SUN-377 Hyperthyroidism to Heart Failure: Armour Thyroid as a Catalyst for Takotsubo Cardiomyopathy

Abstract Disclosure: Y. Abdullah: None. S.H. Ali: None. M.N. Kulkarni-Date: None. P.V. Kumar: None. Introduction: Takotsubo cardiomyopathy (TC), or stress-induced cardiomyopathy, involves systolic dilation and weakening of the left ventricle without myocardial infarction (MI). Hyperthyroidism can result from excessive thyroid hormone intake, termed iatrogenic hyperthyroidism. This case report details TC induced by iatrogenic hyperthyroidism from Armour Thyroid supplementation. Case Presentation: A 58-year-old female with Hashimoto's Thyroiditis, on Armour Thyroid, presented after minor head trauma. Her Armour dose was recently increased to 180 mg (∼300 mcg Levothyroxine) two weeks prior. She exhibited severe anxiety and palpitations but no chest pain or shortness of breath. ECG showed normal sinus rhythm with inverted T waves in V1 and V2 and poor R wave progression. Initial Troponin I was 0.85 ng/L, rising to 20.46 ng/L within 6 hours, raising concern for NSTEMI. Emergent left heart catheterization revealed no obstructive coronary artery disease. Left ventriculography showed moderate to severely reduced left ventricular ejection fraction (EF 37%). Transthoracic echocardiogram (TTE) confirmed TC with reduced EF (35%), apical akinesis, and mid-ventricular hypokinesis. Incidental findings included a bicuspid aortic valve, a dilated aortic root (4.1 cm), and a dilated ascending aorta (5.4 cm). The patient was started on metoprolol tartrate, and Armour Thyroid was discontinued, replaced by Levothyroxine 75 mcg daily. Symptoms improved before discharge, with outpatient follow-ups arranged. A repeat TTE three months post-discharge showed improved EF (63%) without regional wall motion abnormalities. Her TSH was elevated at 11.66, prompting an increase in Levothyroxine dosage. Discussion: Armour Thyroid, derived from desiccated porcine thyroid glands, contains thyroxine (T4) and triiodothyronine (T3). Variability in GI absorption and potency compared to synthetic levothyroxine can lead to hyperthyroidism and cardiovascular effects, including TC. This case highlights Armour Thyroid-induced hyperthyroidism as a precipitating factor for TC, a relationship not extensively studied. Diagnostic tools included ECG, troponin levels, left heart catheterization, and TTE to differentiate TC from other cardiac conditions. Management involved stabilizing cardiovascular status and correcting thyroid dysfunction, leading to symptom resolution and improved cardiac function. Although TC is commonly triggered by stressors, hyperthyroidism-induced TC is rare. This case emphasizes recognizing this correlation for early intervention and management, demonstrating TC's reversible nature with appropriate treatment. Conclusion: This case underscores the need to recognize Armour Thyroid-induced hyperthyroidism as a potential cause of TC. A comprehensive diagnostic approach and prompt intervention are crucial for optimal patient outcomes. Presentation: Sunday, July 13, 2025