Case Presentation: A 61-year-old woman with a remote history of provoked pulmonary embolism presented to the emergency department with persistent, substernal chest pain associated with nausea and dyspnea. Vital signs revealed a heart rate of 137, blood pressure of 182/94, and hypoxia requiring 4L oxygen. On exam, she appeared uncomfortable and cardiac exam was notable for tachycardia with regular rhythm. Neurologic and pulmonary exams were normal. Bloodwork was notable for an elevated alkaline phosphatase of 186 U/ and a BNP of 372 pg/mL with no known baseline. EKG demonstrated sinus tachycardia and 1-2mm ST elevations in the anterior and the inferior leads. The first troponin level was 6.0 ng/mL. Under the presumptive diagnosis of a STEMI, she underwent a coronary angiogram which revealed unobstructed, normal coronary arteries. Additional history was obtained which revealed a 20lb weight loss over last 3 months, recent hair loss, palpitations, and fatigue. Following the coronary angiogram, she had worsening tachycardia and salvos of supraventricular tachycardia requiring intravenous adenosine. An echocardiogram revealed that she had severe left ventricular dysfunction with severe hypokinesis of the mid- and apical segments. A TSH drawn prior to the procedure was undetectable (<0.01), with fT4 4.2 and total T3 254. She was ultimately diagnosed with stress cardiomyopathy secondary to thyroid storm from Grave’s Disease. She was treated with propylthiouracil, high-dose hydrocortisone, Lugol’s iodine solution, and an esmolol infusion for tachycardia and made a full recovery.
Discussion: Our diagnostic approach was challenging given this patient’s initial presentation of unremitting chest pain. Further investigation revealed that the patient had experienced symptoms that are associated with hyperthyroid disease. A worsening of these symptoms can occur when patients with untreated hyperthyroidism are exposed to iodinated contrast, which in this case was from the coronary angiogram. The diagnosis of thyroid storm is often clinical and requires the presence of life-threatening conditions such as severe cardiac dysfunction. The severity of the patient’s symptoms and objective evidence of heart failure, were consistent with this disease. The typical imaging finding of Takotsubo cardiomyopathy is apical ballooning, which reflects the depressed mid and apical ventricular segments. Natriuretic peptides and troponin levels are often elevated in these patients. Therefore, it is important to exclude obstructive CAD or the presence of acute plaque ruptures. Takotsubo cardiomyopathy has often been reported in the setting of physical or emotional stress, suggesting that the effect of cathecholamines on myocardial tissue may contribute to the pathophysiology.
Conclusions: We suspect that this patient’s heart failure was provoked by a massive sympathetic discharge secondary to high circulating levels of thyroid hormone resulting in a high output cardiac state. Prompt reduction of thyroid hormone levels and treatment with goal-directed medical therapy is critical in improving the mortality in these patients.