7659 Iodinated Contrast Induced Thyrotoxicosis Leading to Takotsubu Cardiomyopathy

Abstract Disclosure: A. Jain: None. E. Naous: None. S. Sedrakyan: None. A.T. Sweeney: None. Background: Thyrotoxicosis may cause many cardiovascular manifestations including tachycardia, hypertension, atrial fibrillation and heart failure. Iatrogenic exposure to iodinated contrast media (ICM) precipitating iodine induced thyrotoxicosis (or the Jod-Basedow phenomenon) is often overlooked. Here, we describe a case of iodine induced thyrotoxicosis leading to takotsubu cardiomyopathy, following multiple exposures to ICM. Case Presentation: An 88-year-old male with a history of hypertension, dyslipidemia, chronic obstructive pulmonary disease, and an ED visit one month ago for hemoptysis for which a CT Angiography (CTA) of the chest was obtained (which excluded Pulmonary Embolism(PE)), presented with fever and shortness of breath. On physical examination his temperature was 100.3F, heart rate was 104bpm, blood pressure 130/62mmHg, respiratory rate was 20/min and saturation was 88% (room air). He was frail but his examination was otherwise unremarkable. Electrocardiogram (EKG) revealed sinus tachycardia. Chest CTA excluded PE. Transthoracic echocardiogram (TTE) showed an ejection fraction (EF) of 73% and no wall motion abnormalities. He was admitted to the hospital for a viral upper respiratory infection and was treated conservatively with bronchodilators. Odynophagia prompted a CT with contrast of the neck soft tissue, which was unrevealing. He was planned to be discharged the next day, but overnight developed severe abdominal pain, and atrial fibrillation with a rapid ventricular response (Troponin t was 191 ng/L (normal {nl}: <9 ng/L)). EKG showed new T-wave inversions in the anterolateral leads, raising a suspicion of myocardial ischemia. A repeated TTE revealed a new drop in EF from 73 to 41%, with new apical akinesis, suspicious for takotsubo cardiomyopathy. CT of the abdomen with contrast was unrevealing. Lab results showed a suppressed TSH of <0.01uIU/mL (nl: 0.34-5.60 uIU/mL), elevated FT4 of 13ng/dL (nl: 0.93-1.70 ng/dL), and TSI 4.97 IU/ L (nl: 0-0.55 IU/ L). Endocrinology was consulted. His thyroid examination was normal, and he had no eye findings. Neck ultrasound revealed a homogeneous thyroid gland without any nodules. His clinical course was consistent with the diagnosis of acute thyrotoxicosis precipitating takotsubu cardiomyopathy. He likely developed iodine induced thyrotoxicosis from multiple exposures to ICM, in a background of previously undiagnosed Graves’ disease. Discussion: Screening for thyroid disease is critical in patients with new onset tachyarrhythmias and stress cardiomyopathy. Iodine induced thyrotoxicosis typically presents after patients with underlying thyroid disease are exposed to iodinated contrast. Prior to ordering studies requiring ICM, it is important to thoroughly evaluate patients for possible pre-existing thyroid disease. Presentation: 6/2/2024