2009; Juraszek et al. 2022; Lombardi et al. 2020). In Stanford Type A dissection, the ascending aorta is involved, whereas in Type B, it is spared. DeBakey type I and II are defined based on the involvement of the descending aorta. Type A dissections typically require surgery, while type B dissections may be managed non‐surgically under most conditions (Iribarren et al. 2000). The present case had a Stanford type A (DeBakey type II) dissection. However, the cat survived for six months after the diagnosis. Of the four cases of cats with type A dissection reported in the literature, one died shortly after diagnosis (Scollan and Sisson 2014), one was euthanised (Scollan and Sisson 2014), one survived for a year and was euthanised due to other causes (Gouni et al. 2018) and the remaining one was asymptomatic and survived until the last follow‐up (Wey and Atkins 2000). In humans, the mortality rate in acute type A AD in the first 48 h can be > 50% and the condition is considered an emergency (Howard et al. 2021). Although the exact moment in which the initial symptoms appear could be difficult to determine in cats, its chronicity and severity, the degree of compression and the detailed haemodynamic effect of AD are not comparable, suggesting that the mortality rate of AD in this species could be lower than that observed in humans.

Among the various imaging modalities employed to diagnose AD, echocardiography is non‐invasive and fast, but it does not allow for the evaluation of the entire aorta and adjacent structures. In humans, CT angiography of the aorta is considered the investigation of choice, as it allows not only for detailed diagnosis and classification but also for the evaluation of the distal aorta with sensitivity and specificity of 98 to 100% (Foundation A 2010; LePage et al. 2001). In the present case, CT findings correlated with post‐mortem findings, suggesting that this imaging technique can be useful for accurate diagnosis of AD in cats as well. However, the size of the AD measured on the CT was slightly larger than that measured at the post‐mortem exam, which could be either due to the small size of the defect and motion artefact of cardiac structures. In addition, although not observed in this case, a CT exam is useful for the assessment of end‐organ ischaemia and perfusion disorders that can occur with AD (Wey and Atkins 2000). Thus, echocardiography and CT exams should be considered for accurate evaluation when AD is suspected in cats. Although surgical intervention of AD has not been reported in the veterinary literature, thorough evaluation of AD characteristics is a prerequisite for further surgical plans.

In conclusion, this report describes the AD features in a cat with aortic calcification and chylothorax, diagnosed via echocardiography, CT and post‐mortem examination. This is the first report describing both CT and post‐mortem features of AD in a cat. Although rare, AD should be considered as a potential complication in cats with systemic hypertension, aortic degeneration, HCM phenotype and as a differential diagnosis of cats with chylothorax.

Author Contributions

Ji Y: conceptualisation, formal analysis, investigation, methodology, project administration, resources, supervision, visualisation, writing original draft, writing – review and editing. Yoon H: data curation, formal analysis, investigation, methodology, project administration, resources, supervision, validation, visualization, writing ¬ original draft, writing – review and editing. Kim M: formal analysis, investigation, methodology, resources, supervision. Oh B: formal analysis, methodology, Kim B: investigation, methodology, Oh S: investigation, methodology.

Ethics Statement

Ethical approval was not required for as it involved a single case report and relied solely on data collected during the patient's routine clinical diagnosis. Conflicts of Interest

Conflicts of Interest

The authors declare no conflicts of interest.

Peer Review

The peer review history for this article is available at https://publons.com/publon/10.1002/vms3.70359.

Acknowledgements

The authors would like to thank the professors and clinicians of Veterinary Medical Imaging Department of Jeonbuk National University and Shine Animal Medical Center for their assistance.

Funding: The research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (2019R1A6A1A03033084).

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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