Primary cardiac tumors are rare, with a prevalence of about 0.001-0.03% in autopsy series and myxomas constituting the most common subtype. Cardiac myxomas predominantly originate in the left atrium (75%) and, less frequently, the right atrium (15-20%). Although biologically benign, myxomas carry a risk of embolization associated with complications such as strokes, transient ischemic attacks (TIAs), and neurological deficits. Herein, a 46-year-old female presented with symptoms including dizziness, shortness of breath, and general fatigue. Initial electrocardiogram (ECG) evaluation revealed an inverted T wave in leads aVL and V1, poor R-wave progression (PRWP), nonspecific ST-T wave changes (NSSTTWC), and a right ventricular conduction delay (RVCD) with a primitive epsilon wave in lead V1. A 2D transthoracic echocardiography showed impaired diastolic filling, diminished relaxation, mild left atrium dilation, and a pedunculated mass suggestive of a right atrial myxoma. Cardiothoracic surgery successfully excised the mass weighing 35 grams and measuring 4.7 x 4.5 x 3.5 cm. Histopathological examination confirmed the cardiac myxoma diagnosis and revealed compelling additional findings of multiple dark red hemorrhagic foci and an inflammatory infiltrate, implying an atypical proinflammatory phenotype with potential postoperative complications. Despite successful resection of the myxoma, follow-up ECGs showed persistent inverted T wave morphology in leads aVL and V1, a primitive epsilon wave associated with RVCD, and a right axis deviation, though the NSSTTWC and PRWP patterns resolved. Subsequent echocardiograms noted no structural abnormalities, ruling out remnant intracavitary masses or atrial appendage thrombosis. These persistent electrophysiological abnormalities suggest underlying structural or conduction system abnormalities resembling a pseudo-arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) constellation. The mechanism(s) remains in question; however, genetic predisposition, mild congenital anomalies, and/or inflammation-induced fibrotic changes might have contributed to altered electrical conduction. In conclusion, our case highlights the complexity of cardiac myxoma presentations, offers insights into persistent conduction abnormalities, and suggests immunophenotyping to predict postoperative recovery while facilitating targeted therapies.