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Compendium March 2013 (Vol 35, No 3)

Clinical Snapshot: A Cardiac Mass in a Golden Retriever

by Kevin J. Schabbing, DVM, George A Kramer, DVM, DACVIM (Cardiology)

    Case Presentation

    A 3-year-old neutered golden retriever presented through our emergency service for a cardiology consultation for a 2-week history of exertional syncope, lethargy, decreased appetite, and weight loss. There was no known history of congenital heart disease, the patient was current on vaccinations, and heartworm preventive had been given periodically throughout the preceding year. A presumptive diagnosis of bacterial endocarditis had been made by the referring veterinarian based on a mobile echocardiogram that had been performed by a non–board-certified veterinarian.

    On initial examination by the emergency clinician, the patient appeared bright, alert, and responsive. A sinus tachycardia was noted (heart rate: 154 bpm; normal: 80 to 120 bpm), and a grade III/VI left systolic murmur with a point of maximal intensity over the fifth intercostal space was noted on physical examination. The patient was eupneic, and no rales were ausculted. Upon admission, blood and urine samples were submitted to a commercial laboratory for culture and susceptibility testing. A urinalysis performed by the same laboratory revealed 2+ proteinuria and a pH of 7.5. Blood urea nitrogen and creatinine levels were measured by the in-house laboratory and were 8.3 mg/dL (normal: 7 to 27 mg/dL) and 1.8 mg/dL (normal: 0.5 to 1.8), respectively. Systolic blood pressure was measured at 100 mm Hg (normal: 80 to 120 mm Hg) using Doppler ultrasonography. Cefazolin (22 mg/kg IV three times daily) was started before consultation with the cardiologist. Continuous electrocardiography was implemented to monitor for cardiac arrhythmias. Results of a blood chemistry test and a complete blood count (CBC) submitted to a commercial laboratory showed no abnormalities except a monocytosis of 1.17 × 103/µL (normal: 0 to 0.84 × 103/µL).

    On day two, echocardiography and abdominal ultrasonography were performed. The echocardiogram showed a 2.5 × 2.6–cm, mottled, hyperechoic mass on the posterior mitral valve leaflet and a 4.3 × 2.7–cm mass with similar echogenicity on the anterior mitral valve leaflet (FIGURE A). The mass on the anterior leaflet created a dynamic outflow obstruction of the left ventricular outflow tract, resulting in an increased aortic outflow velocity of 3.8 m/sec (normal: 1.15 ± 0.15 m/sec).1 Moderate mitral regurgitation was present. The contractility was mildly decreased with a shortening fraction of 25% (normal: 27% to 55%). No pleural or pericardial effusion was present.

    Figure A. The yellow arrows outline the mass invading the myocardium and mitral valve (blue arrow). The mitral valve is thickened and irregular. Notice the moderate dilation of the left atrium due to the combination of the left ventricular outflow obstruction created by the mass and regurgitation from the mitral valve. Ultrasonographically, the mass has a mottled appearance. This primary cardiac tumor took on a nodular form.

    The abdominal sonogram indicated mildly decreased renal corticomedullary architecture and no evidence of an abdominal mass. Thoracic radiography showed mild, patchy pulmonary infiltrates with some areas of hypolucency. Antibiotic therapy was switched to enrofloxacin (15 mg/kg IV once a day) for potential bacterial endocarditis pending blood culture results. Blood and urine culture results were negative after 48 hours.

    Based on the uniform echogenicity of the mitral valve masses, a presumptive diagnosis of cardiac myxoma was made.

    1. What clinical pathologic abnormalities would be expected on a CBC in a patient with infective endocarditis (IE)?

    2. What is an appropriate differential diagnosis for a primary cardiac mass in a young dog?

    3. What diagnostic tests or procedures could be used to confirm a cardiac mass and aid in making a histologic diagnosis of a primary cardiac tumor?

