Pulmonary Vascular Disease |

Pulmonary Hypertension Induced by Hyperthyroidism FREE TO VIEW

Niktha Kasinathan, MD
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Hackensack University Medical Center-Mountainside, Lyndhurst, NJ

Chest. 2015;148(4_MeetingAbstracts):991A. doi:10.1378/chest.2260372
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SESSION TITLE: Pulmonary Vascular Disease Student/Resident Case Report Posters

SESSION TYPE: Student/Resident Case Report Poster

PRESENTED ON: Tuesday, October 27, 2015 at 01:30 PM - 02:30 PM

INTRODUCTION: Hyperthyroidism frequently causes cardiac complications. Common cardiac manifestations related to hyperthyroidism are atrial dysrhythmias, sinus tachycardia, decreased diastolic pressure, increased cardiac output, widened pulse pressure, and cardiac failure. Isolated right heart failure, tricuspid regurgitation, and pulmonary hypertension in patients with thyrotoxicosis have rarely been reported.

CASE PRESENTATION: A 27-year-old male with history of untreated hyperthyroidism for 3 years presented with complaints of dyspnea, unintentional weight loss of 100 pounds, fatigue, and palpitations. Physical examination revealed a diffuse, non-tender and soft goiter with prominent thyroid bruit was noted. Other findings were significant for presence of lid lag, mild proptosis, JVD of 7cm, pansystolic murmur at the left sternal border, hepatomegaly, and bilateral lower extremity edema. EKG showed sinus tachycardia. Laboratory evaluation revealed suppressed TSH of 0.01 uIu/ml (0.34-4.82 uIu/ml), Free T4 of 4.45 ng/dl (0.70-1.48 ng/dl), total T3 of 181 ng/dl (58-159 ng/gl), and normal metabolic panel. Presence of a large goiter with thyroid bruit, mild ophthalmopathy and substantial elevation of thyroid receptor antibodies confirmed Graves’ disease. Treatment with methimazole and propranolol was instituted. 2D echocardiogram showed severe pulmonary hypertension with pulmonary artery systolic pressure of 100 mmHg, trace tricuspid regurgitation and ejection fraction of 65%. No evidence of structural or valvular abnormalities. Initial work up for alternative causes of pulmonary hypertension was negative for parenchymal lung disease, pulmonary thromboembolic disease, hypoxemia, collagen vascular disease, HIV, drugs and toxins. Within three weeks our patient had clinical resolution of dyspnea and lower extremity edema with diuretics and antithyroid therapy. He is scheduled for a repeat 2D Echocardiogram and right heart catheterization once euthyroid status is achieved to confirm the reversibility of hyperthyroidism induced pulmonary hypertension.

DISCUSSION: This case illustrates a rare case of pulmonary hypertension in association with severe hyperthyroidism. Proposed mechanisms of pulmonary hypertension in such cases include high cardiac output-induced endothelial injury, increased metabolism of intrinsic pulmonary vasodilating substances resulting in elevated pulmonary vascular resistance, and autoimmune phenomenon associated with endothelial dysfunction.

CONCLUSIONS: Given it’s treatable entity, it is important to include hyperthyroidism in the differential diagnosis of pulmonary hypertension or unexplained right heart failure.

Reference #1: Ismail H. Reversible pulmonary hypertension and isolated right-sided heart failure associated with hyperthyroidism. Soc Gen Intern Med. 2007; 22: 148-150

Reference #2: Siu C, et al. Hemodynamic changes in hyperthyroidism-related pulmonary hypertension: A prospective echocardiographic study. J Clin Endocrinol Metab. 2007; 92: 1736-1742

DISCLOSURE: The following authors have nothing to disclose: Niktha Kasinathan

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