Beyond Atrial Fibrillation: A Case of Thyrotoxicosis-Associated Ischemic Stroke in a Young Patient

While it is presumed that thyrotoxicosis is a contributing factor for cardioembolic stroke secondary to atrial fibrillation (AF), cerebrovascular events in patients without cardiac arrhythmias remain exceptionally rare. We present the case of a 41-year-old African female patient with no traditional stroke risk factors who presented with sudden-onset left hemiplegia and dizziness (National Institutes of Health Stroke Scale (NIHSS) 9). Imaging revealed a right middle cerebral artery (MCA) territory infarct with hemorrhagic transformation and malignant edema (midline shift 3 mm), necessitating emergent decompressive craniectomy. Postoperatively, she developed refractory fever, extreme tachycardia, and hypertension despite broad-spectrum antibiotics for presumed sepsis. Endocrine workup confirmed thyroid storm, and the patient was treated aggressively with propylthiouracil, cholestyramine, and bisoprolol in addition to stress-dose glucocorticoids. Subsequent labs uncovered refractory hypercalcemia, prompting further evaluation that confirmed hyperparathyroidism. Notably, her presentation occurred in the absence of AF. The cardiovascular effects of hyperthyroidism are well-established, with sinus tachycardia and AF being the most common electrocardiographic abnormalities. Emerging evidence further implicates thyroid dysfunction in coagulation pathway dysregulation, which may predispose patients to thromboembolic events independent of cardiac arrhythmias. This case underscores the importance of considering thyrotoxicosis in cryptogenic stroke, even without AF, and highlights gaps in current guidelines regarding anticoagulation therapy for this high-risk population.