    Answers and Explanations

    1. In a case of bacterial endocarditis, a mature leukocytosis with a left shift is likely to be seen on a CBC. If the patient is septic, a leukopenia with a left shift may be encountered. Additionally, thrombocytopenia and anemia have been described.2 Thrombocytopenia may be associated with states of disseminated intravascular coagulation (DIC) or consumption from the active disease process. Anemia, if present, may be regenerative or nonregenerative due to hemolysis or chronic inflammation, respectively.

    2. Thrombus formation and neoplasia (hemangiosarcoma [HSA], chemodectoma). Thrombus formation is much more likely than a primary cardiac tumor in a young dog. Underlying disease processes causing secondary thrombus formation should be ruled out before considering a primary cardiac tumor. Diagnostic differentials for secondary thrombus formation include a wide array of inflammatory conditions, protein-losing nephropathy (PLN) or protein-losing enteropathy (PLE), and hyperadrenocorticism. Possible inflammatory conditions include sepsis, pyometra, pancreatitis, immune-mediated hemolytic anemia, systemic lupus erythematosus, DIC, and neoplasia. PLN may include glomerulonephritis, amyloidosis, and pyelonephritis. PLE may include inflammatory bowel disease, lymphoma, and lymphangiectasia. PLE and PLN both induce thrombus formation due to the loss of antithrombin through the gastrointestinal tract and kidneys, respectively.

    3.After establishing a diagnosis of a cardiac mass with echocardiography, cardiac catheterization or thoracoscopy may allow collection of a histologic sample. Ultrasound-guided biopsy is another option, depending on the location of the mass, but carries a greater risk of hemorrhage.

    If a mass is invading the lumen of a great vessel or heart chamber, cardiac catheterization is an ideal procedure for collection of a histologic sample. Thoracoscopy provides an intrathoracic approach for an extraluminal mass. Thoracotomy is an option but is associated with significantly more morbidity. An effective, definitive treatment plan depends on a histologic diagnosis.

    Diagnosis and Outcome

    We recommended surgical resection of the masses. Surgery for resection of valvular myxomas or myxosarcomas requires cardiopulmonary bypass (which was available at our hospital), since inflow occlusion would be unlikely to result in enough time to resect the masses. The owner declined surgery.

    Blood and urine samples were submitted to acommercial laboratory for a full coagulation profile, antithrombin III level, and urine protein:creatinine (UPC) ratio on day three. The UPC ratio was 0.5 (normal: <1.0). The coagulation profile showed a decreased partial thromboplastin time of 9.7 seconds (normal: 10 to 25 seconds), a prothrombin time of 8.3 seconds (normal: 6 to 12 seconds), a platelet count of 203,000/µL (normal: 170,000 to 400,000/µL), a fibrinogen level of 348 mg/dL (normal: 150 to 400 mg/dL), and a D-dimer level of <250 ng/mL (normal: 0 to <250 ng/mL). The antithrombin III level was within normal range at 96% (normal: 75% to 120%). Heparin (200 U/kg SC q8h) was instituted to prevent any further potential thrombus formation and embolic sequelae.

    On day four, a repeat CBC performed in house noted a monocytosis of 1.56 × 103/µL (normal: 0.1 × 103to 1.40× 103/µL), suggesting chronic inflammation (possibly secondary to the presence of the tumor). The patient experienced a syncopal episode and was noted to have intermittent ventricular premature contractions (VPCs) and sinus tachycardia throughout the evening. The following morning, the patient was considerably weaker, reluctant to stand or walk, and anorectic. Physical examination revealed a mild increase in bronchovesicular sounds bilaterally, weak femoral pulses, and intermittent VPCs. Due to the rapid decline, syncope, and sinus tachycardia, the patient was started on digoxin (0.25 mg [0.007 mg/kg] PO q12h) for rate control. Furosemide (2 mg/kg IV q12h) was initiated due to the increased bronchovesicular sounds, although congestive heart failure (CHF) was considered less likely based on the echocardiogram. With the patient’s progressive decline, poor prognosis, and lack of response to treatment, the owner elected for humane euthanasia.

