A common link between Endocrinology and Cardiology is T3, the active form of thyroid hormone. Approximately 5-25% of patients with hyperthyroidism have atrial fibrillation, but a far less common cardiovascular disease (CVD) associated with thyrotoxicosis is myocardial infarction (MI). There are few reported cases of hyperthyroidism causing STEMI, NSTEMI, coronary vasospasm, and autoimmune myocarditis. We present a previously healthy 58-year-old female seen at the emergency department (ED) for nighttime/early morning chest pain, dyspnea and diaphoresis. She denied prior episodes or family history of CVD. EKG showed incomplete right bundle branch block and anterior T-wave inversions. Troponin peaked at 13 ng/mL. Echocardiogram was unremarkable. Left heart catherization demonstrated non-obstructive coronary artery disease concerning for vasospasm. Pertinent laboratories showed decreased TSH (< 0.005 μU/mL) and elevated total T3 and free T4 (2.19 ng/dL). Differentials for thyrotoxicosis included primary hyperthyroidism, spurious results (patient was taking supplement with biotin and iodine), and stress-induced thyroid function alteration. Further workup revealed negative Thyroid Stimulating Immunoglobulin (TSI) and positive TSH Receptor Antibodies (TRAb). Chest pain resolved and she was discharged, but returned days later with same complaints and elevated troponin. Cardiac differentials were myocarditis in the setting of autoimmune thyroiditis vs vasospastic angina. Serial EKGs had no signs of myocarditis. She denied prior viral infection, autoimmune conditions, recreational drugs, appetite suppressants, ephedrine, or migraine medications. Cardiac MRI was not consistent with myocarditis, instead suspicion was raised for subacute MI with nonobstructive coronary arteries (MINOCA). Based on Coronary Vasomotion Disorders International Study Group (COVADIS) criteria, she had nitro-sensitive vasospastic angina. In the setting of thyrotoxicosis and positive TRAb, she was diagnosed with coronary vasospasm NSTEMI triggered by Graves'. Autoimmune thyroid disease may be undiagnosed 50% of the time, unknowingly contributing to CVD. T3 has direct and indirect cardiovascular effects. It promotes catecholaminergic stimulation and acts as a positive ionotrope and chronotrope. Excess T3 creates a hypermetabolic state that can rarely trigger severe coronary vasospasm. MI with < 50 % stenosis is defined as MINOCA, accounting for 6% of acute infarctions that undergo angiography. Non-atherosclerotic etiologies of MINOCA include coronary vasospasm, embolism/thrombus, anemia, hypotension, and thyrotoxicosis. Our patient had two of these, and to the best of our knowledge, this is the first reported case of a troponin >0.5 ng/mL secondary to Graves’ disease induced MINOCA.