Chemoreceptor organs are sensitive to changes in the carbon dioxide and oxygen content and pH of the blood. They aid in the regulation of respiration and circulation. Although chemoreceptor tissue appears to be widely distributed in the body, tumors (chemodectomas) develop principally in the aortic bodies (more frequent in animals) and carotid bodies (more frequent in humans).
Etiology and Pathogenesis of Chemodectomas in Animals
A chemodectoma is a tumor arising from chemoreceptor cells.
Multicentric neoplastic transformation of chemoreceptor tissue occurs frequently in brachycephalic breeds of dogs. Although the etiology of carotid and aortic body tumors is unknown, it has been suggested that a genetic predisposition aggravated by chronic hypoxia may account for the higher risk in certain brachycephalic breeds. Carotid bodies of several mammalian species, including dogs, have undergone hyperplasia when subjected to chronic hypoxia by living in a high-altitude environment.
The carotid bodies are located at the carotid bifurcation, whereas the aortic bodies are found near the base of the heart. Aortic body tumors are often referred to as heart-base tumors. Another type of heart-base tumor is due to ectopic thyroid carcinoma.
Aortic body carcinomas may infiltrate the wall of the pulmonary artery to form papillary projections into the lumen or invade through the wall into the lumen of the atria. Although tumor cells often invade blood vessels, metastases to the lungs and liver are infrequent in dogs with aortic body carcinomas. Nonetheless, the local and physiologic effects are important, including those of adenomas.
Aortic body tumors tend to be more benign than carotid body tumors. They grow slowly by expansion and exert pressure on the vena cava and atria. Aortic body carcinomas may invade locally into the atria, pericardium, and adjacent large, thin-walled vessels. Aortic body tumors in animals are not functional (ie, they do not secrete excess hormone into the circulation); however, as space-occupying lesions, they may result in various functional disturbances.
Epidemiology of Chemodectomas in Animals
Chemodectomas are found primarily in dogs and rarely in cats and cattle. They are more common in older animals. Aortic body tumors are more common in domestic species than are carotid body tumors.
Brachycephalic breeds of dogs, such as the Boxer and Boston Terrier, are predisposed to tumors of the aortic and carotid bodies. Dogs with carotid body tumors often concomitantly have aortic body tumors. In dogs, malignant aortic body tumors occur less frequently than adenomas.
Aortic body tumors occur more often in male dogs.
In cats, chemodectomas mostly occur in domestic shorthaired cats, with no sex predilection.
Clinical Features of Chemodectomas in Animals
Chemodectomas may arise from chemoreceptors in the cardiovascular system (ie, the aortic and carotic bodies).
Aortic body tumors appear most frequently as single masses or as multiple nodules within the pericardial sac near the base of the heart. They vary considerably in size (0.5–12.5 cm), with carcinomas generally larger than adenomas.
Solitary, small adenomas either are attached to the adventitia of the pulmonary artery and ascending aorta or are embedded in the adipose connective tissue between these major vascular trunks. Larger adenomas may indent the atria or displace the trachea, are multilobular, and partially surround the major arterial trunks at the base of the heart.
Aortic body tumors can result in clinical signs including right-side congestive heart failure. Clinical signs may include cardiac decompensation due to pressure on the atria or vena cava (or both) associated with larger aortic body adenomas and carcinomas.
Clinical signs associated with the mass effects of aortic body tumors include pericardial effusion and evidence of right-side congestive heart failure.
Carotid body tumors arise near the bifurcation of the common carotid artery, usually as a unilateral, slow-growing mass. Adenomas are usually 1–4 cm in diameter. The bifurcation of the carotid artery is incorporated in the mass, and tumor cells are firmly adherent to the tunica adventitia.
Clinical signs associated with carotid body tumor growth include esophageal dysfunction and dyspnea.
Malignant carotid body tumors are larger and more coarsely multinodular than adenomas. Although carcinomas appear to be encapsulated, tumor cells invade the capsule and penetrate into the walls of adjacent vessels and lymphatics. The external jugular vein and several cranial nerves may be incorporated by the neoplasm.
Diagnosis of Chemodectomas in Animals
A presumptive diagnosis of chemodectoma can be made based on signalment, history, clinical signs, physical examination findings, and radiographic evaluation.
Histologic evaluation is the gold standard for diagnosis of carotid or aortic body tumors. However, because of their location, it is often difficult to obtain biopsy specimens. Tumors can be found incidentally or diagnosed at necropsy. The histologic characteristics of chemodectomas are essentially similar whether derived from the carotid or aortic body.
Treatment and Prognosis of Chemodectomas in Animals
Treatment and prognosis of chemodectomas vary by tumor type.
Pericardiectomy is reported to be effective potential surgical treatment for aortic body tumors.
Complete excision or biopsy of carotid body tumors is often is difficult because of the high vascularity and intimate relationship with major arterial trunks in the neck.
Metastases of carotid body tumors occur in ~30% of cases and have been found in the lung, bronchial and mediastinal lymph nodes, liver, pancreas, and kidneys.
Aortic body tumors are more common in domestic species than are carotid body tumors.
Aortic body tumors can result in clinical signs including right-side congestive heart failure.
Clinical signs associated with carotid body tumors include esophageal dysfunction and dyspnea.
For More Information
Treggiari E, Pedro B, Dukes-McEwan J, Gelzer AR, Blackwood L. A descriptive review of cardiac tumours in dogs and cats. Vet Comp Oncol. 2015;15(2):273-288. doi:10.1111/vco.12167
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