Case Presentation: A 49-year-old male with a history of OSA on CPAP, Parkinson’s disease, hyperlipidemia, and obesity presented to the emergency department with a three-week history of progressive dyspnea on exertion (DOE) and abdominal pain on exertion that radiated into his chest, neck, and jaw that resolved after rest. He had an intentional 50-lb weight loss in the past six months. He denied any fevers, chills, cough, gastrointestinal symptoms, and leg swelling. His vital signs were HR 100s, BP 113/84 mm/Hg, SaO2 >94% on room air. Physical exam showed jugular venous distention and trace lower extremity edema. CBC and BMP were unremarkable, troponin negative, D-dimer 308 ng/mL, and proBNP 7110 pg/mL. ECG demonstrated non-specific ST-T wave changes. He underwent CTA chest which was negative for pulmonary embolus but showed dilation of the main pulmonary artery suggestive of pulmonary hypertension, mild bilateral bibasilar pulmonary edema, and small bilateral pleural effusions. Echocardiogram showed reduced systolic function (EF 30%), systolic pulmonary artery hypertension (65 mmHg), mild dilatation of the aortic root, mild mitral and tricuspid regurgitation, and mild dilatation of the left atrium with a mass measuring 7.3 cm x 3.9 cm prolapsing across the mitral valve into the left ventricle concerning for myxoma. Coronary angiography showed two-vessel coronary artery disease (CAD) and moderate-severe functional mitral stenosis. Cardiac MRI demonstrated the origin of the atrial mass arising from the interatrial septum, four chamber enlargement, and an EF of 21%. Excision of the mass was deemed urgent and he underwent resection via atriotomy. The mass measured 7 x 4 x 5 cm and pathology confirmed myxoma. Given the patient´s severe LAD and LCX stenosis, he also underwent CABG. The patient was discharged home three days after his operations and his EF will be evaluated in six months via echocardiogram.

Discussion: Myxomas are the most common primary cardiac tumor but are extremely rare. The clinical manifestations are non-specific cardiopulmonary symptoms like DOE, pulmonary and pedal edema which are often attributed to more common cardiopulmonary diseases like heart failure (1). While this patient did have heart failure confirmed via echocardiogram, the severity (EF-21%) pointed to an additional pathology hindering left ventricular function. In his case, it was due to severe LAD and LCX stenosis requiring CABG. CAD with concomitant atrial myxomas has been scantly documented in literature (2). The pathogenesis of CAD in the setting of myxomas is still being established. Most commonly, it is due to thrombotic plaques dislodging from the myxoma to the coronary arteries (5). There is also an overproduction of interleukins 6 and 8 in the setting of myxomas, which may induce a prothrombotic state, neutrophil migration, and myxoma cell fragment adhesion to coronary artery endothelium (5). These interleukins are observed to cause a negative inotropic effect on cardiac tissue, leading to further cardio depression (5).

Conclusions: Reassessing EF following resection is key to further understanding CAD and recovery of EF in patients with myxomas.