12199 Uncontrolled Graves Disease Leading To The Development Of Pulmonary Hypertension

Abstract Disclosure: A. Agrawal: None. N. Shaykh: None. C. Marsalisi: None. L. Lam: None. C. Harrison: None. G.Y. Gandhi: None. Introduction: Graves’ disease can cause cardiorespiratory complications by increasing cardiac output, inducing endothelial dysfunction, and increasing the metabolism of intrinsic pulmonary vasodilating substances. Case: A 26-year-old female with a one-year history of Graves’ disease presented with chest pressure, shortness of breath, worsening orthopnea, a 40-pound weight loss, and subjective fevers. Her home methimazole dose was 10 mg daily, which she had missed for four days before admission. Her BP was 153/90 mmHg, heart rate 117 bpm, and temperature 100.7° F. She had mild bilateral proptosis and an enlarged but non-tender thyroid, which caused her difficulty swallowing. TSH was undetectable less than 0.005 mIU/L (0.27-4.2 mIU/L), and thyroid hormone levels were significantly elevated free T4 greater than 7.77 ng/dL (0.8-1.7 ng/dL) and free T3 29.1 pg/mL (2-4.4 pg/mL). TSI was high at 5.66 IU/L (0-0.55 IU/L) as was BNP at 1,642 pg/mL (0-125 pg/mL). Cardiac troponin was 105 ng/dL (less than 14 ng/dL) with a peak of 106 ng/dL. A Burch-Warsofsky score of 50 was highly suggestive of thyroid storm. She initially received 1 mg of IV propranolol, 1,000 mg of PTU, and 4 mg of dexamethasone followed by hydrocortisone 100 mg, methimazole 20, propanol 20 mg, and two doses of SSKI. A transthoracic echocardiogram was remarkable for severe right atrial and ventricular enlargement, and pulmonary artery pressure measured 55 mmHg (normal 20-30 mmHg). Autoimmune testing, including ANA, c-ANCA, p-ANCA, rheumatoid factor, anti-CCP, anti-SS-A, anti-SS-B antibodies, ultrasound for deep vein thrombosis, and ventilation-perfusion scan were negative. There was no history of congenital heart defects or valvulopathy. The patient reached a euthyroid state and was discharged home on methimazole 20 mg daily. Discussion: Although frequently underappreciated, pulmonary hypertension is present in 30 to 65% of Graves’ disease patients when systematically ascertained. Elevated thyroid hormones can increase heart rate, contractility, venous return, and cardiac output. An imbalance between vasoconstriction and vasodilation, along with endothelial dysfunction, can cause pulmonary vascular effects of hyperreactivity, remodeling, and thrombosis. An autoimmune mechanism is plausible due to an association between antithyroid antibodies and pulmonary hypertension. Right heart catheterization remains the gold standard for diagnosis, though in this case, it was not pursued in the acute setting. This case reinforces the importance of screening for pulmonary hypertension in patients with Graves’ disease and possibly normalizing pulmonary hypertension, thereby avoiding irreversible complications. Clinicians should consider reassessing for pulmonary hypertension even after long-term control of the thyrotoxic state, as about 30% of these patients have persistent pulmonary hypertension. Presentation: 6/3/2024