Abstract
SESSION TITLE: Pulmonary Manifestations of Systemic Disease 1 SESSION TYPE: Med Student/Res Case Report PRESENTED ON: 10/09/2018 03:45 PM - 04:45 PM INTRODUCTION: Graves' disease and other hyperthyroid states are known to have significant effects on the cardiovascular system. These may include increase in heart rate, increase in cardiac output, and decrease in systemic vascular resistance[1]. When heart failure is present, left ventricular dysfunction is frequently reported[2,3]. Thyrotoxicosis rarely presents with pulmonary hypertension and isolated right heart failure. CASE PRESENTATION: A 42-year-old African-American female with no past medical history was sent into the hospital by her outpatient physician for tachycardia. History revealed unintentional 70-pound weight loss over one year. Vital signs were notable for tachycardia identified as atrial fibrillation with rapid ventricular response(>150bpm) on ECG[Figure 1]. Physical exam revealed exophthalmos, symmetrically enlarged and non-tender thyroid, JVD 11 cm, irregularly-irregular tachycardia, decreased breath sounds right lung base, bilateral 2+ pitting edema of lower extremities, and hyperreflexia. Laboratory values indicated suppressed TSH(<0.004 uIU/mL) with elevated T3 Total, T4, and TSH-receptor antibody(494ng/dL, 23.14ug/dL, 111.10IU/L respectively). Diagnosis of Graves' disease was made. Burch-Wartofsky Point Scale of 55 suggesting thyroid storm. Treatment initiated with propranolol, methimazole, glucocorticoids. Chest x-ray showed right pleural effusion, cardiomegaly, and mediastinal widening[Figure 2]. Ultrasound thyroid showed enlarged, heterogeneous, hypervascular gland. Radioactive iodine scan showed diffuse uptake. Echocardiogram showed severe pulmonary hypertension(PASP 88mmHg), right ventricular systolic dysfunction, severe tricuspid regurgitation, left ventricular ejection fraction of 60%. Workup for causes of pulmonary hypertension negative for HIV, connective tissue disease, drugs, toxins, underlying pulmonary disease, and thromboembolic disease. Patient discharged after radioiodine ablation of thyroid gland. Follow up echocardiogram approximately six months after treatment showed significant improvement of both pulmonary hypertension (PASP 35 mmHg) and right heart systolic function. DISCUSSION: This case demonstrates that thyrotoxicosis can induce pulmonary hypertension and right-sided heart failure independent of left-heart disease. Proposed mechanisms of pulmonary hypertension in thyrotoxicosis include autoimmune endothelial dysfunction, endothelial damage from high cardiac output, changes in metabolism of vasodilators or vasoconstrictors, and sympathetic pulmonary vasoconstriction. CONCLUSIONS: It is important to consider thyrotoxicosis in patients with pulmonary hypertension and right heart failure since normalizing thyroid hormones can reverse even severe cardiopulmonary disease. Reference #1: Klein, I., & Ojamaa, K. (2001). Thyroid hormone and the cardiovascular system. The New England Journal of Medicine, 344(7), 501-509. https://doi.org/10.1056/NEJM200102153440707 Reference #2: Klein, I., & Danzi, S. (2007). Thyroid Disease and the Heart. Circulation, 116(15), 1725-1735. https://doi.org/10.1161/CIRCULATIONAHA.106.678326 Reference #3: Siu, C.-W., Yeung, C.-Y., Lau, C.-P., Kung, A. W. C., & Tse, H.-F. (2007). Incidence, clinical characteristics and outcome of congestive heart failure as the initial presentation in patients with primary hyperthyroidism. Heart (British Cardiac Society), 93(4), 483-487. https://doi.org/10.1136/hrt.2006.100628 DISCLOSURES: No relevant relationships by Mina Bushra, source=Admin input No relevant relationships by Kevin Rabii, source=Web Response No relevant relationships by Sally Ziatabar, source=Web Response
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