Abstract 13293: Albuterol and Hyperthyroidism as Potential Causes of Stress Cardiomyopathy

Introduction Takotsubo cardiomyopathy (TCM) is a recognized reversible process associated with emotional or physical stressors characterized by left ventricular apical ballooning in the absence of obstructive coronary artery disease. We present a unique case of TCM after albuterol use in the setting of hyperthyroidism. Results A 74-year-old woman with history of hyperthyroidism and asthma presented with acute substernal chest pain and progressive dyspnea. She was diagnosed with an asthma exacerbation, started oral prednisone 3 days before presentation, and reported using 16 puffs of her albuterol inhaler the day before. Examination revealed blood pressure 157/100 mmHg, heart rate 135 beats per minute, respiratory rate of 35 breaths per minute, and SpO2 94% on a 5-liter nasal cannula. Lung exam revealed bilateral end-expiratory wheezes, and she appeared in respiratory distress. The remainder of the exam was unremarkable, including cardiac exam. ECG revealed atrial tachycardia with ST elevations in the anterolateral leads concerning for injury. High sensitivity troponin was 1484 ng/L (ref <19), free T4 level 3.63 ng/dL (ref 0.56-1.64 ng/dL), TSH <0.02 μU/mL (ref 0.35-3.30 μU/mL ) with TSH-receptor Ab 8.62 IU/L (ref <1.75 IU/L) consistent with worsening hyperthyroidism when compared to one month prior (free T4: 1.19 ng/dL; TSH: 0.84 μU/mL/mL). Emergent cardiac catheterization showed non-obstructive coronary artery disease and reduced ejection fraction (EF) of 30% with akinesia of the anterolateral, apical, and diaphragmatic segments consistent with TCM. She had a full recovery of systolic function noted on repeat echocardiogram 10 weeks after treatment with guideline-directed therapy. Conclusion TCM is primarily driven by a high catecholamine state that, paradoxically, increases β-2 adrenergic receptor inhibitory signaling, thus, causing preferential depression of apical myocardial function possibly due to topographic receptor distribution. Hyperthyroidism mimics a state of adrenergic excess partially mediated by the upregulation of β-adrenergic receptors by thyroid hormones, and the use of β-2 agonists potentiated the development of TCM.