INTRODUCTION

Thyrotoxicosis is caused by excess thyroid hormone levels from inappropriately high circulating hormone concentrations that can cause multi-organ dysfunction. One of the well-known cardiovascular manifestations includes stress cardiomyopathy, coronary vasospasm, myocarditis, and even mimic ST-segment elevation myocardial infarction (STEMI).¹ Thyrotoxicosis and hyperthyroidism are known to cause high-output failure and left ventricular hypertrophy due to sustained increases in both cardiac output and preload from increased expression of myocardial sarcoplasmic reticulum calcium-dependent adenosine triphosphate (ATP), which results in increased heart rate and myocardial contractility.^2-3 Untreated hyperthyroidism may result in STEMI, which is rarely encountered as its first clinical manifestation.⁴

CASE DESCRIPTION

A 51-year-old female with no known disease sought consultation because of sudden onset severe chest pain accompanied by one week history of easy fatigability, palpitations, and three pillow orthopnea. Upon arrival at the ED, there was persistent chest pain characterized as continuous, sharp, and nonradiating accompanied by vomiting, tachycardia as high as 140 beats per minute (BPM), and hypotension as low as 70/50 mmHg in both arms. There was no carotid bruit with a jugular venous pressure of 8 mmHg above the sternal angle. On cardiac examination, there were distinct S1 and S2 sounds, no heaves, thrills, murmurs, or S3 gallop. Pulses were full and equal in all extremities with no bipedal edema. The patient was initially administered fluid resuscitation of 1 L of crystalloid solution, hooked to a low-dose norepinephrine drip, and given analgesia using morphine. Blood pressure was stabilized; however, she was still tachycardic; hence, esmolol IV was administered. The electrocardiogram (ECG) showed STEMI in lead aVR with ST depression on leads V2–V6 (Figure 1A) with an elevated troponin T of 79 ng/L. She was also started on an acute coronary syndrome (ACS) regimen, namely aspirin 300mg, ticagrelor 180mg, enoxaparin 60 mg, and rosuvastatin 40 mg. Coronary angiogram revealed normal coronary arteries (Figure 1B). She was eventually admitted to the cardiology critical care unit. Ancillaries were performed to determine the etiology of the disease (See Table 1). These tests showed severe hyperthyroidism with TSH of <0.01 uIU/mL, FT4 >12 ng/dL and FT3 >20 pg/mL with Burch Wartofsky score of 50. Neck ultrasound showed diffuse parenchymal enlargement of the thyroid gland with TSH receptor antibodies (TRAb) of 32.47 IU/L, suggestive of Graves’ disease. Inflammatory markers, specifically high-sensitivity C-reactive protein (hs-CRP) and D-dimer, were normal. There was elevated NT-proBNP (1394 pg/mL), and echocardiogram showed a reduced EF of 28.7% with dilated LV and global hypokinesia with mild pulmonary hypertension. There was an increasing norepinephrine requirement; hence, started on dobutamine drip. There was immediate initiation of hyperthyroid regimen, specifically methimazole, propranolol, and steroids. Vasopressors were eventually titrated off. The patient was also managed as heart failure with reduced ejection fraction; hence, guided directed medical therapy was started by administering sacubitril-valsartan, empagliflozin, and spironolactone. The patient was closely monitored during critical care and was eventually transferred to a regular room. When she was out of thyroid storm, additional ancillaries were performed, specifically myocardial perfusion imaging using technetium-99m sestamibi scan, which showed no scintigraphic evidence of resting ischemia with markedly improved LV systolic function with ejection fraction of 61% (Figure 1C). She was eventually discharged with methimazole, propranolol, and the pillars of heart failure therapy.