    A necropsy was performed. Histopathology results were consistent with a grade I myxosarcoma of the mitral valve. The tumor consisted of spindle-shaped to stellate cells embedded in a myxomatous matrix. Nuclei were oval and pleomorphic and contained prominent nucleoli, and mitoses were few. This particular lesion grew outward, forming a mass, and infiltrated the endocardium and myocardium of the left atrium (FIGURE A). Marked inflammation was noted throughout various sections of the lungs.  Pulmonarythrombosis with accompanying hemorrhage and marked neutrophilic bronchial inflammation was present. The pulmonary changes were likely related to the presence of the tumor.


    Primary cardiac tumors are rare in humans and domestic small animals.3 Reports of cardiac myxomas and myxosarcomas are rare in the veterinary literature. Roberts4 reported the first case of a cardiac myxoma in a dog in 1959, involving a 14-year-old spayed schnauzer. Primary cardiac tumors in dogs have a quoted incidence of 0.19%,3 the most common being HSA arising from the right auricle or atrium, followed by chemodectoma. HSA is believed to account for 40% to 69% of all primary cardiac tumors in dogs.5 In humans, the prevalence of primary cardiac tumors is 0.002% to 0.25%, and the most common cardiac tumor is myxoma, with 86% developing from the left atrium.6

    Cardiac tumors have been described as involving intracavitary, intramural, pericardial, or heart- base locations as well as great vessels. The clinical signs associated with cardiac tumors can be numerous and vague, typically reflecting signs that are directly related to the anatomic location and size of the neoplasm.3 Common clinical signs associated with primary cardiac tumors include syncope, weakness, anorexia, and exercise intolerance; pericardial effusion, cardiac tamponade, pulmonary edema, CHF, pleural effusion, conduction disturbance arrhythmias, and pulmonary and systemic emboli have also been associated with cardiac tumors.3,5 Human case reports have described two morphologic types of cardiac myxomas, solid and papillary,7 while veterinary case reports have described polypoid and nodular cardiac myxomas.

    Some debate still exists as to the exact origin of cardiac myxosarcomas. Cardiac myxomas are believed to develop in the subendocardial layer, arising from a multipotential mesenchymal cell.8 Myxomas are nonencapsulated, infiltrative tumors with poorly defined margins.9,10 These tumors differ from fibrosarcomas in their abundance of intercellular matrix, predominantly made of mucin.9 Histologically, myxomas consist of stellate to spindle-shaped cells scattered through an abundant myxoid matrix.10 Grossly, myxomas and myxosarcomas appear gray-white with a soft texture and clear mucoid fluid. The distinction between a myxoma and myxosarcoma is based on cellular changes and criteria for malignancy. Cytologic atypia is sparse to nonexistent in myxomas.10 Myxosarcomas, however, are unique in their consistent identification and increase in mitotic figures, mitosis, the degree of anisocytosis and anisokaryosis, and the malignant biologic behavior for separate local and distant metastasis.11

    The gold standard for the identification of cardiac masses in small animals is two-dimensional, real-time echocardiography. A skilled ultrasonographer can readily and accurately discern, localize, and determine the surgical accessibility of the tumor.12

    Given the exceptional rarity of canine myxosarcoma, this case is of particular interest because it entailed a primary cardiac tumor without metastases in a dog only 3 years of age. Additionally, it highlights the importance of not eliminating neoplasia as a diagnostic differential in a young animal, even when a tumor is considered to be rare.

    Most cases of primary cardiac tumors in dogs involve animals between the ages of 7 and 15 years.3 The sex of the dog does not seem to affect tumor incidence, although castrated males are slightly more at risk than intact males.3 The most prominent presenting signs are syncope, lethargy, and anorexia. In this particular case, a negative outcome was due to pulmonary thrombosis and marked inflammation, which was likely a result of ongoing pulmonary embolisms secondary to the neoplasia. Thromboembolic disease and its sequelae are common in humans. In people, the treatment of choice for cardiac myxoma is surgical resection because of the high frequency of systemic emboli.5 The location of the tumor may be predictive of clinical sequelae. In humans, septal location correlated with CHF and extraseptal locations with neurologic and systemic embolization.7

    Lidocaine was not instituted in this particular case because only single intermittent VPCs were present. It is prudent to monitor patientswith intermittent VPCsclosely for the development of ventricular tachycardia, for which treatment would be indicated.

