History
A 7-year-old 42.8-kg (94.2-lb) castrated male German Shepherd Dog was evaluated at the Kansas State University Veterinary Health Center on an emergency basis because of a sudden onset of lethargy. While in the waiting room, the dog had an episode of syncope. The owner did not report any previous clinical signs.
Clinical and Gross Findings
On physical examination, the dog had weak pulses, muffled heart sounds, and pale mucous membranes. Results of a CBC were unremarkable. Serum biochemical analysis revealed hypoalbuminemia and azotemia. Thoracic radiography revealed cardiomegaly and an enlarged vena cava. Limited echocardiographic examination revealed pericardial effusion with tamponade secondary to a large (8 × 4-cm), lobular, oval, slightly hypoechoic homogeneous mass located at the heart base, adjacent to the aorta and pulmonary trunk. Pericardiocentesis was performed, and 280 mL of frank blood was removed from the pericardial sac. The dog was discharged from the hospital and remained apparently healthy for 2 years until it was again evaluated on an emergency basis because of an episode of lethargy, collapse, and a distended abdomen. Treatments for congestive heart failure and ventricular tachycardia were initiated. The dog became refractory to treatment 7 months later, and its clinical signs and azotemia worsened. The owners elected euthanasia on the basis of the patient's deteriorating condition and requested that only the dog's heart be examined during necropsy.
At necropsy, the abdomen was severely distended and contained many liters of clear, serosanguineous fluid. At the base of the heart were multiple, firm, smooth masses, one of which extended into the mediastinum. The largest mass, which appeared to be multiple coalescing masses, measured 6.5 × 3.5 × 3.5 cm. It was adhered to the pericardial sac and had infiltrated the pulmonary trunk. Additional masses of variable size were located adjacent to each other. One was found partially occluding the right atrium (Figure 1); others were found between the right atrium and the adjacent right ventricular wall, in the space between the right auricle and the pulmonary trunk, and at the base of the aorta. There was a 3-cm-diameter spherical nodule adjacent to the aorta at the brachiocephalic trunk. A lobulated, soft, red mass (7.5 × 5.0 × 3.0 cm) filled much of the right atrium and auricle and bulged into the right ventricle. The tracheobronchial lymph nodes were moderately enlarged and firm.
Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page→
Histopathologic Findings
Microscopically, the heart masses were composed of densely cellular sheets of polygonal or round cells with discrete cell borders that were subdivided into distinct packets or lobules by fine fibrovascular septa (Figure 2). The cells had a moderate amount of eosinophilic, finely granular cytoplasm and a round basophilic nucleus with abundant, coarsely stippled chromatin. Mitotic figures were rare, with a mean mitotic rate of 0 to 1/10 hpf (400×). There were scattered areas of necrosis. Multiple vessels in the soft tissue at the base of the heart were filled by tumor emboli composed of solid sheets of neoplastic cells. Tissues thought to be lymph nodes at necropsy were solid sheets of the same neoplastic cells that composed the heart masses. Immunohistochemical staining for chromogranin A revealed strong, diffuse, granular cytoplasmic staining in the neoplastic cells.
Morphologic Diagnosis and Case Summary
Morphologic diagnosis: aortic body carcinoma at the base of the heart with vascular invasion and spread to surrounding soft tissue.
Case summary: aortic body carcinoma in a dog.
Comments
The anatomic location and gross and histopathologic findings for the heart masses in the dog of the present report were consistent with aortic body carcinoma, a malignant neoplasm of the chemoreceptor cells located along the heart base. These chemoreceptors belong to a dispersed collection of neuroendocrine cells that originate embryologically from the neural crest ectoderm. They detect changes in blood pH and blood concentrations of oxygen and carbon dioxide.1,2 The neuroendocrine nature of the neoplastic cells in this dog was confirmed by immunohistochemical reaction with chromogranin A, a protein that is present in the secretory granules of normal and neoplastic cells of neuroendocrine lineage. Studies3–5 evaluating the correlation between the expression of chromogranin A and the malignant potential of canine chemodectomas have provided contrasting results. It has been shown that the expression of chromogranin A decreases with increasing malignancy in canine chemodectomas3,4; however, a more recent study5 revealed no correlation. More research is likely needed to determine the relationship between chromogranin A expression and malignancy in this tumor type.
