Not even a zebra: when an ‘ordinary acute coronary syndrome’ turns out to be a thyrotoxicosis-associated takotsubo syndrome

A 75-year-old female patient presented to the emergency department with dyspnoea without chest pain. The personal history was significant for chronic obstructive pulmonary disease, smoking, and major depression. The electrocardiogram showed sinus tachycardia with ST elevations in V2 to V5 (Panel A). Clinical chemistry was significant for elevated N-terminal of prohormone brain natriuretic peptide (2892  ng/L), dynamic elevation of troponin T (baseline 21 ng/L, peak 78 ng/L), and normal creatine kinase. Echocardiography revealed left ventricular systolic dysfunction with reduced left ventricular ejection fraction around 40% with apical hypo- to akinesia and left ventricular thrombus (Panels D, E andF, Supplementary material online, VideosSupplementary material online,Videos). Acute myocardial infarction was suspected. However, urgent coronary angiography ruled out significant coronary artery disease (Panel I). Thyroid function tests revealed hyperthyroidism with a suppressed thyroid-stimulating hormone (<0.01 mU/L) and elevated free thyroxine (42.2  pmol/L). Thyroid ultrasound showed a cystic nodule (4 cm) in the left thyroid lobe suggestive for toxic adenoma (Panel J). Thyroid suppressive therapy was initiated with carbimazole alongside with usual heart failure therapy and anticoagulation. Over the following 5  days, the clinical status significantly improved with regression of dyspnoea, tachycardia, and electrocardiographic abnormalities (Panels B andC). Echoc...
Source: European Heart Journal - Category: Cardiology Source Type: research