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Ann Thorac Surg 2007;83:1882-1884
© 2007 The Society of Thoracic Surgeons
a Department of Cardiology, Akron General Medical Center, Akron, Ohio
b Department of Pathology, Akron General Medical Center, Akron, Ohio
c Department of Neurology, Akron General Medical Center, Akron, Ohio
d Department of Cardiothoracic Surgery, Akron General Medical Center, Akron, Ohio
Accepted for publication December 6, 2006.
* Address correspondence to Dr Hayek, Akron General Medical Center, Department of Cardiology, 400 Wabash Ave, Akron, OH 44307 (Email: hayeke{at}adelphia.net).
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A 58-year-old man with longstanding stage II hypertension presented to the hospital with the acute onset of chest pain and expressive aphasia while riding a stationary bicycle. His physical examination was notable for hypertension (161/94 mm Hg) and mild expressive aphasia and dysarthria.
Results of an urgent brain computed tomography (CT) and CT angiography, with intravenous contrast administration, were normal. There was no evidence of significant stenosis of the distal common carotid arteries, carotid bifurcations, internal carotid arteries, distal vertebral arteries, basilar artery, circle of Willis, or proximal intracranial vasculature. The patient was begun on aspirin and unfractionated intravenous heparin and experienced complete resolution of the neurologic deficits within 7 hours of symptom onset.
Diffusion-weighted brain magnetic resonance imaging (MRI) the next day demonstrated increased signal within a focal area of the cortex in the left parietal lobe just above the sylvian fissure, consistent with an acute ischemic stroke [1].
Serial cardiac enzymes on admission were mildly elevated, consistent with myocardial infarction. Left heart catheterization demonstrated minimal coronary atherosclerosis, and a vascular mass was visualized on contrast injection of the right coronary artery (Fig 1). Transesophageal echocardiography (TEE) demonstrated a well-circumscribed round mass located within the anterior wall of the right atrium near the atrioventricular groove and a patent foramen ovale (PFO) with right-to-left shunt (Fig 2).
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Preoperatively, the patient’s blood pressure required treatment with amlodipine, lisinopril, metoprolol, and nitroglycerin for adequate control. After excision of the tumor, his blood pressure remained normal without antihypertensive treatment. He was discharged 6 days after surgery. The patient had an uneventful postoperative recovery, and 2 months after surgery was normotensive and exercising in cardiac rehabilitation.
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Although hypertension represents the most common clinical presentation, functional tumors may also cause symptoms related to catecholamine excess, including palpitations, headache, and sweating [3]. Constitutional symptoms, chest pain, heart failure, mitral insufficiency, embolic phenomenon, hypertensive crisis, and compressive or obstructive symptoms have also been reported [5].
Once excess plasma or urinary catecholamines or their metabolites are demonstrated, localization of cardiac pheochromocytoma represents a significant diagnostic challenge. Multiple techniques, including CT, MRI, iodine-131-meta-iodobenzylguanidine scintigraphy, indium-octreotide scintigraphy, coronary angiography, TEE, and staged venous sampling for catecholamines have been used to successfully localize the tumor.
Treatment consists of preoperative 
-adrenergic and ß-adrenergic blockers, and surgical resection on total cardiopulmonary bypass. These tumors are highly vascular, frequently being supplied by the coronary arteries, and are locally invasive; thus, complete resection is often technically difficult. Patients may require extensive cardiac reconstruction, cardiac autotransplantation, or orthotopic cardiac transplantation [6, 7]. Most of the tumors are benign, and most patients in whom complete excision is possible have a good long-term prognosis [3].
In this patient, the cardiac paraganglioma presented with a paradoxical embolic stroke and myocardial infarction. With the exception of the rare demonstration of paradoxical embolus in transit, this diagnosis is usually one of exclusion. Because our patient demonstrated no evidence of significant carotid artery or intracranial stenosis, had no hematologic disorder that would predispose to acute ischemic stroke, and TEE demonstrated no other possible cardiac or aortic source of embolus, paradoxical embolus of the right-atrial based tumor across a PFO is the most likely mechanism of stroke. Although catecholamine levels were not measured in this patient, the prompt resolution of severe hypertension after excision supports the probable functionally active nature of this tumor.
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  F. Kargar and M. H. Aazami Right Atrial Chemodectoma With Atypical Chest Pain: A 6-Year Surgical Follow-Up Ann. Thorac. Surg., September 1, 2008; 86(3): 1006 - 1008. [Abstract] [Full Text] [PDF]
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 R. Kennelly, R. Aziz, M. Toner, and V. Young Right atrial paraganglioma: an unusual primary cardiac tumour Eur. J. Cardiothorac. Surg., June 1, 2008; 33(6): 1150 - 1152. [Abstract] [Full Text] [PDF]
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 S. Yendamuri, M. Elfar, J.-C. Walkes, and M. J. Reardon Aortic paraganglioma requiring resection and replacement of the aortic root Interactive CardioVascular and Thoracic Surgery, December 1, 2007; 6(6): 830 - 831. [Abstract] [Full Text] [PDF]
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