The term chemodectoma is applied to paragangliomas that originate from aortic or carotid bodies. Chemodectomas from the aortic body are the most commonly reported chemoreceptor tumor or paraganglioma in dogs. There is a significantly higher incidence of chemodectomas in some brachiocephalic dogs, specifically Boxers and Boston Terriers.6 Aortic body tumors usually have a more prolonged, benign course than do carotid body tumors. Aortic body tumors are typically not functional but grow slowly and exert pressure on the atria, eventually causing the appearance of clinical signs.7 These tumors may invade the vena cava, atria, pericardium, and adjacent thin-walled veins. If metastasis occurs, the lungs and liver are usually first affected.5,7 It is difficult to predict the malignant potential of chemodectomas on the basis of defined histopathological features such as nuclear pleomorphism, high rate of mitotic figures, or high nuclear-to-cytoplasmic ratio. In the dog of the present report, the tumor invaded beyond the capsule into the walls of multiple vessels and neighboring tissues, thereby favoring a diagnosis of an aortic body carcinoma.
Heart tumors can be diagnosed on the basis of clinical signs and confirmation of the presence of a mass via echocardiography.7 Clinical signs may vary, but commonly include exercise intolerance, syncope, and difficulty breathing.1,7 Development of cardiac tamponade, as in the dog of the present report, results in secondary venous congestion and lowered cardiac output.8 Affected dogs, however, may have no clinical signs.7 A major differential diagnosis for chemodectoma is hemangiosarcoma, the most common primary cardiac tumor of dogs.8 The only way to definitively diagnose the tumor type is by histologic examination of tumor tissue samples. Cytologic evaluation of fine-needle aspirates does not usually provide conclusive findings because these tumors do not exfoliate well. The case described in the present report had histologic features characteristic of canine aortic body tumors.5 In addition, we did not observe any primitive follicular structure or colloid containing follicles in the tissue sections, thereby ruling out ectopic tumors of thyroid origin.
Treatment of aortic body carcinoma is quite difficult. Very rarely can these tumors be completely excised during surgery.1 Even if a mass is resectable, surgery generally has a high risk because of the location and vascularity of aortic body carcinomas.7 Pericardiectomy is a palliative option when a mass cannot be removed. Pericardiectomy may increase survival time by preventing an increase in diastolic filling pressure, which subsequently reduces signs of right-sided heart failure.1,7 Overall prognosis for affected dogs varies; in 1 study7 of dogs with heart-base masses, the survival time ranged from 0 to 1,096 days.
References
1. Ehrhart N, Ehrhart EJ, Willis J, et al. Analysis of factors affecting survival in dogs with aortic body tumors. Vet Surg 2002;31:44–48.
2. Deim Z, Szalay F, Glavits R, et al. Carotid body tumor in dog: a case report. Can Vet J 2007;48:865–867.
3. Aresu L, Tursi M, Iussich S, et al. Use of S-100 and chromogranin antibodies as immunohistochemical markers in detection of malignancy in aortic body tumours in dog. J Vet Med Sci 2006;68:1229–1233.
4. Noszczyk-Nowak A, Nowak M, Paslawska U, et al. Cases with manifestation of chemodectoma diagnosed in dogs in Department of Internal Diseases with Horses, Dogs and Cats Clinic, Veterinary Medicine Faculty, University of Environmental and Life Sciences, Wroclaw, Poland. Acta Vet Scand 2010;52:35–41.
5. Yamamoto SR, Fukushima R, Hirakawa A, et al. Histopathological and immunohistochemical evaluation of malignant potential in canine aortic body tumours. J Comp Pathol 2013;149:182–191.
6. Patnaik AK, Liu SK, Hurvitz AI, et al. Canine chemodectoma (extra-adrenal paragangliomas)—a comparative study. J Small Anim Pract 1975;16:785–801.
7. Vicari ED, Brown DC, Holt DE, et al. Survival times of and prognostic indicators for dogs with heart base masses: 25 cases (1986–1999). J Am Vet Med Assoc 2001;219:485–487.
8. Ware WA, Hopper DL. Cardiac tumors in dogs: 1982–1995. J Vet Intern Med 1999;13:95–103.