Abstract 17328: A Case of Reversible Severe Systolic Cardiomyopathy; Thinking Outside the Box

Abstract

Introduction: Non-ischemic systolic cardiomyopathy is associated with significant morbidity and mortality. Prompt evaluation and timely removal of the potential insult may lead to reverse remodeling and recovery of the left ventricular (LV) systolic function. Case: A 39-year-old female with BMI 40 presented with dyspnea and bilateral lower extremity edema. Vital signs significant for mild tachycardia and hypertension. ECG showed sinus tachycardia. Physical exam revealed bibasilar crackles and 3+ pitting edema of the lower extremities. Laboratory significant for NTpro BNP 563 pg/dL and TSH <0.005 IU/mL with a free T4 of 2.73 ng/dL. Chest x-ray showed pulmonary vascular congestion. Echocardiogram showed severely reduced LV systolic function with ejection fraction (EF) of 27%, global LV hypokinesis and diastolic LV diameter of 6.85 cm. No significant atrial or ventricular arrhythmias noted on Telemetry. A CT angiography of the coronary arteries showed no evidence of calcification or obstructive coronary disease. Additional labs revealed severely elevated TSH receptor antibody and thyroid stimulating immunoglobulin. Diffuse thyroid enlargement noted on ultrasound. Patient was diagnosed with Grave’s disease (GD) with Burch-Wartofsky score of 30 indicating an impending thyroid storm. She was treated with Metoprolol and Methimazole. She underwent intravenous diuresis and was started on guideline-directed medical therapy for systolic cardiomyopathy. In follow-up after 6 months, her TSH had normalized. On repeat imaging, her LVEF improved to > 50% with diastolic LV diameter of 5.6 cm. Discussion: This patient was diagnosed with non-ischemic dilated systolic cardiomyopathy due to severe hyperthyroidism from GD. Thyrotoxicosis-induced systolic cardiomyopathy occurs in about 1% of patients with GD and is associated with increased morbidity and mortality. Excess thyroid hormones in thyrotoxicosis can affect multiple regulatory and structural genes of cardiac myocytes resulting in abnormal intracellular calcium regulation and impaired LV systolic and diastolic function. Our experience is consistent with literature demonstrating the importance of timely diagnosis and treatment of this reversible cause of systolic cardiomyopathy.