Aortic mineralization in a cat︓A case report
Chiaki Morita, MVS１, Yusuke Yamashita, BVS２, Takayoshi Miyabayashi, BVS, MS,PhD, Dipl. ACVR１
１︓iVEAT Fukuoka Veterinary Specialty Practice, 2︓Aoi Animal Hospital
History
A 9-year-old, neutered male, American shorthair cat had resection of a bladdermass (urothelial carcinoma) at a university hospital and was discharged after
three days. The following day, after subcutaneous fluid administration at a
primary veterinary clinic, the patient developed dyspnea and diagnosed withpleural effusion, pulmonary edema, and cardiomyopathy. Pleural drainage andcardiac treatment (Pimobendan and ACE inhibitor) were initiated. Seven days
later, the patient came to Aoi Animal Hospital for a second opinion.
Clinicopathological findings
The results of complete blood count and blood chemistry tests were within anormal limit except for a high SNAP NT-proBNP value. The blood pressure was ahigh end of normal (138 mmHg; normal value is <140mmHg).
Radiographic and CT imaging findings
Radiographic findings
On the right lateral view, there was mineralization of vascular wall from the aortic
root to the abdominal aorta (Figure 1a). In the ventrodorsal (VD) anddorsoventral views, the left ventricular wall was attached to the thoracic wall, andcardiac enlargement was observed (Fig. 1b). In the VD view, the lengths of theleft and right kidneys were 1.7 and 2.5 times of the length of the second lumbar
vertebral body, respectively (Fig. 1b).
Computed tomography (CT) imaging findings
Mineralization was seen from the aortic root to the abdominal aorta (Figure 2a).
Multi-phased, non-selective, intravenous contrast studies were performed. Theinterventricular septum and the papillary muscle appeared thickened (Figure 2c).
Discussion
In cats, aortic mineralization on thoracic radiographs was rare.1-4 Two reportssuggested that the causes of aortic mineralization were arteriosclerosis andmetastatic calcification due to chronic renal failure.1,2
In dogs, aortic mineralization was also rare, and it was considered to have noclinical significance.4
In humans, however, the incidence of aortic mineralization on thoracic

radiographs was 1.9% in men and 2.6% in women (the ages of 30 and 89).5,6
Furthermore, in humans, aortic mineralization was associated witharteriosclerosis, chronic renal failure, aging, and cardiovascular diseases.6-9
In humans, arteriosclerosis was the most common cause of aortic
mineralization.10 The risk factors of arteriosclerotic damage include hypertension,
dyslipidemia, and diabetes mellitus.11 In this case, dyslipidemia and diabetes
mellitus were negative because of blood test results. In this patient, the bloodpressure was within a normal range, but the value was in the high end.12 Thus,
hypertension could not be completely ruled out.
Metastatic calcification due to chronic renal failure was less likely in this patient.
Although the patient had the left renal atrophy, serum calcium levels, urea
nitrogen, and creatinine were all normal on the blood test. On contrast-enhanced
CT imaging, renal excretory function appeared normal.
Aging could cause degenerative changes and dystrophic calcification of aorta.
Thus, the aging factor could not be ruled out.
In human reports, aortic calcification was associated with cardiovasculardiseases.6,13 Aortic calcification could cause adverse effects on vascularcompliance, vasomotion, and plaque stability.14 Aortic stiffness including aortic
calcification correlated with high left ventricular afterload.13 In addition,cardiomyopathy could cause turbulence and reduced perfusion of blood in theaorta, which might have resulted in the aortic mineralization in this case.15,16
Finally, this patient had urothelial carcinoma of the bladder in the past. The aortic
calcification might have occurred due to the presence of carcinoma. In themolecular biological aspects, osteopontin was a multifunctional glycoprotein thatwas involved in cardiovascular disease, cancer, and biomineralization (the processby which organisms produce minerals).17 In humans, overexpression ofosteopontin promoted carcinogenesis, progression, and metastasis of multiple
malignant tumors.18 Notably, in humans, increased osteopontin expression wasobserved in urothelial carcinoma of the urinary bladder.19 We could not examined
osteopontin in this patient.
In this case, both cardiac disease and urothelial carcinoma might be associatedwith the aortic mineralization.
Conclusion
When aortic mineralization was observed in cats, chronic renal failure andunderlying diseases that triggers arteriosclerosis should be examined. In addition,
cardiac diseases should be ruled out for a loss of aortic elasticity and increased

afterload. Molecular biological mechanisms such as osteopontin should be thesubject of future research.

Figures and captions

Figure１a

Figure１b

1a. Right lateral radiograph of the thorax and cranial abdomen (cropped).
Mineralization of the aortic root to abdominal aorta is seen (arrows).
1b. Ventrodorsal radiograph of the thorax and cranial abdomen (cropped). The
cardiac shadow is wide and appears enlarged. The left kidney appears smaller
than normal (arrow).

Figure 2a

Figure２b

Figure２c2a. Sagittal CT image. Mineralization is seen from the aortic arch to abdominalaorta. 2b. Dorsal CT image of the right and left kidneys in the portal venous
phase. The sizes of the left and right kidneys were different, but the renal
excretory function appears to be normal. 2c. Dorsal CT image of the thorax in thelate arterial phase. Cardiac enlargement and mineralization of the aortic wall(arrow) were noted.

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