    Foale et al11 reported successful surgical treatment of a myocardial myxosarcoma in a dog. In this case, a solitary lesion with no gross metastatic disease was detected, surgical intervention was accessible, and the tumor was excised successfully. The dog lived 11 months without recurrence of the previous clinical signs.11 After 11 months, lethargy, weight loss, and diarrhea developed. Metastasiswas noted in the abdominal cavity on ultrasonography.The owners elected for humane euthanasia.

    Patients with primary cardiac tumors affecting the myocardium or pericardium and without metastatic disease may be candidates for cardiothoracic surgery. Intrathoracic surgery to remove primary cardiac tumors is a treatment option in select cases. Some patients may live an acceptable length of time without recurrence of tumor-induced clinical signs after surgery. A subphrenic pericardectomy should be included as a palliative effort to prevent pericardial effusion.5 These measures may involve the use of thoracoscopy to help reduce morbidity.

    The role of radiation therapy for cardiac myxosarcomas has yet to be determined in dogs. Radiation therapy is regularly used to treat intrathoracic tumors (round cell tumors and carcinomas). Treatment for primary cardiac tumors may include surgery, chemotherapy, and radiation therapy alone or in combination.

    To the best of our knowledge, the combination of surgery and chemotherapy or radiation therapy for primary cardiac myxosarcomas has not been evaluated due to the rarity of these tumors. Additional information and reporting on treatment and outcomes of cardiac myxosarcomas in veterinary medicine would be welcomed as they occur. In humans and, ideally, in dogs, open heart surgery with tumor removal is the recommended treatment of choice.


    The authors thank Barbara Powers, DVM, PhD, DACVP, of Colorado State University School of Veterinary Medicine and Biomedical Sciences, for the histopathology results.


    1. Bonagura JD. Appendix 2: canine. In: Boon JA, ed. Veterinary Echocardiography. Ames, IA: Wiley-Blackwell; 2011:531-557.

    2. DeClue A. Sepsis and the systemic inflammatory response syndrome. In: Ettinger SJ, Feldman EC, eds. Veterinary Internal Medicine. St. Louis, MO: Saunders-Elsevier; 2010:523-527.

    3. Ware WA, Hopper DL. Cardiac tumors in dogs: 1982-1995. J Vet Intern Med 1999;13(2):95-103.

    4. Roberts SR. Myxoma of the heart in a dog. J Am Vet Med Assoc 1959;134(4):185-188.

    5. Kisseberth WC. Neoplasia of the heart. In: Withrow SJ, Vail DM, eds. Small Animal Clinical Oncology. 4th ed. Philadelphia, PA: WB Saunders; 2006:809-812.

    6. Mueller DK, Karlheinz P. Benign cardiac tumors.Medscape; 2011. www.emedicine.com/med/topic2999.htm.Accessed February 2013.

    7. Swartz MF, Lutz CJ, Chandan VS, et al. Atrial myxomas: pathologic types, tumor location, and presenting symptoms. J Card Surg 2006;21(4):435-440.

    8. Machida N, Hoshi K, Kobayashi M, et al. Cardiac myxoma of the tricuspid valve in a dog. J Comp Pathol 2003;129(4):320-324.

    9. Theilen GH, Madewell BR. Tumours of skin and subcutaneous tissues. In: Veterinary Cancer Medicine. 2nd ed. Philadelphia, PA: Lea & Febiger; 1987:290.

    10. GoldschmidtMH. Tumors of the skin and soft tissue. In: Meuten DJ, ed. Tumors in Domestic Animals. Ames, IA: Blackwell Publishing Company; 2002:91.

    11. Foale RD, White RA, Harley R, Herrtage ME. Left ventricular myxosarcoma in a dog. J Small Anim Pract 2003;44(11):503-507.

    12. Thomas WP, Sisson D, Bauer TG, Reed JR. Detection of cardiac masses in dogs by two-dimensional echocardiography. Vet Radiol 1984;25(2):65-72.

    References »

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